FOOD TOXINS 1

Lecture No. 7
Copyright Mgr. Zuzana irok, PhD.

Toxic agents in food of plant origin

Glucosides This is the largest group of secondary metabolites. Substances consisting of sugar part and non-sugar part, so called aglycone. These two parts are connected by a bond of ether character by glucosidic bond. Generally speaking, we can say that these substances usually affect blood and circulatory system. These agents are not toxic themselves, but are easily hydrolysed in acid environment and release cyanic acid

Cyanogenic glucosides:
Very common in plants, found in more than one thousand species in more than one hundred families. They are bitter and primarily act as repellents. We know more than fifty cyanogenic glucosides. In table there are some most known ones:

Glucoside
Linamarin

Plants
Manioc, white clover, cultivated flax

HCN (mg/kg) content in fresh flesh Manioc-bitter type

-peel of bulbs 840 -pulp of bulbs 330

Faseolunatin Lotaustralin Linustatin Neolinustatin Prunasin

Sugar bean Birds-food trefoil, white clover, manioc Cultivated flax Plum tree

100-4000

-seeds 200-380

Sambunigrin
Amygdalin Vicianin Taxifyllin Dhurrin

Elder Sambucus nigra

Plum tree, kernels of stone-fruits: bitter almonds, apricot, peach Bob, vetch Common yew, bamboo Sorghum Kernels of these plants approximately 3 %

 Aglycones (non-sugar parts) are formed by hydroxynitriles, which are stabilised by glucosyl bound to hydroxyl group of a sugar.
Aglycone: R1 OH C R2 C N -hydroxynitrile

R1 C

O- -glycosyl

R2 C N cyanogenic glucoside

Manioc (kasawa, cassava):

Originally south-american species from Euphorbiaceae family It is widespread in all tropic areas Root bulbs contain starch and hydrocyanic acid, which can be removed by cooking or baking Bulbs are used as potatoes, they are dried and flour is made of them We distinguish bitter and sweet types of manioc, bitter can contain up to 500 mg/kg of HCN

Sorghum:
From Poaceae family Has been known since ancient Egypt times It is an annual plant, about 3 m high with minute grains containing a lot of starch Dhurrin is mainly in germs, seeds usually dont contain cyanic acid

Almond, apricot, peach:

Contain glucoside called amygdalin HCN is very poisonous, but in plants occurs in quite low concentrations Additionally, releasing process is slow so there is not sufficient amount cumulated in one time Lower concentration of amygdalin is found in plums, blackthorns, cherries, sour cherries and apples.

Mechanism of action:
The carrier of toxicity is HCN, released from glucoside In blood it binds to haemoglobin and methaemoglobin and forms cyanhaemoglobin and cyanmethaemoglobin respectively Its affinity to methaemoglobin (which is higher than to haemoglobin) is used for treatment Cyanides and cyanic acid act as neurotoxins and they also bind to several proteins damaging enzyme systems. They decrease tissue breathing, block cytochromoxidase (HCN binds to Fe and Cu), cause tissue asphyxia (suffocation), because oxygen is not passed on to tissues, blood is oversaturated by oxygen and is of bright brick red colour

 In acute poisoning we can see increased respiration due to chemoreceptors and respiration centre damage Then the decrease of blood pressure, seizures, coma and exitus due to respiratory centre collapse follows In chronic intoxications is typical tremor, conjunctivitis, inappetence, neuropathies, headaches In manioc it is called tropic ataxic neuropathy

Biotransformation:
Dissociation of cyanogenic glucosides goes on in two steps First, -D-glucopyranose is dissociated due to action of enzyme called -D-glucosidase and -hydroxynitrile is formed This substance is dissociated to HCN and aldehyde or ketone due to enzyme hydroxynitrillyase

Dissociation of cyanogenic glucosides:

R1 C R2

O- -glucopyranose C= N + H2O

R1 C R2

OH + glucose C = N -hydroxynitrile

cyanogenic glucoside
glucosidase

R1 C R2

OH

R1 C=O + HCN

C= N

+ H2O

R2 Aldehyde and ketone

-hydroxynitrile

-hydroxynitrillyase

 In normal plant tissues free HCN doesnt occur Described dissociation takes place in mechanically damaged tissues, where glucosides and enzyme, normally stored separately, come into touch and start to react together It can be during cutting of plants, crushing of seeds, if the plant is frozen, in extreme drought Efficient glucosidase is also a part of bacterial microflora in GIT of mammals Released HCN must be detoxified in plant or in animal somehow - product of detoxification is thiocyanate SCN This change is possible thanks to one of two enzymes sulphurtransferases. Cyanide-sulphurtransferase, also called rhodanase, which is a part of mitochondria and 3 merkaptopyruvatesulphurtransferase (also in mitochondria)

Detoxification of cyanides:
S2O3 thiosulphate
+

CNnitrile rhodanase

SO32sulphite

+ SCNthiocyanate SCN-

CH2 - C - COOH + CNtransferase SH O Mercaptopyruvate

CH3- C -COOH O Pyruvate

3-merkaptopyruvatesulphur

thiocyanate

 Similar mechanism is found in animals It takes place in liver and thiocyanates are excreted by urine or faeces Detoxification is dependent on sufficient amount of sulphur substances in an organism

Treatment:
Administration of nitrites formation of methaemoglobin, which binds cyanides formation of cyanmethaemoglobin administration of thiosulphates cyanides released from methaemoglobin react with them and form thiocyanates Now a new antidote is tested hydroxocobalamin with cyanides in blood forms cyanocobalamin (vitamin B12) Lethal doses: - In fruit containing amygdalin they are 5-25 pieces of seed for children. - Lethal dose for humans is 0,5 3,5 mg/kg HCN

Glycoalkaloids of potatoes (Solanum tuberosum, Solanaceae)

Potatoes are fourth most important crop-plant in the world Toxic glycoalkaloids are found in the whole plant of potato Solanum tuberosum, and also in majority of other species from family Solanaceae, e.g. tomato or aubergine - Solanum melongena A)These alkaloids are so called steroid glycoalkaloids (SGA), or pseudoalkaloids, R)because their precursors are not aminoacids like in genuine alkaloids They can be also classified as glucosides they contain glucosidic bond in their molecule Glycoalkaloids are formed of: - polar, in water soluble saccharide part mono-tetrasaccharide - non-polar steroid (aglycone)

Potatoe:
The whole overground part of the plant is poisonous In green parts, germs and berries there is solanin and less potent solanidin, in tubers, there are solanin and chaconin In general we call all these alkaloids Solanin The concentration of alkaloids varies according to many conditions (warm, dryness, humidity). Also quality of soil, fertilizers added, stress factors (e.g. insect attacks, mechanical damage or light) influence the concentration These stress factors and increased amount of magnesium in soil increase the concentration of alkaloids, on the other hand, molybdenum in soil decreases their concentration

 In starch parenchyma of tubers, there is only about 1 % of solanin Glycoalkaloids are termostable, so you cannot destroy them by cooking, frying or drying. They bear temperatures higher than 300C. But during cooking potatoes in water majority of alkaloids pass to water Solanin in fresh unpeeled tubers there can be concentration of solanin more than 100 mg/kg. The limit for potatoes determined to eat is 200 mg/kg. But at about 150 mg/kg, the taste starts to be bitter and in higher concentration this taste disallows to eat them. In tubers for consumption , the vast majority of glycoalkaloids is in 1.5 mm thick part of cortex, of peel

 By peeling we remove 60-95 % of solanin It is recommended not to expose them to light. Tuber reacts with rapid synthesis of alkaloids as a defence against stress Once formed, these alkaloids cannot be removed during storage in dark Another danger is mechanical damage which also leads to alkaloid synthesis Data on temperature and humidity differs among sources, low temperatures lengthen high quality of tubers, but cold can cause increased synthesis of alkaloids A)For decreasing of alkaloid formation we use chemical retardants or vacuum package, R)because lack of oxygen and decreased respiration block metabolism in tubers

Toxic effects of glycoalkaloids:

They posses two mechanisms of action: - First: they disturb cell membranes containing steroid substances (an effect similar to those in saponines) - Second: they inhibit serum cholinesterase too (similar to organophosphates) Glycoalkaloids cause gut mucosa and liver damage Early signs of intoxication are colic, diarrhoea with blood in excrements, apathy, halucinations. Then follow seizures, coma and respiration paralysis We suppose, that many of slight intoxications are considered as common gut problems and we dont attribute them to potatoes For humans, toxic dose is 2-5 mg/kg of body weight and lethal dose between 3-6 mg/kg body weight Other group of glycoalkaloids in potatoes are leptins. They are natural pesticides and genetics try to put the gene for leptins to other plants to protect them Tubers also contain so called protease inhibitors, which dissociate trypsine, chymotrypsine, kathepsine D and karboxypeptidases. These inhibitors can be removed and destroyed by exposure to heat BEWARE - Inhibitors are also in: - peanuts, wheat, red beet, onion, soya beans

Organ, tissue Germs Roots Stalk Leaves Flowers Berry Whole tuber (bulb) Peel

Content (mg/kg) 2000-4000 180-400 20-30 400-1000 3000-5000 4200 75 300-500