of DMA synthesis (see also discussion, on vrt 012 in chap 1 SBC II, lor explanation)

) This leads to inhibition of cell division which in turn leads lo greater amount of PNA accumulation within the cell (as RNA synthesis has nol been hampered) This means, The cells become bigger than normal and remain immature. This is seen typically in the bane marrow of patients suffering from pernicious anemia and such abnormal cells are ceiled megalobJasts. However, on theoretical grounds such abnormality should be present universally m all the cells of the body, although m practice that is not seen The rnegaLoblasts develop into macrocyles (= bigger cells) which appear in the cirulation FQUC ACID like vif B12, most of the important issues on the folic acid have been discussed in connection with the factors required Tor erythropoiesis [chap II 1) Some additional issues are discussed below In Ihe 1930s Will and her colleagues reported a particular type of megaloblastic anemia occurring in the Hindu (Indian] pregnant women, which was different from pernicious anemia (The classical pemicrous anemia is very rare in India) A new factor, called Wills factor' could cure it Subsequent investigations established thal this Will's factor'was different from the vit B12 and eventually Will's factor was found 10 be folic acid Chemistry and mode of action Folic acid has the following structure (fig 7. 14 6) Fig 7 .14. 6. Monoqlutamale form of folic acid (pteroyl glutamic acid) The structure shown in fig 7. 14 .6. is a monoglutamate form of folic acid This form of folic acid is seen in the blood In the tissues of our body (as well as in the food), folic acids is in polyglulamate form, that is, there are several glutamic acids (upto seven) in a single molecule of folic acid The food polyglutamale form of folic acid is converted into monoglutamate form in the intestine and absorbed Ultimately it (= the monoglutamate form) comes to the tissue where it becomes 5. 10 melhylene fetrahydrofolic acid (5.10. methylene THF). which is required for The DNA synthesis Wnile doing This some 5.10. methylene THF become 5 methyl I tetrahydrofolic acid Vit B12 is required for converting 5 methyl tetrahydrofolic acid into 5.10 methylene THF so that the 5, 10 melhylene THF is regenerated Conclusion is, either lack of food folic acid or vi[ B12 should cause inhibition of DMA synthesis and can cause megaloblastic anemia (see also factors for erythropoiesis. chap II I) Finally, the student should remember a fundamental difference in the clinical feature of folate deficiency which differentiates it self from vit B12 deficiency This is important because the hematological (bone marrow and peripheral blood pictures) features of folate (folic acid) deficiency and B12 deficiency are remarkably identical, only dependable difference being the concentration of vit B12 and folate in blood That is. in pure B12 deficiency (pernicious anemia) the blood concentration of vit Bt2 falls whereas that of folate falls in folate deficiency (sea chap 1 sec I! for details) The clinical difference (expected in advanced cases), mentioned above. is as follows in vit B12 deficiency neurological signs may appear due lo degeneration of some tracts of spinal cord Q symptoms and signs include loss of motor as well as sensory (particularly sense of vibration and posmon sense) functions In folate deficiency they do nol appear In a book like this, the probable explanations need not fie discussed VIT C (ASCORBIC ACID) Chemistry Vit C (ascorbic acid) rs water soluble vilamm. The structural formula of ascorbic acrd and its oxidized form, dehydroascorbic acid is given in fig 7 147 note that there is an asymmetric C atom in the molecule