摘要Oxidative stress (OS) occurs when the production of reactive oxygen species (ROS) overrides the body’s natural defence. When the cell nucleus represents the target, macromolecular damage may result in mutations. Cancer is a disease of mutations, and DNA damages that are not repaired or mis-repaired during cell proliferation are necessary but not sufficient for cancer development. A role of ROS for cancer initiation depends on the likelihood of interaction between reactive electrophilic molecules and nuclear DNA. As described in part one of this presentation, the physico-chemical properties of the ROS involved in OS and of the ensuing DNA lesions are of major importance. Current knowledge dictates that emphasis should be shifted from oxidative DNA damages of low genotoxicity towards pro-mutagenic lesions induced by reaction products of nitrogen monoxide and complex highly reactive carbonyls, e.g. from the peroxidation of lipids. Based on the determination of pro-mutagenic DNA adducts in human tissues there is compelling evidence for a causal relation between OS and cancers of the liver, colon/rectum, cervix, pancreas and stomach. However, modulation by the simultaneous presence of an ubiquitous high background of potent pro-carcinogenic DNA adducts, which are not generated by ROS should be taken into account. Ionizing radiation is established human carcinogenic agent, and generate some of the same oxidative ROS as those involved in OS. However, the cancer spectrum from whole body radiation exposure differs in some important respects from that associated with OS. The scientific support for a causal link between exposure to non-ionizing electromagnetic radiation and human cancer is judged to be insufficient. As exemplified by diabetes, a common shortcoming when assessing the role of OS in disease is the failure to distinguish between cause and effect - i.e. could the indicators of harmful oxidative stress be the result of the pathological condition in question, rather than its cause.