Cho C H, Fong L Y, Wong S H, Ogle C W
Department of Pharmacology, Faculty of Medicine, University of Hong Kong.
Drug Nutr Interact. 1988;5(4):289-95.
The effects of zinc deficiency on ethanol-induced ulcers were studied. Rats fed with zinc-deficient diets for 5 weeks showed markedly lowered serum zinc levels and body weights. Ethanol 30% given orally produced gastric mucosal lesions and reduced the glutathione content in the gastric glandular mucosa in their pair-fed non-zinc-deficient controls. Zinc deficiency potentiated the glutathione-depleting and ulcer-producing effects of ethanol. N-acetylcysteine, a sulfhydryl-containing agent, protected non-zinc-deficient rats from lesions produced by 50% ethanol, whereas N-ethylmaleimide, a sulfhydryl-blocking agent, worsened ulceration. It appears that zinc deficiency intensifies ethanol-induced ulceration by permitting greater depletion of the glutathione content in the stomach.
研究了锌缺乏对乙醇诱导溃疡的影响。用缺锌饮食喂养5周的大鼠血清锌水平和体重显著降低。口服30%乙醇会导致胃黏膜损伤,并降低其配对喂养的非缺锌对照组胃腺黏膜中的谷胱甘肽含量。锌缺乏增强了乙醇消耗谷胱甘肽和产生溃疡的作用。含巯基的药物N-乙酰半胱氨酸可保护非缺锌大鼠免受50%乙醇所致的损伤,而巯基阻断剂N-乙基马来酰亚胺则会加重溃疡。看来锌缺乏通过使胃中谷胱甘肽含量更大程度地消耗,从而加剧了乙醇诱导的溃疡形成。