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Title: ARSENIC DEPRIVATION AFFECTS HOMOCYSTEINE REMETHYLATION IN RATS FED HOMOCYSTINE AND CHOLINE

Author
item Uthus, Eric

Submitted to: North Dakota Academy of Science Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 2/20/2001
Publication Date: 5/31/2001
Citation: Uthus, E.O. 2001. Arsenic deprivation affects homocysteine remethylation in rats fed homocystine and choline. Proceedings of the North Dakota Academy of Science. 55:65.

Interpretive Summary: Dietary arsenic (As) is thought to have a physiological role affecting the sulfur amino acid methionine. These findings suggest that arsenic could be important in the formation of methionine from its precursor homocysteine. There are two ways by which methionine can be formed from homocysteine. One pathway needs the vitamin folic acid. The other pathway needs the vitamin. This study assessed in rats the effect of dietary arsenic on these 2 pathways. The results obtained suggest that dietary arsenic affects the formation of methionine from homocysteine. The data show that arsenic-deprived rats fed low amounts of folic acid can not as efficiently make more methionine. This suggests that arsenic has a physiological role that could be important to maintain adequate amounts of methionine in the body. These data support the notion that a small amount of arsenic is needed by humans.

Technical Abstract: Dietary arsenic (As) is thought to have a physiological role in methionine (Meth) metabolism. Some studies suggest that arsenic may be important in the remethylation of homocysteine to methionine. There are two pathways by which homocysteine can be remethylated to form methionine. One pathway, catalyzed by the enzyme methionine synthase (MS), derives its methyl group from the C1 (folic acid) pool. The other pathway derives its methyl group from choline and is catalyzed by the enzyme betaine- homocysteine methyltransferase (BHMT). Thus, the objective of this study was to assess in rats the effect of arsenic deprivation on these 2 pathways. The pathways were altered by feeding either methionine or homocystine in conjunction with either folic acid or choline deficiency. The experiment was a 2 x 2 x 2 design with dietary variables arsenic (0 or 0.5 ug/g), DL-methionine or DL-homocystine (one or the other in the diet), and choline or folic acid (one or the other in the diet). The basal diet was lacking in folic acid and choline. After 54 days the arsenic deprived rats fed choline tended to weigh less than those fed supplemental As; this was not true in the FA-fed rats. MS activity was decreased in rats fed choline (no folic acid). BHMT was decreased by arsenic deprivation in rats fed dietary choline. The results suggest that dietary arsenic does affect remethylation of homocysteine. The data show that arsenic-deprived rats fed choline (no folic acid) can not as efficiently compensate with the enzyme BHMT to produce methionine. This suggests that arsenic has a physiological role related to BHMT or in the metabolism of betaine from choline, or that arsenic deprivation results in more S- adenosylhomocysteine which inhibits BHMT.