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Diazinon
IUPAC name[hide]
O,O-Diethyl O-[4-methyl-6-(propan-2-yl)pyrimidin-2-yl]
phosphorothioate
Other names[hide]
Diethoxy-[(2-isopropyl-6-methyl-4-pyrimidinyl)oxy]thioxophosphorane
Identifiers
CAS number
333-41-5
PubChem
3017
ChemSpider
2909
UNII
YUS1M1Q929
KEGG
D07856
ChEBI
CHEBI:34682
ChEMBL
CHEMBL388560
ATCvet code
QP53AF03
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C12H21N2O3PS
Molar mass
304.35 g mol1
Appearance
Density
Solubility in water
40 mg/L[2]
log P
3.81 (octanol/water)[3]
?)
Infobox references
Diazinon (IUPAC name: O,O-Diethyl O-[4-methyl-6-(propan-2-yl)pyrimidin-2-yl]
phosphorothioate, INN -Dimpylate), a colorless to dark brown liquid, is a thiophosphoric acid ester
developed in 1952 by Ciba-Geigy, a Swiss chemical company (later Novartis and then Syngenta). It is a
nonsystemic organophosphate insecticide formerly used to control cockroaches, silverfish, ants,
and fleas in residential, non-food buildings. Diazinon was heavily used during the 1970s and early
1980s for general-purpose gardening use and indoor pest control. A bait form was used to control
scavenger wasps in the western U.S. Diazinon is used in flea collars for domestic pets in Australia and
New Zealand. Residential uses of diazinon were outlawed in the U.S. in 2004 but it is still approved for
[4]
agricultural uses. An emergency antidote is atropine.
Contents
[hide]
History[edit]
Diazinon was developed in 1952 by the Swiss company Ciba-Geigy as a replacement for the insecticide
DDT. Diazinon became available for mass use in 1955, as DDT production tapered. Prior to 1970
diazinon had issues with contaminants in the solution. However, by the 1970s, alternative purification
methods were utilized to reduce residual materials. After this, diazinon became an all-purpose indoor
and outdoor commercial pest control product. In 2004, U.S. residential use of diazinon was outlawed,
except for agricultural purposes and cattle ear tags .
Synthesis[edit]
According to the German Patent bureau, the industrial synthesis of diazinon is as follows:
-isobutyrylaminocrotonic acid amine was cyclized with NaOR (R is either a hydrogen or
aliphatic chain of 1 to 8 carbons) in a mixture of 0 to 100% by weight of water and an alcohol
having 1 to 8 carbon atoms, above 90C (but below the boiling point of the mixture used).
Sodium pyrimidinolate was precipitated out in an inert solvent, such as benzene, with
simultaneous removal of the water formed. The potassium salt is then reacted with
diethylthiophosphoryl chloride by heating for several hours. When the reaction finished, the
potassium chloride formed was washed with water and the solvent was removed under
reduced pressure leaving diazinon.
Colics
Diarrhea and/or Vomiting
Vertigo
Headaches
Miosis
Bradycardia
Sudden Drop in blood pressure
Convulsion
Apnea
Lethal Dose
LD50
Observations
Symptoms in humans[edit]
Intoxication of diazinon produces the following signs and symptoms:
Typically treatments will vary depending on exposure and method of administration of the toxin.
Critical biomarkers such as urine samples, blood content and heart rates are measured while
detoxifying the patient. Common treatments for patients suffering from diazinon poisoning include:
Assisted Breathing
Intravenous fluids (IV)
Irrigation (washing of the skin and eyes)
[5]
Medicinal Treatments; including the antidotes atropine and oxime.
Gastric Lavage
Patients that continue to improve over the first 4 to 6 hours (after medical treatment) usually
recover unscathed. Prolonged treatment often is needed to reverse the poisoning, including
intensive care hospitalization and long-term therapy. Some toxicity may persist for weeks or
months, or even longer.
Saccharin
From Wikipedia, the free encyclopedia
Saccharin[1]
IUPAC name[hide]
2H-16,2-benzothiazol-1,1,3-trione
Other names[hide]
Benzoic sulfimide
Ortho sulphobenzamide
Identifiers
CAS number
81-07-2
PubChem
5143
ChemSpider
4959
UNII
FST467XS7D
KEGG
D01085
ChEBI
CHEBI:32111
ChEMBL
CHEMBL310671
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C7H5NO3S
Molar mass
183.18 g mol1
Appearance
Density
0.828 g/cm3
Melting point
228.8-229.7 C
Solubility in water
1 g per 290 mL
?)
Infobox references
[2]
Saccharin is an artificial sweetener with effectively no food energy which is approximately 300 times
as sweet as sucrose or table sugar, but has a bitter or metallic aftertaste, especially at high
concentrations. It is used to sweeten products such as drinks, candies, cookies, medicines, and
toothpaste.
Origins[edit]
Saccharin derives its name from the word "saccharine", meaning of, relating to, or resembling sugar.
Properties[edit]
[3]
History[edit]
Government regulation[edit]
Starting in 1907, the USDA began investigating saccharin as a direct result of the Pure Food and Drug
Act. Harvey Wiley, then the director of the bureau of chemistry for the USDA, viewed it as an illegal
substitution of a valuable ingredient (sugar) by a less valuable ingredient. In a clash that had career
consequences, Wiley told President Theodore Roosevelt that "Everyone who ate that sweet corn was
deceived. He thought he was eating sugar, when in point of fact he was eating a coal tar product totally
devoid of food value and extremely injurious to health." But Roosevelt himself was a consumer of
saccharin, and, in a heated exchange, Roosevelt angrily answered Wiley by stating, "Anybody who says
[15]
saccharin is injurious to health is an idiot." The episode proved the undoing of Wiley's career.
In 1911, the Food Inspection Decision 135 stated that foods containing saccharin were adulterated.
However, in 1912, Food Inspection Decision 142 stated that saccharin was not harmful.
More controversy was stirred in 1969 with the discovery of files from the FDA's investigations of 1948
and 1949. These investigations, which had originally argued against saccharin use, were shown to
prove little about saccharin being harmful to human health. In 1972, the USDA made an attempt to
[16][full citation needed]
completely ban the substance.
However, this attempt was also unsuccessful, and the
sweetener continued to be widely used in the United States. It is now the most popular artificial
sweetener after sucralose and aspartame.
In the European Union, saccharin is also known by the E number (additive code) E954.
The current status of saccharin is that it is allowed in most countries, and countries like Canada are
[17]
considering lifting their previous ban of it as a food additive. The claims that it is associated with
[18]
bladder cancer were shown to be unfounded in experiments on primates. (It is, however, prohibited to
[19]
mail saccharin tablets or packets to France.)
Saccharin was formerly on California's list of chemicals known to the state to cause cancer for the
[20]
purposes of Proposition 65, but it was delisted in 2001.
Chemistry[edit]
[26]
Saccharin can be produced in various ways. The original route by Remsen & Fahlberg starts
[27]
with toluene; another route begins with o-chlorotoluene. Sulfonation by chlorosulfonic acid gives
the ortho and para substituted sulfonyl chlorides. The ortho isomer is separated and converted to
the sulfonamide with ammonia. Oxidation of the methyl substituent gives the carboxylic acid, which
[28]
cyclicizes to give saccharin free acid:
In 1950, an improved synthesis was developed at the Maumee Chemical Company of Toledo,
Ohio. In this synthesis, anthranilic acid successively reacts with nitrous acid (from sodium
[28]
nitrite and hydrochloric acid), sulfur dioxide, chlorine, and then ammonia to yield saccharin:
The free acid of saccharin has a low pKa of about 2 (the acidic hydrogen being that attached
[29][30]
to the nitrogen).
Saccharin can be used to prepare exclusively
[31]
disubstituted amines from alkyl halides via a nucleophilic substitution, followed by Gabriel
synthesis.
Aspartame
From Wikipedia, the free encyclopedia
(Redirected from Aspertame)
Aspartame[1]
IUPAC name[hide]
N-(L--Aspartyl)-L-phenylalanine,
1-methyl ester
Identifiers
CAS number
22839-47-0
ChemSpider
118630
UNII
Z0H242BBR1
DrugBank
DB00168
KEGG
C11045
ChEBI
CHEBI:2877
ChEMBL
CHEMBL171679
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C14H18N2O5
Molar mass
294.30 g mol1
Density
1.347 g/cm3
Melting point
246247 C
Boiling point
decomposes
Solubility in water
sparingly soluble
Solubility
Acidity (pKa)
4.56.0[2]
Hazards
NFPA 704
1
1
0
Except where noted otherwise, data are given for materials in
?)
Infobox references
Aspartame (APM; /sprtem/ or /sprtem/) is an artificial, non-saccharide sweetener used as
a sugar substitute in some foods and beverages. In the European Union, it is codified as E951.
Aspartame is a methyl ester of the aspartic acid/phenylalanine dipeptide. It was first sold under the
brand name NutraSweet; It was first synthesized in 1965 and the patent expired in 1992.
The safety of aspartame has been the subject of several political and medical
[3][4][5]
controversies, congressional hearings and Internet hoaxes
since its initial approval for use in food
[6]:2
products by the U.S. Food and Drug Administration (FDA) in 1981.
The European Food Safety
Authority concluded in its 2013 re-evaluation that aspartame and its breakdown products are safe for
[7]
[8]
human consumption at current levels of exposure, corroborating other medical reviews. However,
because its breakdown products include phenylalanine, aspartame must be avoided by people with the
genetic condition phenylketonuria (PKU).
Chemistry[edit]
Aspartame is a methyl ester of the dipeptide of the natural amino acids L-aspartic acid and Lphenylalanine. Under strongly acidic or alkaline conditions, aspartame may
generate methanol by hydrolysis. Under more severe conditions, thepeptide bonds are also hydrolyzed,
[9]
resulting in the free amino acids.
[10]
While known aspects of synthesis are covered by patents, many details are proprietary. Two
approaches to synthesis are used commercially. In the chemical synthesis, the two carboxyl groups of
aspartic acid are joined into an anhydride, and the amino group is protected by a compound that will
prevent further reactions of that group. Phenylalanine is methylated and combined with the N-protected
aspartic anhydride, then the blocking group is removed from aspartic acid by acid hydrolysis. The
drawback of this technique is that a byproduct, the bitter tasting -form, is produced when the wrong
carboxyl group from aspartic acid links to phenylalanine. A process using an enzyme from Bacillus
thermoproteolyticus to catalyze the condensation of the chemically altered amino acids will produce high
yields without the -form byproduct. A variant of this method, which has not been used commercially,
uses unmodified aspartic acid, but produces low yields. Methods for directly producing aspartylphenylalanine by enzymatic means, followed by chemical methylation, have also been tried, but not
[11]
scaled for industrial production.
Beta-aspartame differs from aspartame based upon which carboxyl group of aspartate binds to the
nitrogen of phenylalanine.
Aspartame, an artificial sweetener, is approximately 200 times sweeter than sucrose, or table sugar.
Due to this property, even though aspartame produces four kilocalories of energy per gram when
metabolized, the quantity of aspartame needed to produce a sweet taste is so small that its caloric
[8]
contribution is negligible. The taste of aspartame and other artificial sweeteners differs from that of
table sugar in the times of onset and how long the sweetness lasts, though aspartame comes closest to
[10]
sugar's taste profile among approved artificial sweeteners. The sweetness of aspartame lasts longer
than sucrose, so it is often blended with other artificial sweeteners such as acesulfame potassium to
[12]
produce an overall taste more like sugar. Aspartame can be synthesized from its constituent amino
acids, L-phenylalanine andL-aspartate.
Like many other peptides, aspartame may hydrolyze (break down) into its constituent amino acids under
conditions of elevated temperature or high pH. This makes aspartame undesirable as a baking
sweetener, and prone to degradation in products hosting a high pH, as required for a long shelf life. The
stability of aspartame under heating can be improved to some extent by encasing it in fats or
in maltodextrin. The stability when dissolved in water depends markedly on pH. At room temperature, it
is most stable at pH 4.3, where its half-life is nearly 300 days. At pH 7, however, its half-life is only a few
days. Most soft-drinks have a pH between 3 and 5, where aspartame is reasonably stable. In products
that may require a longer shelf life, such as syrups for fountain beverages, aspartame is sometimes
[13]
blended with a more stable sweetener, such as saccharin.
Aspartame's major decomposition products are its cyclic dipeptide (in a 2,5-diketopiperazine, or DKP,
form), the de-esterified dipeptide (aspartyl-phenylalanine), and its constituent
[14]
[15]
[16]
components, phenylalanine, aspartic acid, and methanol. At 180 C, aspartame undergoes
[17]
decomposition to form a diketopiperazine derivative.
In products such as powdered beverages, the amine in aspartame can undergo a Maillard reaction with
the aldehyde groups present in certain aroma compounds. The ensuing loss of both flavor and
sweetness can be prevented by protecting the aldehyde as an acetal.
Descriptive analyses of solutions containing aspartame report a sweet aftertaste as well as bitter and
[18]
off-flavor aftertastes.
Citing data from a Japanese study that had not been available to the members of the PBOI, and after
seeking advice from an expert panel that found fault with statistical analyses underlying the PBOI's
[6]:53
hesitation, yet argued against approval,
FDA commissioner Hayes approved aspartame for use in
[6]
dry goods. In 1983, the FDA further approved aspartame for use in carbonated beverages, and for use
in other beverages, baked goods, and confections in 1993. In 1996, the FDA removed all restrictions
from aspartame, allowing it to be used in all foods.
Several European Union countries approved aspartame in the 1980s, with EU-wide approval in 1994.
The European Commission Scientific Committee on Foodreviewed subsequent safety studies and
reaffirmed the approval in 2002. The European Food Safety Authority reported in 2006 that the
previously establishedAcceptable daily intake was appropriate, after reviewing yet another set of
[24]
studies.
Compendial status[edit]
[25]
British Pharmacopoeia
[26]
United States Pharmacopeia
subsequently. The approval was rescinded the following year, but after outside reviews of the
problematic tests and additional testing, final approval was granted in 1981. Because allegations
[6][31][32]
of conflicts of interest marred the FDA's approval of aspartame,
the U.S. Government
Accountability Office reviewed the actions of involved officials in 1986 and the approval process in 1987;
neither the allegations of conflict of interest nor problems in the final approval process were
[6][33]
substantiated.
In addition, the Centers for Disease Control investigated in 1984 and was unable to find any
[34]
significant epidemiological associations to serious risk or harm.
Since December 1998, a widely circulated email hoax cited aspartame as the cause of numerous
[35]
diseases.
The weight of existing scientific evidence indicates that aspartame is safe at current levels of
[8]
consumption as a non-nutritive sweetener. Reviews conducted by regulatory agencies decades after
[36]
aspartame was first approved have supported its continued availability. The consumer
advocacy group the Center for Science in the Public Interest continues to promote the position that
[37]
aspartame is not safe.
Intake[edit]
The acceptable daily intake (ADI) value for aspartame, as well as other food additives studied, is
defined as the "amount of a food additive, expressed on a body weight basis, that can be ingested daily
[45]
over a lifetime without appreciable health risk." The Joint FAO/WHO Expert Committee on Food
Additives (JECFA) and theEuropean Commission's Scientific Committee on Food has determined this
[46]
value is 40 mg/kg of body weight for aspartame, while FDA has set its ADI for aspartame at
[47]
50 mg/kg.
The primary source for exposure to aspartame in the United States is diet soft drinks, though it can be
consumed in other products, such as pharmaceutical preparations, fruit drinks, and chewing gum
[8]
among others in smaller quantities. A 12 US fluid ounce (355 ml) can of diet soda contains 180
milligrams (0.0063 oz) of aspartame, and for a 75 kg (165 lb) adult, it takes approximately 21 cans of
diet soda daily to consume the 3,750 milligrams (0.132 oz) of aspartame that would surpass the FDA's
[47]
50 milligrams per kilogram of body weight ADI of aspartame from diet soda alone.
Reviews have analyzed studies which have looked at the consumption of aspartame in countries
worldwide, including the United States, countries in Europe and Australia, among others. These reviews
have found that the even high levels of intake of aspartame, studied across multiple countries and
different methods of measuring aspartame consumption, is well below the ADI for safe consumption of
[8][38][41][46]
aspartame.
Reviews have also found that populations that are believed to be especially high
consumers of aspartame such as children and diabetics are below the ADI for safe consumption, even
[8][38]
considering extreme worst-case scenario calculations of consumption.
In a report released on 10 December 2013, the EFSA said that, after an extensive examination of
evidence, it ruled out the "potential risk of aspartame causing damage to genes and inducing cancer,"
[48]
and deemed the amount found in diet sodas an amount safe to consume.
Metabolites[edit]
Aspartame is rapidly hydrolyzed in the small intestines. Even with ingestion of very high doses of
[8]
aspartame (over 200 mg/kg), no aspartame is found in the blood due to the rapid breakdown. These
metabolites have been studied in a wide range of populations including infants, children, adolescents,
and healthy adults. In healthy adults and children, even enormous doses of aspartame do not lead to
plasma levels of metabolites that are a concern for safety.
Upon ingestion, aspartame breaks down into residual components, including aspartic
[49]
[50]
acid, phenylalanine, methanol, in ratio of 4:5:1 by mass and further breakdown products
[51]
including formaldehyde and formic acid, accumulation of the latter being suspected as the major
cause of injury in methanol poisoning. Human studies show that formic acid is excreted faster than it is
formed after ingestion of aspartame. In some fruit juices, higher concentrations of methanol can be
[15]
found than the amount produced from aspartame in beverages.
Aspartate[edit]
Aspartic acid (aspartate) is one of the most common amino acids in the typical diet. As with methanol
and phenylalanine, intake of aspartic acid from aspartame is less than would be expected from other
dietary sources. At the 90th percentile of intake, aspartame provides only between 1% and 2% of the
[52][53]
daily intake of aspartic acid. There has been some speculation
that aspartame, in conjunction with
other amino acids like glutamate, may lead to excitotoxicity, inflicting damage on brain and nerve cells.
[8]
However, clinical studies have shown no signs of neurotoxic effects, and studies of metabolism
suggest it is not possible to ingest enough aspartic acid and glutamate through food and drink to levels
[41]
that would be expected to be toxic.
Methanol[edit]
The methanol produced by the metabolism of aspartame is absorbed and quickly converted
into formaldehyde and then completely oxidized to formic acid, which, due to its long half life, is
considered the primary mechanism of toxicity in methanol poisoning. The methanol from aspartame is
unlikely to be a safety concern for several reasons. The amount of methanol in aspartame is less than
that found in fruit juices and citrus fruits, and there are other dietary sources for methanol such
asfermented beverages. Therefore, the amount of methanol produced from aspartame is likely to be
less than that from natural sources. With regard to formaldehyde, it is rapidly converted in the body, and
the amounts of formaldehyde from the metabolism of aspartame are trivial when compared to the
amounts produced routinely by the human body and from other foods and drugs. At the highest
expected human doses of consumption of aspartame, there are no increased blood levels of methanol
[8]
or formic acid, and ingesting aspartame at the 90th percentile of intake would produce 25 times less
[41]
methanol than what would be considered toxic.
Lactation[edit]
In a study done in 1979, the effect of aspartame ingestion on blood and milk amino acid levels in
[57]
lactating women was tested. In this study, six women from the ages of 20 to 29 with established
lactation were studied after oral administration of aspartame or lactose (50 mg/kg body weight) in a
random order, with the intent to study the differences in breast milk between the two. The study resulted
with the conclusion that aspartame administration at 50 mg/kg body weight has a small effect upon the
milk aspartate levels and although a small increase in aspartate time-effect scores was noted over the
four-hour postabsorptive period, no significant difference was noted over the entire 24-hour watching
[57]
period.
Cancer[edit]
Reviews have found no association between aspartame and cancer. These reviews have looked at
numerous carcinogenicity studies in animals, epidemiologic studies in humans, as well as in
vitro genotoxicity studies. These studies have found no significant evidence that aspartame causes
cancer in animals, damages the genome, or causes cancer in humans at doses currently
[8][38][41]
[58]
used.
This position is supported by multiple regulatory agencies like the FDA and EFSA as well
[47]
as scientific bodies such as the National Cancer Institute.
Concern about possible carcinogenic properties of aspartame was originally raised and popularized in
the mainstream media by John Olney in the 1970s and again in 1996 by suggesting that aspartame may
be related to brain tumors. Reviews have found that these concerns were flawed, due to reliance on
[59]
the ecological fallacy and the purported mechanism of causing tumors being unlikely to actually cause
cancer. Independent agencies such as the FDA and National Cancer Institute have reanalyzed multiple
[41]
studies based on these worries and found no association between aspartame and brain cancer.
As discussed in the article on controversies around aspartame, the Cesare Maltoni Cancer Research
Center of the European Ramazzini Foundation of Oncology and Environmental Sciences released
several studies which claimed that aspartame can increase several malignancies in rodents, concluding
[60][61]
[62]
that aspartame is a potential carcinogen at normal dietary doses.
The EFSA and the
[58]
FDA discounted the study results and found no reason to revise their previously established
acceptable daily intake levels for aspartame.
Headaches[edit]
[8]
Headaches are the most common symptom reported by consumers. While one small review noted
aspartame is likely one of many dietary triggers of migraines, in a list that includes "cheese,
chocolate, citrus fruits, hot dogs, monosodium glutamate, aspartame, fatty foods, ice cream, caffeine
[66]
withdrawal, and alcoholic drinks, especially red wine and beer," other reviews have noted conflicting
[8][67]
studies about headaches
and still more reviews lack any evidence and references to support this
[38][41][65]
claim.
Commercial uses[edit]
Under the trade names Equal, NutraSweet, and Canderel, aspartame is an ingredient in approximately
6,000 consumer foods and beverages sold worldwide, including (but not limited to) diet sodas and other
soft drinks, instant breakfasts, breath mints, cereals, sugar-free chewing gum, cocoa mixes, frozen
desserts, gelatin desserts, juices, laxatives, chewable vitamin supplements, milk drinks, pharmaceutical
drugs and supplements, shake mixes, tabletop sweeteners, teas, instant coffees, topping mixes, wine
coolers and yogurt. It is provided as a table condiment in some countries. Aspartame is less suitable
for baking than other sweeteners, because it breaks down when heated and loses much of its
sweetness.
NutraSweet Company[edit]
In 1985, Monsanto Company bought G.D. Searle, and the aspartame business became a separate
Monsanto subsidiary, the NutraSweet Company. In March 2000, Monsanto sold it to J.W. Childs Equity
[69]
[70]
Partners II L.P. European use patents on aspartame expired starting in 1987, and the U.S. patent
expired in 1992. Since then, the company has competed for market share with other manufacturers,
including Ajinomoto, Merisant and the Holland Sweetener Company.
Ajinomoto[edit]
[10]
Many aspects of industrial synthesis of aspartame were established by Ajinomoto. In 2004, the
market for aspartame, in which Ajinomoto, the world's largest aspartame manufacturer, had a 40
percent share, was 14,000 metric tons a year, and consumption of the product was rising by 2 percent a
[71]
[72]
year. Ajinomoto acquired its aspartame business in 2000 from Monsanto for $67M.
In 2008, Ajinomoto sued British supermarket chain Asda, part of Wal-Mart, for a malicious falsehood
action concerning its aspartame product when the substance was listed as excluded from the chain's
[73]
[74]
product line, along with other "nasties". In July 2009, a British court found in favour of Asda. In
June 2010, an appeals court reversed the decision, allowing Ajinomoto to pursue a case against Asda
[75]
to protect aspartame's reputation. Asda said that it would continue to use the term "no nasties" on its
[76]
own-label products, but the suit was settled in 2011 with ASDA choosing to remove references to
[77]
aspartame from its packaging.
In November 2009, Ajinomoto announced a new brand name for its aspartame sweetener
[78]
AminoSweet.
Competing products[edit]
Because sucralose, unlike aspartame, retains its sweetness after being heated, and has at least twice
[82]
the shelf life of aspartame, it has become more popular as an ingredient. This, along with differences
in marketing and changing consumer preferences, caused aspartame to lose market share to
[83][84]
sucralose.
In 2004, aspartame traded at about $30/kg and sucralose, which is roughly three times
[85]
sweeter by weight, at around $300/kg.
Dicalcium phosphate
From Wikipedia, the free encyclopedia
Dicalcium phosphate
IUPAC name[hide]
Calcium hydrogen phosphate dihydrate
Other names[hide]
Calcium monohydrogen phosphate
Phosphoric acid, calcium salt (1:1)
Identifiers
CAS number
7757-93-9
7789-77-7
(dihydrate)
PubChem
104805
ChemSpider
10605753
UNII
L11K75P92J
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
CaHPO4
Molar mass
136.06 g/mol
Appearance
white powder
Density
2.929 g/cm3
Solubility in water
0.02 g/100 mL
Hazards
EU Index
Not listed
NFPA 704
0
1
0
Flash point
Non-flammable
?)
Infobox references
Dicalcium phosphate, also known as dibasic calcium phosphate or calcium monohydrogen
phosphate, is a type ofcalcium phosphate that is dibasic. It is usually found as the dihydrate, with the
chemical formula of CaHPO42H2O, but it can be thermally converted to the anhydrous form, which has
[1]
been referred to by the abbreviation 'DPCA'. It is practically insoluble in water, with a solubility of 0.02
g per 100 mL at 25 C. It contains about 29.5 percent calcium in its anhydrous form. On contact with
water, it converts to hydroxyapatite, which is insoluble solid, and phosphoric acid
Preparation[edit]
Dicalcium phosphate is produced by the reaction of calcium chloride and phosphoric acid:
CaCl2 + H3PO4 + 2 NaOH CaHPO4 + 2 NaCl + 2 H2O
Calcium carbonate is also used in place of the calcium chloride and sodium hydroxide.
Uses[edit]
Dicalcium phosphate is mainly used as a dietary supplement in prepared breakfast cereals, dog
treats, enriched flour, and noodle products. It is also used as a tableting agent in some
pharmaceutical preparations, including some products meant to eliminate body odor. It is used in
poultry feed. It is also used in some toothpastes as a tartar control agent.
Potassium chloride
From Wikipedia, the free encyclopedia
This article is about the chemical compound. For other uses, see KCL.
Potassium chloride
Other names[hide]
Sylvite
Muriate of potash
Identifiers
CAS number
7447-40-7
PubChem
4873
ChemSpider
4707
UNII
660YQ98I10
DrugBank
DB00761
KEGG
D02060
ChEBI
CHEBI:32588
ChEMBL
CHEMBL1200731
RTECS number
TS8050000
ATC code
A12BA01,B05XA01
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
KCl
Molar mass
74.5513 gmol1
Appearance
Odor
odorless
Density
1.984 g/cm3
Melting point
770 C
Boiling point
1420 C
Solubility in water
Solubility
Acidity (pKa)
~7
Refractive index(nD)
Crystal structure
Std molar
83 Jmol1K1[2]
entropy So298
Std enthalpy of
436 kJmol1[2]
formation fHo298
Hazards
MSDS
ICSC 1450
EU Index
Not listed
NFPA 704
0
1
0
Flash point
Non-flammable
LD50
Other anions
Potassium fluoride
Potassium bromide
Potassium iodide
Other cations
Lithium chloride
Sodium chloride
Rubidium chloride
Caesium chloride
Related compounds
Potassium chlorate
Potassium perchlorate
?)
Infobox references
The chemical compound potassium chloride (KCl) is a metal halide salt composed
of potassium and chlorine. In its pure state, it is odorless and has a white
or colorless vitreous crystal appearance, with a crystal structure that cleaves easily in three directions.
Potassium chloride crystals are face-centered cubic. Potassium chloride was historically known as
"muriate of potash". This name is occasionally still encountered in association with its use as
a fertilizer. Potash varies in color from pink or red to white depending on the mining and recovery
process used. White potash, sometimes referred to as soluble potash, is usually higher in analysis and
is used primarily for making liquid starter fertilizers. KCl is used inmedicine, scientific applications,
and food processing. It occurs naturally as the mineral sylvite and in combination withsodium
chloride as sylvinite.
Chemical properties[edit]
Solubility of KCl in various solvents
(g KCl / 1 kg of solvent at 25C)[4]
H2O
360
Liquid ammonia
0.4
0.41
Methanol
5.3
Formic acid
192
Sulfolane
0.04
Acetonitrile
0.024
Acetone
0.00091
Formamide
62
Acetamide
24.5
Dimethylformamide
0.170.5
In chemistry and physics, it is a very commonly used standard, for example as acalibration standard
solution in measuring electrical conductivity of (ionic) solutions, since carefully prepared KCl solutions
have well-reproducible and well-repeatable measurable properties.
Potassium chloride can react as a source of chloride ion. As with any othersoluble ionic chloride, it will
precipitate insoluble chloride salts when added to asolution of an appropriate metal ion:
Physical properties[edit]
Potassium chloride has a crystalline structure like many other salts. Its structure is facecentered cubic. Its lattice constant is roughly 6.3. Some other properties are
Sylvite
Sylvinite
Potassium chloride occurs naturally as sylvite, carnallite, and potash, and it can be extracted
from these ores. It is also extracted from salt water and can be manufactured by crystallization
from solution, flotation or electrostatic separation from suitable minerals. It is a by-product of
the making of nitric acid from potassium nitrate and hydrochloric acid.
Synthesis[edit]
Potassium chloride is inexpensively available and is rarely prepared intentionally in the
laboratory. It can be generated by two routes that are of instructive but not practical value:
One way is to treat potassium hydroxide (KOH) with hydrochloric acid:
KOH + HCl KCl + H2O
This conversion is an acid-base neutralization reaction. The resulting salt can then be
purified by recrystallization. Another method would be to allow potassium to burn in the
presence of chlorine gas, also a very exothermic reaction:
2 K + Cl2 2 KCl
Uses[edit]
The majority of the potassium chloride produced is used for making fertilizer, since
the growth of many plants is limited by their potassium intake. As a
chemical feedstock, it is used for the manufacture of potassium
hydroxide and potassiummetal. It is also used in medicine, lethal
injections, scientific applications, food processing, and as a sodium-free substitute
for table salt (sodium chloride).
It is sometimes used in water as a completion fluid in petroleum and natural
gas operations, as well as being an alternative to sodium chloride in
household water softener units. KCl is useful as a beta radiation source
for calibration ofradiation monitoring equipment, because natural potassium contains
40
0.0118% of the isotope K. One kilogram of KCl yields
16350 becquerels of radiation consisting of 89.28% beta and 10.72% gamma with
1.46083 MeV. Potassium chloride is used in some deicing products that are
designed to be safer for pets and plants, though these are inferior in melting quality
to calcium chloride (lowest usable temperature 12 F (11 C) v. 25 F (32 C)). It
is also used in various brands of bottled water, as well as in bulk quantities for fossil
fuel drilling purposes.
Potassium chloride was once used as a fire extinguishing agent, used in portable
and wheeled fire extinguishers. Known as Super-K dry chemical, it was more
effective than sodium bicarbonate-based dry chemicals and was compatible
with protein foam. This agent fell out of favor with the introduction of potassium
bicarbonate (Purple-K) dry chemical in the late 1960s, which was much
less corrosive and more effective. It is rated for B and C fires.
Along with sodium chloride and lithium chloride, potassium chloride is used as
a flux for the gas welding of aluminium.
Potassium chloride is also an optical crystal with a wide transmission range from
210 nm to 20 m. While cheap, KCl crystal is hygroscopic. This limits its application
to protected environments or short term uses such as prototyping. Exposed to free
air, KCl optics will "rot". Whereas KCl components were formerly used for infrared
optics, it has been entirely replaced by much tougher crystals like zinc selenide.
Potassium chloride has also been used to create heat packs which
[5]
employ exothermic chemical reactions, but these are no longer being created due
to cheaper and more efficient methods, such as the oxidation of metals ('Hot Hands',
one time use products) or the crystallization of sodium acetate (multiple use
products).
Potassium chloride is used as a scotophor with designation P10 in dark-trace CRTs,
e.g. in the Skiatron.
Precautions[edit]
Orally, potassium chloride is toxic in excess; the LD50 is around 2.5 g/kg (meaning
that a lethal dose for 50% of people weighing 75 kg (165 lb) is about 190 g
(6.7ounces)). However, this is not far from oral toxicity of sodium chloride (table salt),
of 3.75 g/kg, thus potassium chloride is harmless for alimentation (and even good for
health, see previous paragraph). But intravenously, without the step of digestive
[14]
absorption, this is reduced to just over 30 mg/kg. Most concerns are its severe
effects on the cardiac muscles: high doses can cause cardiac arrest and rapid death,
thus the aforementioned use as the third and final drug delivered in the lethal
injection process.
Ascorbic acid
From Wikipedia, the free encyclopedia
This article is about the molecular aspects of ascorbic acid. For information about its role in nutrition,
see Vitamin C.
L-Ascorbic acid
IUPAC name[hide]
(5R)-[(1S)-1,2-dihydroxyethyl]-3,4-dihydroxyfuran-2(5H)-one
Other names[hide]
Vitamin C
Identifiers
CAS number
50-81-7
PubChem
5785
ChemSpider
10189562
UNII
PQ6CK8PD0R
EC number
200-066-2
KEGG
D00018
ChEBI
CHEBI:29073
ChEMBL
CHEMBL196
ATC code
A11GA01,G01AD03,S01XA15
Jmol-3D images
Image 1
Image 2
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C6H8O6
Molar mass
176.12 g mol1
Appearance
Density
1.65 g/cm3
Melting point
Solubility in water
330 g/L
Solubility inethanol
20 g/L
Solubility inglycerol
10 g/L
Solubility inpropylene
50 g/L
glycol
Solubility in other
insoluble in diethyl
solvents
ether,chloroform, benzene,petroleum
ether, oils, fats
Acidity (pKa)
MSDS
JT Baker
Oxford University
NFPA 704
1
1
0
LD50
?)
Infobox references
Ascorbic acid is a naturally occurring organic compound with antioxidant properties. It is a white solid,
but impure samples can appear yellowish. It dissolves well in water to give mildly acidic solutions.
Ascorbic acid is one form ("vitamer") of vitamin C. It was originally called L-hexuronic acid, but, when it
was found to have vitamin C activity in animals ("vitamin C" being defined as a vitamin activity, not then
a specific substance), the suggestion was made to rename L-hexuronic acid. The new name for Lhexuronic acid is derived from a- (meaning "no") and scorbutus (scurvy), the disease caused by a
deficiency of vitamin C. Because it is derived from glucose, many animals are able to produce it, but
humans require it as part of their nutrition. Other vertebrates lacking the ability to produce ascorbic acid
include other primates, guinea pigs, teleost fishes, bats, and some birds, all of which require it as a
[2]
dietary micronutrient (that is, in vitamin form).
There exists a D-ascorbic acid, which does not occur in nature. It may be synthesized artificially. It has
identical antioxidant properties to L-ascorbic acid yet has far less vitamin C activity (although not quite
[3]
zero). This fact is taken as evidence that the antioxidant properties of ascorbic acid are only a small
part of its effective vitamin activity. To be specific, L-ascorbate is known to participate in many specific
enzyme reactions that require the correct epimer (L-ascorbate and not D-ascorbate). L-ascorbic acid
has a specific rotation of
[4]p. 35
History[edit]
From the middle of the 18th century, it was noted that lemon juice could help prevent sailors from
getting scurvy. At first, it was supposed that the acid properties were responsible for this benefit;
however, it soon became clear that other dietary acids, such as vinegar, had no such benefits. In 1907,
two Norwegian physicians reported an essential disease-preventing compound in foods that was distinct
from the one that prevented beriberi. These physicians were investigating dietary-deficiency diseases
using the new animal model of guinea pigs, which are susceptible to scurvy. The newly discovered foodfactor was eventually called vitamin C.
From 1928 to 1932, the Hungarian research team led by Albert Szent-Gyrgyi, as well as that of
the American researcherCharles Glen King, identified the antiscorbutic factor as a particular single
chemical substance. At the Mayo clinic, Szent-Gyrgyi had isolated the chemical hexuronic acid from
animal adrenal glands. He suspected it to be the antiscorbutic factor but could not prove it without a
biological assay. This assay was finally conducted at the University of Pittsburgh in the laboratory of
King, which had been working on the problem for years, using guinea pigs. In late 1931, King's lab
obtained adrenal hexuronic acid indirectly from Szent-Gyrgyi and, using their animal model, proved
that it is vitamin C, by early 1932.
This was the last of the compound from animal sources, but, later that year, Szent-Gyrgyi's group
discovered thatpaprika pepper, a common spice in the Hungarian diet, is a rich source of hexuronic
acid. He sent some of the now-more-available chemical to Walter Norman Haworth, a British sugar
[5]
chemist. In 1933, working with the then-Assistant Director of Research (later Sir) Edmund Hirst and
their research teams, Haworth deduced the correct structure and optical-isomeric nature of vitamin C,
[6]
and in 1934 reported the first synthesis of the vitamin. In honor of the compound's antiscorbutic
properties, Haworth and Szent-Gyrgyi now proposed the new name of "a-scorbic acid" for the
compound. It was named L-ascorbic acid by Haworth and Szent-Gyrgyi when its structure was finally
[7]
proven by synthesis.
In 1937, the Nobel Prize for chemistry was awarded to Haworth for his work in determining the structure
of ascorbic acid shared with Paul Karrer, who received his award for work on vitamins and the
prize for Physiology or Medicine that year went to Albert Szent-Gyrgyi for his studies of the biological
functions of L-ascorbic acid.
The American physician Fred R. Klenner, M.D. promoted vitamin C as a cure for many diseases in the
1950s by elevating the dosages greatly to as much as tens of grams vitamin C daily by injection. From
1967 on, Nobel prize winner Linus Pauling recommended high doses of ascorbic acid as a prevention
against cold and cancer; he took 18 grams daily. The results of Klenner have been controversial as yet,
[8]
since his investigations do not meet the modern methodologic standards.
Acidity[edit]
Antioxidant mechanism[edit]
The oxidized forms of ascorbate are relatively unreactive and do not cause cellular damage.
However, being a good electron donor, excess ascorbate in the presence of free metal ions
can not only promote but also initiate free radical reactions, thus making it a potentially
dangerous pro-oxidative compound in certain metabolic contexts.
Reactions[edit]
Food chemistry[edit]
Ascorbic acid and its sodium, potassium, and calcium salts are commonly used
as antioxidant food additives. These compounds are water-soluble and, thus, cannot
protect fats from oxidation: For this purpose, the fat-soluble esters of ascorbic acid with
long-chain fatty acids (ascorbyl palmitate or ascorbyl stearate) can be used as food
[9]
antioxidants. Eighty percent of the world's supply of ascorbic acid is produced in China.
The relevant European food additive E numbers are:
1.
2.
3.
4.
5.
It creates volatile compounds when mixed with glucose and amino acids in 90 C.
It is a cofactor in tyrosine oxidation.
[15]
Biosynthesis[edit]
Main article: Vitamin C
Industrial preparation[edit]
Ascorbic acid is prepared in industry from glucose in a method based on the
historical Reichstein process. In the first of a five-step process, glucose is
catalyticallyhydrogenated to sorbitol, which is then oxidized by
the microorganism Acetobacter suboxydans to sorbose. Only one of the six hydroxy
groups is oxidized by this enzymatic reaction. From this point, two routes are available.
Treatment of the product with acetone in the presence of an acid catalyst converts four of
the remaininghydroxyl groups to acetals. The unprotected hydroxyl group is oxidized to
the carboxylic acid by reaction with the catalytic oxidant TEMPO (regenerated by sodium
hypochlorite bleaching solution). Historically, industrial preparation via the Reichstein
process used potassium permanganate as the bleaching solution. Acid-catalyzed
hydrolysis of this product performs the dual function of removing the two acetal groups
and ring-closing lactonization. This step yields ascorbic acid. Each of the five steps has a
[27]
yield larger than 90%.
A more biotechnological process, first developed in China in the 1960s, but further
developed in the 1990s, bypasses the use of acetone-protecting groups. A
secondgenetically-modified microbe species, such as mutant Erwinia, among others,
oxidises sorbose into 2-ketogluconic acid (2-KGA), which can then undergo ring-closing
lactonization via dehydration. This method is used in the predominant process used by
the ascorbic acid industry in China, which supplies 80% of world's ascorbic
[28]
acid. American and Chinese researchers are competing to engineer a mutant that can
carry out a one-pot fermentation directly from glucose to 2-KGA, bypassing both the need
[29]
for a second fermentation and the need to reduce glucose to sorbitol.
The outdated, but historically-important industrial synthesis of ascorbic acid from glucose
via the Reichstein process.
Determination[edit]
The traditional way to analyze the ascorbic acid content is the process of titrationwith
an oxidizing agent, and several procedures have been developed, mainly relying
on iodometry. Iodine is used in the presence of a starch indicator. Iodine is reduced by
ascorbic acid, and, when all the ascorbic acid has reacted, the iodine is then in excess,
forming a blue-black complex with the starch indicator. This indicates the end-point of the
titration. As an alternative, ascorbic acid can be treated with iodine in excess, followed by
[30]
back titration with sodium thiosulfate using starch as an indicator. The preceding
iodometric method has been revised to exploit reaction of ascorbic acid
with iodate and iodide in acid solution. Electrolyzing the solution of potassium iodide
produces iodine, which reacts with ascorbic acid. The end of process is determined
by potentiometric titration in a manner similar to Karl Fischer titration. The amount of
ascorbic acid can be calculated by Faraday's law.
An uncommon oxidising agent is N-bromosuccinimide, (NBS). In this titration, the NBS
oxidizes the ascorbic acid in the presence of potassium iodide and starch. When the NBS
is in excess (i.e., the reaction is complete), the NBS liberates the iodine from the
potassium iodide, which then forms the blue-black complex with starch, indicating the
end-point of the titration.
Potassium sorbate
From Wikipedia, the free encyclopedia
Potassium sorbate[1][2]
IUPAC name[hide]
Potassium (2E,4E)-hexa-2,4-dienoate
Other names[hide]
E202
Sorbistat-K
Sorbistat potassium
Identifiers
CAS number
24634-61-5
PubChem
23676745
ChemSpider
4445644
KEGG
D02411
ChEBI
CHEBI:77868
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C6H7KO2
Molar mass
150.22 g mol1
Appearance
White crystals
Odor
yes
Density
1.363 g/cm3
Melting point
270 C (decomp.)
Solubility in water
Insoluble in benzene
Hazards
NFPA 704
1
2
0
LD50
?)
Potassium sorbate is the potassium salt of sorbic acid, chemical formula CH3CH=CH-CH=CH-CO2K. It
is a white salt that is very soluble in water (58.2% at 20 C). It is primarily used as a food preservative (E
[3]
number 202). Potassium sorbate is effective in a variety of applications including food, wine,
and personal care products. While sorbic acid is naturally occurring in some berries, virtually all of the
world's production of sorbic acid, from which potassium sorbate is derived, is manufactured
synthetically.
Production[edit]
Potassium sorbate is produced industrially by neutralizing sorbic acid with potassium hydroxide. The
precursor sorbic acid is produced in a two-step process via the condensation
[4][5][6]
of crotonaldehyde and ketene.
Uses[edit]
Potassium sorbate is used to inhibit molds and yeasts in many foods, such
[7]
as cheese, wine, yogurt, dried meats, apple cider, soft drinks and fruit drinks, and baked goods. It is
used in the preparation of items such as Sweet maple syrup and Milk shakes served by fast
[8] [9] [10]
food conglomerates such as Mc Donalds.
It can also be found in the ingredients list of
many dried fruit products. In addition, herbal dietary supplement products generally contain potassium
sorbate, which acts to prevent mold and microbes and to increase shelf life, and is used in quantities at
[11]
which there are no known adverse health effects, over short periods of time. Labeling of this
preservative on ingredient statements reads as "potassium sorbate" or "E202". Also, it is used in
many personal care products to inhibit the development ofmicroorganisms for shelf stability. Some
manufacturers are using this preservative as a replacement for parabens. Tube feeding of potassium
[12]
sorbate reduces gastric burden of pathogenic bacteria.
Also known as "wine stabilizer", potassium sorbate produces sorbic acid when added to wine. It serves
two purposes. When active fermentation has ceased and the wine is racked for the final time after
clearing, potassium sorbate will render any surviving yeast incapable of multiplying. Yeast living at that
moment can continue fermenting any residualsugar into CO2 and alcohol, but when they die no new
yeast will be present to cause future fermentation. When a wine is sweetened before bottling, potassium
sorbate is used to prevent refermentation when used in conjunction with potassium metabisulfite. It is
primarily used with sweet wines, sparkling wines, and some hard ciders but may be added to table
wines which exhibit difficulty in maintaining clarity after fining.
Some molds (notably some Trichoderma and Penicillium strains) and yeasts are able to detoxify
sorbates bydecarboxylation, producing piperylene (1,3-pentadiene). The pentadiene manifests as a
[13]
typical odor of kerosene orpetroleum.
Toxicology[edit]
[14]
Potassium sorbate is a skin, eye and respiratory irritant. Although some research implies it has a long
[15]
term safety record, in vitro studies have shown that it is both genotoxic and mutagenic to human
blood cells. Potassium sorbate is found to be toxic to human DNA in peripheral blood lymphocytes, and
[16]
hence found that it negatively affects immunity. It is often used with ascorbic acid and iron salts as
they increase its effectiveness but this tends to form mutagenic compounds that damage DNA
[17]
molecules.
Typical usage rates of potassium sorbate are 0.025% to 0.1% (see sorbic acid), which in a 100 g
serving yields intake of 25 mg to 100 mg. Acceptable daily intakes for human is 12.5 mg/kg, or 875 mg
daily for an average adult (70 kg), according to FAO/World Health Organization Expert Committee on
[11]
Food Additives.
Sulfonic acid
From Wikipedia, the free encyclopedia
(Redirected from Sulphonic acid)
General structure of a sulfonic acid with the blue marked functional group
A sulfonic acid (or sulphonic acid) refers to a member of the class of organosulfur
compounds with the general formula RS(=O)2OH, where R is an
organic alkyl or aryl group and the S(=O)2OH group a sulfonyl hydroxide.[1] A sulfonic
acid can be thought of as sulfuric acid with one hydroxyl group replaced by an
organic substituent. The parent compound (with the organic substituent replaced by
hydrogen) is the hypothetical compound sulfurous acid. Salts or esters of sulfonic acids
are called sulfonates.
Preparation[edit]
Sulfonic acid is produced by the process of sulfonation. Usually the sulfonating agent
is sulfur trioxide. A particularly large scale application of this method is the production of
alkylbenzenesulfonic acids:
RC6H5 + SO3 RC6H4SO3H
In this reaction, sulfur trioxide is an electrophile and
the arene undergoes electrophilic aromatic substitution.[1]
Thiols can be oxidized to sulfonic acids:
RSH + 3/2 O2 RSO3H
Certain sulfonic acids, such as perfluorooctanesulfonic acid are prepared
by electrophilic fluorination of preformed sulfonic acids. The net conversion can
be represented simplistically:
C8H17SO3H + 17 F2 C8F17SO3H + 17 HF
Properties[edit]
Sulfonic acids are much stronger acids than the
corresponding carboxylic acids. p-Toluenesulfonic acid, with a pKa of -2.8, is
about a million times stronger acid thanbenzoic acid, with a pKa of 4.2.
Similarly, methanesulfonic acid, pKa = -1.9, is also about one million times
stronger acid than acetic acid. Because of their polarity, sulfonic acids tend
to be crystalline solids. They are also usually colourless and nonoxidizing,
which is convenient. Because of their high acidity, sulfonic acids are often
soluble in water or exhibit detergent-like properties.
The structure of sulfonic acids is illustrated by the
prototype, methanesulfonic acid. The sulfonic acid group, RSO2OH features
a tetrahedral sulfur centre, meaning that sulfur is at the center of four atoms:
three oxygens and one carbon. The overall geometry of the sulfur centre is
reminiscent of the shape of sulfuric acid.
Taurine, a bile acid, and one of the few naturally occurring sulfonic acids
(shown in uncommontautomer).
Applications[edit]
Although both alkyl and aryl sulfonic acids are known, most of the
applications are associated with the aromatic derivatives.
Detergents and surfactants[edit]
Detergents and surfactants are molecules that combine highly nonpolar and
highly polar groups. Traditionally, soaps are the popular surfactants, being
derived fromfatty acids. Since the mid-20th century, the usage of sulfonic
acids has surpassed soap in advanced societies. For example, an estimated
2 billion kilograms ofalkylbenzenesulfonates are produced annually for
diverse purposes. Lignin sulfonates, produced by sulfonation of lignin are
components of drilling fluids and additives in certain kinds of concrete.[2]
Dyes[edit]
Many if not most of the anthroquinone dyes are produced or processed via
sulfonation.[3] Sulfonic acids tend to bind tightly
to proteins and carbohydrates. Most "washable" dyes are sulfonic acids (or
have the functional sulfonyl group in them) for this reason. pCresidinesulfonic acid is used to make food dyes.
Acid catalysts[edit]
Being strong acids, sulfonic acids are also used as catalysts. The simplest
examples are methanesulfonic acid, CH3SO2OH and p-toluenesulfonic acid,
which are regularly used in organic chemistry as acids that are lipophilic
(soluble in organic solvents). Polymeric sulfonic acids are also
useful. Dowex resin are sulfonic acid derivatives of polystyrene and is used
as catalysts and for ion exchange (water softening).Nafion, a fluorinated
polymeric sulfonic acid is a component of proton exchange membranes
in fuel cells.[4]
Drugs[edit]
Antibacterial drugs sulfa drugs are produced from sulfonic acids.
Flow Batteries[edit]
Methanesulfonic acid is used as the supporting electrolyte of the zinccerium and lead-acid (methanesulfonate) flow batteries.
Neem oil
From Wikipedia, the free encyclopedia
Neem oil is a vegetable oil pressed from the fruits and seeds of the neem (Azadirachta
indica), an evergreen tree which isendemic to the Indian subcontinent and has been
introduced to many other areas in the tropics. It is the most important of the commercially
available products of neem for organic farming and medicines.
Neem oil varies in color; it can be golden yellow, yellowish brown, reddish brown, dark
brown, greenish brown, or bright red. It has a rather strong odor that is said to combine
the odours of peanut and garlic. It is composed mainly of triglycerides and contains
many triterpenoid compounds, which are responsible for the bitter taste. It
is hydrophobic in nature; in order to emulsify it in water for application purposes, it must
be formulated with appropriate surfactants.
Azadirachtin is the most well known and studied triterpenoid in neem oil. The
azadirachtin content of neem oil varies from 300ppm to over 2500ppm depending on the
extraction technology and quality of the neem seeds crushed. Neem oil also
contains steroids(campesterol, beta-sitosterol, stigmasterol).
Average composition of neem oil fatty acids
Common Name
Acid Name
Composition range
Omega-6
Linoleic acid
6-16%
Omega-9
Oleic acid
25-54%
Palmitic acid
Hexadecanoic acid
16-33%
Stearic acid
Octadecanoic acid
9-24%
Omega-3
Alpha-linolenic acid
?%
Palmitoleic acid
9-Hexadecenoic acid
?%
Uses[edit]
Neem oil is not used for cooking purposes. In India, it is used for
preparing cosmetics (soap, hair products, body hygiene creams, hand creams) and
in Ayurvedic,Unani and folklore traditional medicine, in the treatment of a wide range of
afflictions. The most frequently reported indications in ancient Ayurvedic writings are skin
diseases, inflammations and fevers, and more recently rheumatic disorders, insect
repellent and insecticide effects.[1]
Traditional Ayurvedic uses of neem include the treatment of acne, fever, leprosy, malaria,
ophthalmia and tuberculosis. Various folk remedies for neem include use as
an anthelmintic, antifeedant, antiseptic, diuretic, emmenagogue, contraceptive, febrifuge,
parasiticide, pediculocide and insecticide. It has been used in traditional medicine for the
treatment of tetanus, urticaria, eczema, scrofula and erysipelas. Traditional routes of
administration of neem extracts included oral, vaginal and topical use. Neem oil has an
extensive history of human use in India and surrounding regions for a variety of
therapeutic purposes. Puri (1999) has given an account of traditional uses and
therapeutic indications and pharmacological studies of this oil, in his book on neem.[2]
Formulations made of neem oil also find wide usage as a biopesticide for organic
farming, as it repels a wide variety of pests including the mealy bug, beet
armyworm,aphids, the cabbage worm, thrips, whiteflies, mites, fungus gnats, beetles,
moth larvae, mushroom flies, leafminers, caterpillars, locust, nematodes and
the Japanese beetle. Neem oil is not known to be harmful to mammals, birds,
earthworms or some beneficial insects such as
butterflies, honeybees and ladybirds (ladybugs in US English) if it is not concentrated
directly into their area of habitat or on their food source. It can be used as a household
pesticide for ant, bedbug, cockroach, housefly,sand
fly, snail, termite and mosquitoes both as repellent and larvicide.[2] Neem oil also
controls black spot, powdery mildew, anthracnose and rust fungi.
Neem seed oil has also been found to prevent implantation and may even have an
abortifacient effect similar to pennyroyal, juniper berries, wild ginger, myrrh andangelica.
The effects were seen as many as ten days after fertilization in rats though it was most
effective at no more than three days. (Sinha, et al., 1984)[not specific enough to verify]; (Lal et al.,
1985)[not specific enough to verify]. In a study on rats, neem oil was given orally eight to ten days
after implantation of the fetuson the uterine wall. In all cases, by day 15, the embryos
were all completely resorbed by the body. The animals regained fertility on the next cycle
showing no physical problems. Detailed study of the rats revealed increased levels
of gamma interferon in the uterus. The neem oil enhanced the local immune response in
the uterus.(Mukherjee, 1996)[3][not specific enough to verify] Post coital use of neem oil as birth
control does not appear to work by hormonal changes but produces changes in the
organs that make pregnancy no longer viable (Tewari, 1989)[not specific enough to
verify]
Neem seed oil has also been used as a renewable source for the preparation of
polymeric coatings. It has been converted into various polymeric resins, including
polyesteramides and polyetheramides. These resins may be utilized further for
preparation of polyurethane coatings.[4][5] Ashok Chaudhari, Anil Kuwar, Pramod
Mahulikar, Dilip Hundiwale, Ravindra Kulkarni and Vikas Gite, RSC Advances, 2014, 4,
1786617872
Toxicity[edit]
Studies done when Azadirachtin (the primary active pesticidal ingredient in neem oil) was
approved as a pesticide showed that when neem leaves were fed to male albino rats for
11 weeks, 100% (reversible) infertility resulted.[6]
Neem oil and other neem products such as neem leaves and neem tea should not be
consumed by pregnant women, women trying to conceive, or children.[citation needed]
There is some evidence that internal medicinal use may be associated with liver damage
in children.[7]
Calcium propanoate
From Wikipedia, the free encyclopedia
(Redirected from Calcium propionate)
Calcium propanoate[1]
IUPAC name[hide]
Calcium propanoate
Other names[hide]
Calcium propionate
Calcium dipropionate
Mycoban
Identifiers
CAS number
4075-81-4
PubChem
19999
ChemSpider
18840
EC number
223-795-8
Jmol-3D images
Image 1
SMILES
[show]
InChI
[show]
Properties
Molecular formula
C6H10CaO4
Molar mass
186.2192 g/mol
Appearance
Solubility in water
49 g/100 mL (0 C)
55.8 g/100 mL (100 C)
Solubility
slightly soluble
in methanol,ethanol
insoluble in acetone,benzene
Structure
Crystal structure
monoclinic
Hazards
NFPA 704
1
2
0
Except where noted otherwise, data are given for materials in
their standard state (at 25 C (77 F), 100 kPa)
(verify) (what is:
?)
Infobox references
Calcium propanoate or calcium propionate has the formula Ca(C2H5COO)2. It is the calcium salt
of propanoic acid.
Uses[edit]
As a food additive, it is listed as E number 282 in the Codex Alimentarius. Calcium propanoate is used
as a preservative in a wide variety of products, including but not limited to bread, other baked goods,
[2]
processed meat, whey, and other dairy products. In agriculture, it is used, amongst other things, to
[3]
prevent milk fever in cows and as a feed supplement Propanoates prevent microbes from producing
the energy they need, like benzoates do. However, unlike benzoates, propanoates do not require an
[4]
acidic environment.
[5]
Calcium propanoate is used in bakery products as a mold inhibitor, typically at 0.1-0.4% (though
animal feed may contain up to 1%). Mold contamination is considered a serious problem amongst
[6]
bakers, and conditions commonly found in baking present near-optimal conditions for mold growth.
[7]
A few decades ago, Bacillus mesentericus (rope), was a serious problem, but today's improved
sanitary practices in the bakery, combined with rapid turnover of the finished product, have virtually
[citation needed]
eliminated this form of spoilage.
Calcium propanoate and sodium propanoate are effective
[8]
against both B. mesentericus rope and mold.
Metabolism of propanoate begins with its conversion to propionyl coenzyme A (propionyl-CoA), the
usual first step in the metabolism of carboxylic acids. Since propanoic acid has three carbons, propionylCoA can directly enter neither beta oxidation nor the citric acid cycles. In most vertebrates, propionylCoA is carboxylated to D-methylmalonyl-CoA, which is isomerised to L-methylmalonyl-CoA. A vitamin
B12-dependent enzyme catalyzes rearrangement of L-methylmalonyl-CoA to succinyl-CoA, which is an
intermediate of the citric acid cycle and can be readily incorporated there.
When propanoic acid is infused directly into rodents' brains, it produces reversible behavior changes
(e.g. hyperactivity, dystonia, social impairment, perseveration) and brain changes (e.g. innate
[9]
neuroinflammation, glutathione depletion) that may be used as a model of human autism in rats.
[10]
According to the Pesticide Action Network North America, calcium propionate is slightly toxic. This
rating is not uncommon for food products; vitamin C is also rated by the same standards as being
[11]
[12]
slightly toxic.
Calcium propanoate can be used as a fungicide on fruit.