Reference

Metabolism of methylmalonic acid in rats

Metabolism of methylmalonic acid in rats. Is methylmalonyl-coenzyme A racemase deficiency symptomatic in man?. Montgomery, J. A.; Mamer, O.In this study， 9024-03-7 and 516-05-2 are also used. A.; Scriver, C. R. (Biomed. Mass Spectrometry Unit, McGill Univ., Montreal, PQ H3A 1A3, Can.). J. Clin. Invest., 72(6), 1937-47 (English) 1983. CODEN: JCINAO. ISSN: 0021-9738. DOCUMENT TYPE: Journal CA Section: 14 (Mammalian Pathological Biochemistry) Vitamin B12-deficient and normal rats were loaded with methylmalonic (MMA) and ethylmalonic acids labeled with 13C in the carboxyl groups and with 2H in the alkyl groups. Significant fractions of the administered acids were excreted in both the B12-deficient and the normal animal, having undergone exchange of both their 13C-labeled carboxyl groups with endogenous 12C. The exchange of the a-1H of MMA in 2H2O at 25° and pH 7.5 was found by 1H-NMR to have a half-life of 28.3 min. These results show that a fraction of in vivo metab. through the propionate-to-succinate pathway occurs via a shunt involving free MMA. The enzymes of this pathway are thought to utilize only CoA esters. To allow for the exchange of the 2nd CoA-bound carboxyl group, it is proposed the deacylation of the once exchanged acid with spontaneous racemization (relative to the 13C-carboxyl group), followed by reacylation, thus exposing the labeled carboxyl to decarboxylation. The significance of this mechanism involving free MMA is that racemization of methylmalonyl (MM)-CoA may also occur without the intervention of MM-CoA racemase. A deficiency of this enzyme need not result in symptomatic methylmalonic aciduria. .

Vitamins and periodic fasting as possible factors of experimental prolongation of the life span

Vitamins and periodic fasting as possible factors of experimental prolongation of the life span. Konoplya, E. F.; Dubina, T. L.; Zelezinskaya, G. A.; Dyundikova, V. A.; Pokrovskaya, R. V.; Gul'ko, V. V.; Mazhul, L. M.; Gatsko, G. G. (Sect. Gerontol., Acad. Sci., Minsk, USSR). Fiziol. Zh. (Kiev), 30(1), 16-24 (Russian) 1984. CODEN: FIZHDO. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) Periodic fasting decreased the aging process in rats given during the refeeding period a vitamin mix contg. thiamin [59-43-8], riboflavin [83-88-5], pyridoxine [65-23-6], nicotinic acid [59-67-6], pantothenic acid [79-83-4], vitamin B12 [68-19-9], folic acid [59-30-3], ascorbic acid [50-81-7], and vitamin D [1406-16-2]. The rats were obsd. from 6-6.5 to 20-20.There are some commonly used reagents with their cas registry numbers 1406-16-2 and 68-19-9 in this article.5 mo of age, and the courses of fasting-refeeding lasted 6 wk (4-9 courses). The conventional biol. age value calcd. from data on live wt., skin, heart, and aorta collagen levels, and liver glucose 6-phosphate dehydrogenase [9001-40-5] was less in vitamin-supplemented periodically fasting rats than in vitamin-supplemented nonfasting or nonsupplemented fasting controls. Fasting without vitamin supplementation increased the conventional biol. age value compared to nonfasting controls. Combination of fasting with vitamin supplementation increased liver aminopyrine demethylase [9037-69-8] and succinate dehydrogenase [9002-02-2], heart NADP dehydrogenase [9001-68-7], and brain lactate dehydrogenase [9001-60-9] and succinate dehydrogenase activities compared to controls. Fasting + vitamins increased the level of glycogen [9005-79-2] in the muscles and decreased it in the liver. .