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Zinc Deficiency and Oxidation of L-Methionine-methyl-¹⁴C in Rats

Biochemistry Research Laboratory, Veterans Administration Hospital, and the Department of Biochemistry, The Johns Hopkins University, Baltimore, Maryland

Studies were undertaken to determine the effect of zinc deficiency on the patterns of oxidation of various ¹⁴C-labeled compounds to respiratory CO₂. Significantly higher percentages of L-methionine-methyl-¹⁴C were oxidized by zinc-deficient rats. This increase was apparently not due to differences in body weight and was observed with tracer as well as with carrier doses of the amino acid. Intraperitoneal injection of 400 µg zinc daily for 3 consecutive days prevented this occurrence. The specific involvement of the methyl group of methionine was indicated by the observation of normal oxidations of methionine-1-¹⁴C and methionine-2-¹⁴C. Oxidations of tracer doses of ¹⁴C-labeled acetate, glutamic acid and formic acid were essentially unaffected by zinc deficiency. Oxidations of glycine-1-¹⁴C, cystine-1-¹⁴C, tryptophan-2-¹⁴C and formaldehyde-¹⁴C, however, were enhanced in zinc-deficient rats.