Erythropoiesis is the process in which new erythrocytes are produced.

These new erythrocytes

replace the oldest erythrocytes (normally about one percent) that are phagocytosed and destroyed
each day. Folate, vitamin B12, and iron have crucial roles in erythropoiesis. Erythroblasts require
folate and vitamin B12 for proliferation during their differentiation. Deficiency of folate or vitamin B12
inhibits purine and thymidylate syntheses, impairs DNA synthesis, and causes erythroblast apoptosis,
resulting in anemia from ineffective erythropoiesis. Erythroblasts require large amounts of iron for
hemoglobin synthesis. Large amounts of iron are recycled daily with hemoglobin breakdown from
destroyed old erythrocytes. Many recently identified proteins are involved in absorption, storage, and
cellular export of nonheme iron and in erythroblast uptake and utilization of iron. Erythroblast heme
levels regulate uptake of iron and globin synthesis such that iron deficiency causes anemia by
retarded production rates with smaller, less hemoglobinized erythrocytes.

As folic acid is biochemically inactive, it is converted by dihydrofolate reductase to tetrahydrofolic acid and
methyltetrahydrofolate. These folic acid congeners are transported by receptor-mediated endocytosis across
cells where they are needed to maintain normal erythropoiesis

Vitamin b12 in erythropoisis

Erythropoiesis is a term used to indicate the process of red blood cell formation. Red blood
cells carry oxygen to the tissues and organs throughout your body, and when red blood cell
formation is hampered, your health can be negatively impacted. Vitamin B12 plays a key role
in the formation of red blood cells.

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Mechanism

Vitamin B12 works in conjunction with folate in the formation and maturation of red blood
cells, according to the Merck Manual Home Edition. Your liver stores vitamin B12 in
quantities that should last up to five years before the supply is exhausted. When you no
longer have sufficient supplies of B12, your red blood cells can become depleted in number
and abnormally large, a condition known as megaloblastic anemia.


Deficiency
Vitamin B12 deficiency can inhibit your body’s ability to create red blood cells to transport
oxygen to the organs that depend on it. As a result of vitamin B12 deficiency, anemia can
occur, leaving you feeling tired and weak. Neuropathy, or nerve damage, is another potential
result of vitamin B12 deficiency.

Causes

Vitamin B12 deficiency, and the anemia that results from it, can be the result of either dietary
inadequacies or health problems that inhibit your ability to absorb adequate amounts of
vitamin B12 from the foods you eat. MedlinePlus states that chronic alcoholism, Crohn’s
disease, celiac disease, tapeworm infections, gastrointestinal surgery, pernicious anemia and
chronic use of heartburn medications can all hamper your ability to absorb a sufficient
amount of vitamin B12.

Erythropoiesis is the process in which new erythrocytes are produced.

These new erythrocytes replace the oldest erythrocytes (normally about one percent)
that are phagocytosed and destroyed each day. Folate, vitamin B
12
, and iron have
crucial roles in erythropoiesis. Erythroblasts require folate and vitamin B
12
for prolif-
eration during their differentiation. Deficiency of folate or vitamin B
12
inhibits purine
and thymidylate syntheses, impairs DNA synthesis, and causes erythroblast apopto-
sis, resulting in anemia from ineffective erythropoiesis. Erythroblasts require large
amounts of iron for hemoglobin synthesis. Large amounts of iron are recycled daily
with hemoglobin breakdown from destroyed old erythrocytes. Many recently identi-
fied proteins are involved in absorption, storage, and cellular export of nonheme iron
and in erythroblast uptake and utilization of iron. Erythroblast heme levels regulate
uptake of iron and globin synthesis such that iron deficiency causes anemia by retarded
production rates with smaller, less hemoglobinized erythrocytes

New Insights into Erythropoiesis: The Roles of Folate, Vitamin B12, and Iron (PDF
Download Available). Available from:
https://www.researchgate.net/publication/8518428_New_Insights_into_Erythropoiesis_The_
Roles_of_Folate_Vitamin_B12_and_Iron [accessed Mar 04 2018].
Vitamin B12 and/or folate deficiency can cause a characteristic megaloblastic anemia with
ineffective erythropoiesis • The anemia of Cobalamin deficiency may be accompanied by
characteristic neurologic abnormalities. • The megaloblastic features are identical in deficiencies of
FA and Cbl. • The two vitamins are intertwined biochemically so that the final common pathway that
impairs DNA synthesis in hematopoietic cells is the same when either vitamin is deficient • However,
neuropathy occurs only with Cbl deficiency,. • Megaloblastic anaemia results from impaired
nucleotide biosynthesis (DNA Synthesis) due to a block in purine and thymidine biosynthesis. • Block
in purine and thymidine biosynthesis is consequence of vitamin B12 deficiency as it prevents the
synthesis of THF derivatives (Foliate metabolism) required for the purine and thymidine nucleotide.
Vitamin B12; Deficiency • Liver can store up to six years worth of vitamin B12, hence

Folic acid and cobalamin are B-group vitamins that play an essential role in
many cellular processes. Deficiency in one or both of these vitamins
causes megaloblastic anaemia, a disease characterized by the presence of
megaloblasts. Megaloblasts occur when inhibition of DNA synthesis causes
asynchronous maturation between the nucleus and the cytoplasm. Clinical
manifestations are similar to those of other types of anaemia, with the
exception of cobalamin deficiency megaloblastic anaemia, which presents
distinctive neurological symptoms. An understanding of the metabolism of
these vitamins will enable clinicians to make the best use and interpretation
of laboratory studies and monitor therapeutic strategies, which consist
mainly of administering supplements to restore body reserves.

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