Possible interrelationship between vitamins E and b12 in the disturbance in methylmalonate metabolism in vitamin E deficiency.
1. The disturbance in 2-methylmalonate metabolism resulting in its increased urinary excretion observed in vitamin E deficiency is not caused by increased formation of methylmalonate from propionate as is evident from the activity of the enzyme propionyl-CoA carboxylase (EC 6.4.1.3), but can be traced to an impairment in the conversion of methylmalonate into succinate by the vitamin B12-requiring enzyme, methylmalonyl-CoA mutase (EC 5.4.99.2) in rat liver. 2. It is shown that the decrease in the activity of methylmalonyl-CoA mutase in vitamin E deficiency is not a consequence of a secondary vitamin B12 deficiency. Peroxidative destruction of the coenzyme in vitamin E deficiency was also ruled out. The results suggest a defect in the conversion of cyanocobalamin into its coenzyme form.
D000818:Animals; D003038:Cobamides / Q000378:metabolism*; D066298:In Vitro Techniques; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008297:Male; D008314:Malonates / Q000378:metabolism*; D008764:Methylmalonic Acid / Q000378:metabolism* / Q000652:urine; D011422:Propionates / Q000378:metabolism; D051381:Rats; D013386:Succinates / Q000378:metabolism; D014805:Vitamin B 12 / Q000494:pharmacology; D014810:Vitamin E / Q000378:metabolism*; D014811:Vitamin E Deficiency / Q000378:metabolism*
D003038:Cobamides; D008314:Malonates; D011422:Propionates; D013386:Succinates; D014810:Vitamin E; D008764:Methylmalonic Acid; D014805:Vitamin B 12