Role of dietary mutagens in cancer and atherosclerosis

Purpose of review To provide an updated summary of dietary mutagens and their potential role in the etiology of cancer and atherosclerosis. Recent findings Compelling evidence supports an accumulation of somatic mutations during carcinogenesis, leading to the activation of oncogenes or inactivation of tumor suppressor genes or both. There is also suggestive evidence that mutation provides an early event in atherosclerosis. Genome-wide association studies (GWAS) identify genes associated with familial cancers and atherosclerosis, but genes involved in sporadic events are less well characterized. Many dietary components are mutagenic, including natural dietary components, mutagens generated during cooking and processing of food or through contamination. Molecular epidemiology associates specific mutagens with specific types of cancer. Although chromosome mutations may provide a risk biomarker for atherosclerosis, they are not necessarily causal. Summary Association studies, supported by molecular epidemiology, provide evidence that certain dietary mutagens, including aflatoxin B1, aristolochic acid and benzo[a]pyrene, are causal in some human cancers. Similar studies have correlated the level of oxidative DNA damage, DNA adducts and clastogenesis in arterial smooth muscle cells with atherogenic risk factors described through traditional epidemiology, However, establishing whether or not dietary mutagens lead to mutations that are causal in atherosclerosis remains a challenge for the newer genomic technologies.