White K L M, Chalmers D M, Martin I G, Everett S M, Neville P M, Naylor G, Sutcliffe A E, Dixon M F, Turner P C, Schorah C J
Molecular Epidemiology Unit, Epidemiology and Health Services Research, University of Leeds, LS2 9JT, UK.
Br J Nutr. 2002 Sep;88(3):265-71. doi: 10.1079/BJN2002619.
Free radicals and reactive species produced in vivo can trigger cell damage and DNA modifications resulting in carcinogenesis. Dietary antioxidants trap these species limiting their damage. The present study evaluated the role of vitamins C and E in the prevention of potentially premalignant modifications to DNA in the human stomach by supplementing patients who, because of hypochlorhydria and possible depletion of gastric antioxidants, could be at increased risk of gastric cancer. Patients undergoing surveillance for Barrett's oesophagus (n 100), on long-term proton pump inhibitors were randomized into two groups: vitamin C (500 mg twice/d) and vitamin E (100 mg twice/d) for 12 weeks (the supplemented group) or placebo. Those attending for subsequent endoscopy had gastric juice, plasma and mucosal measurements of vitamin levels and markers of DNA damage. Seventy-two patients completed the study. Plasma ascorbic acid, total vitamin C and vitamin E were elevated in the supplemented group consistent with compliance. Gastric juice ascorbic acid and total vitamin C levels were raised significantly in the supplemented group (P=0.01) but supplementation had no effect on the mucosal level of this vitamin. However, gastric juice ascorbic acid and total vitamin C were within normal ranges in the unsupplemented group. Mucosal malondialdehyde, chemiluminescence and DNA damage levels in the comet assay were unaffected by vitamin supplementation. In conclusion, supplementation does not affect DNA damage in this group of patients. This is probably because long-term inhibition of the gastric proton pump alone does not affect gastric juice ascorbate and therefore does not increase the theoretical risk of gastric cancer because of antioxidant depletion.
体内产生的自由基和活性物质可引发细胞损伤和DNA修饰,从而导致癌症发生。膳食抗氧化剂可捕获这些物质,限制其造成的损害。本研究通过对因胃酸过少和胃内抗氧化剂可能耗竭而患胃癌风险增加的患者进行补充维生素C和E,评估了它们在预防人类胃部潜在癌前DNA修饰方面的作用。对100名正在接受巴雷特食管监测且长期服用质子泵抑制剂的患者进行随机分组:一组服用维生素C(500毫克,每日两次)和维生素E(100毫克,每日两次),持续12周(补充组),另一组服用安慰剂。接受后续内镜检查的患者进行了胃液、血浆维生素水平及DNA损伤标志物的检测。72名患者完成了研究。补充组血浆中的抗坏血酸、总维生素C和维生素E升高,表明患者依从性良好。补充组胃液中的抗坏血酸和总维生素C水平显著升高(P = 0.01),但补充对该维生素的黏膜水平没有影响。然而,未补充组的胃液抗坏血酸和总维生素C在正常范围内。补充维生素对彗星试验中的黏膜丙二醛、化学发光及DNA损伤水平没有影响。总之,补充维生素对该组患者的DNA损伤没有影响。这可能是因为仅长期抑制胃质子泵不会影响胃液中的抗坏血酸盐,因此不会因抗氧化剂耗竭而增加患胃癌的理论风险。