Møller Peter, Loft Steffen
Institute of Public Health, c/o Department of Pharmacology, University of Copenhagen, The Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark.
Mutat Res. 2004 Jul 13;551(1-2):79-89. doi: 10.1016/j.mrfmmm.2004.02.018.
Cells are constantly exposed to oxidants from metabolic and other biochemical reactions as well as external factors, suggesting that DNA repair systems and nutritional antioxidants are important determinants for low levels of DNA damage and cancer risk. The effects of single antioxidants, as well as various vegetables, fruits and carotenoid- and polyphenolic-rich products, have been assessed with biomarkers, mainly including DNA damage in white blood cells (WBC), urinary excretion of oxidized bases and nucleosides and DNA repair capacity. The basal levels of oxidative DNA damage, and effects of the interventions have been rather variable, possibly reflecting differences in the populations, regimens, and the type of assays. In general, single dose antioxidant interventions have shown protective effects with respect to WBC DNA oxidation. Studies with continuous ingestion of antioxidants show mixed results with respect to effects on oxidative DNA damage in WBC, possibly due to various problems with design, statistical power and period effects. Studies with only male subjects appear to show consistent antioxidant effects in terms of reduced levels of oxidized pyrimidines. Investigations of oxidatively stressed subjects, e.g. HIV-infected patients or diabetics, suggest beneficial outcomes in populations with high initial levels of oxidative DNA damage. Recent research on the effect of antioxidants on DNA repair enzymes suggest effects in terms of increased removal of oxidized purines, whereas mRNA levels of the relevant DNA repair genes appears to be unaffected by an antioxidant-rich diet. In the future, care should be taken with respect to design of intervention studies and considerations of gender effect, genotypes of defence enzymes as well as DNA repair capacity.
细胞不断暴露于来自代谢及其他生化反应的氧化剂以及外部因素中，这表明DNA修复系统和营养抗氧化剂是低水平DNA损伤和癌症风险的重要决定因素。单一抗氧化剂以及各种蔬菜、水果和富含类胡萝卜素及多酚的产品的效果已通过生物标志物进行评估，这些生物标志物主要包括白细胞（WBC）中的DNA损伤、氧化碱基和核苷的尿排泄以及DNA修复能力。氧化DNA损伤的基础水平以及干预措施的效果差异很大，这可能反映了人群、方案和检测类型的不同。一般来说，单剂量抗氧化剂干预已显示出对白细胞DNA氧化的保护作用。持续摄入抗氧化剂的研究在对白细胞氧化DNA损伤的影响方面结果不一，这可能是由于设计、统计效力和周期效应等各种问题所致。仅针对男性受试者的研究似乎在氧化嘧啶水平降低方面显示出一致的抗氧化作用。对氧化应激受试者（如HIV感染患者或糖尿病患者）的调查表明，在初始氧化DNA损伤水平较高的人群中会有有益结果。近期关于抗氧化剂对DNA修复酶影响的研究表明，在增加氧化嘌呤清除方面有作用，而相关DNA修复基因的mRNA水平似乎不受富含抗氧化剂饮食的影响。未来，在干预研究设计以及性别效应、防御酶基因型和DNA修复能力等方面的考虑上应谨慎。
