In vivo methylation capacity is not impaired in healthy men during short-term dietary folate and methyl group restriction.

Ten healthy adult men were fed a diet low in folate and exogenous methyl groups to study the effects on in vivo methylation capability. The men were housed in a metabolic unit for the entire 108 d of the study. After a 9-d baseline period (Period 1), the men were fed a soy-product-amino acid defined diet for 45 d, which provided 25 micrograms/d of folate for 30 d (Period 2) and, with a folate supplement, 99 micrograms/d for 15 d (Period 3). During Period 2 and Period 3, the low methionine and choline diet was supplemented with methionine for half the subjects to vary the dietary methyl group intake. The periods were then repeated over the next 54 d (Periods 4-6), with a crossover of methionine intakes in Period 5 and Period 6. A 1-g oral dose of nicotinamide was given at the end of each period and methylated urine metabolites determined. Other measures related to in vivo methylation capability included urine creatinine, and plasma and urine carnitine. Even with moderate folate depletion, none of these measures was decreased by low methionine and choline intakes. Plasma methionine concentrations were unchanged throughout. Limiting exogenous methyl group intake by restricting dietary methionine and choline did not impair in vivo methylation capabilities for the variables tested, even at low folate intake.

Cellular ascorbate depletion in healthy men.

To clarify the relationship of plasma ascorbic acid to cellular ascorbic acid levels, we determined plasma, lymphocyte, buccal cell and semen ascorbic acid in eight healthy men consuming controlled ascorbic acid intakes of 5, 10, 20, 60 or 250 mg/d over 13 wk while living in a metabolic unit. Levels of ascorbic acid in all four specimen types were significantly lower during the three lowest intakes (5, 10, or 20 mg/d) compared with the 60 or 250 mg/d intakes, but only plasma and lymphocyte ascorbic acid levels discriminated between these intakes unequivocally and with no overlap. Priority for maintenance of intracellular lymphocyte ascorbic acid was indicated by rapid repletion of lymphocytes compared with plasma and semen at 60 mg/d intake. Strong correlations of plasma with lymphocyte ascorbic acid within individuals indicated that plasma levels would reliably reflect low lymphocyte levels in nutrition monitoring surveys. Buccal cell ascorbic acid may be useful as a noninvasive screening test for ascorbic acid deficiency. Semen and sperm qualities were unchanged despite an average decline in semen ascorbic acid to 24% of baseline. Short-term ascorbic acid depletion in healthy men did not adversely affect sperm qualities related to fertility nor did moderate supplementation improve them.

Immunocompetence and oxidant defense during ascorbate depletion of healthy men.

To determine nonscorbutic effects of moderate vitamin C deficiency we measured immune function and oxidative damage in eight healthy men (25-43 y) who consumed 5-250 mg/d of ascorbic acid over 92 d on a metabolic unit. During ascorbic acid intakes of 5, 10, or 20 mg/d, subjects attained a state of moderate ascorbic acid deficiency as ascorbic acid concentrations in plasma, leucocytes, semen, and buccal cells dropped to less than 50% of baseline with no scorbutic symptoms observed. No changes in cell proliferation, erythrocyte antioxidant enzymes, and DNA strand breaks were observed; however, blood levels of glutathione and NAD(P) decreased during ascorbic acid deficiency, as did delayed hypersensitivity responsiveness. Concentrations of the oxidatively modified DNA base, 8-hydroxydeoxyguanosine in sperm DNA and fecapentaenes, ubiquitous fecal mutagens, were increased during ascorbic acid depletion. Moderate vitamin C deficiency, in the absence of scurvy, results in alteration of antioxidant chemistries and may permit increased oxidative damage.