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American Journal of Clinical Nutrition, Vol 54, 1302S-1309S, Copyright © 1991 by The American Society for Clinical Nutrition, Inc
ORIGINAL RESEARCH COMMUNICATIONS |
RA Jacob, DS Kelley, FS Pianalto, ME Swendseid, SM Henning, JZ Zhang, BN Ames, CG Fraga and JH Peters
Western Human Nutrition Research Center, USDA Agricultural Research Service, Presidio of San Francisco, CA 94129.
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.
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