Diet, genetic polymorphisms, detoxification, and health risks.

摘要: Modulation of detoxification enzymes is one mechanism by which diet may influence risk cancer and other diseases. However, genetic differences in taste preference, food tolerance, nutrient absorption, metabolism response target tissues all potentially the effect on disease risk. Thus, prevention at individual population level needs to be evaluated context totality background exposures both causative agents chemopreventive compounds. Polymorphisms that alter protein expression and/or function can modify individuals exposed relevant substrates. Diet a mixture carcinogens, mutagens, protective are metabolized enzymes. Genotypes associated with more favorable handling carcinogens less phytochemicals. For example, glutathione S-transferases (GST) detoxify polycyclic aromatic hydrocarbons present grilled meats. GSTs also conjugate isothiocyanates, compounds found cruciferous vegetables. GSTM1 GSTT1 genes result complete lack GSTM1-1 GSTT1-1 proteins, respectively. In some observational studies cancer, vegetable intake confers greater protection these polymorphisms; however, studies, converse observed. A recent study sulforaphane pharmacokinetics suggests enzyme rapid excretion sulforaphane. Many phytochemicals conjugated glucuronide sulfate moieties, excreted urine bile. UDP-glucuronosyltransferases (UGT) sulfotransferases (SULT) contribute variability phytochemical clearance efficacy. The effects UGT polymorphisms flavonoid have not been examined, but affect glucuronidation several drugs steroid hormones. Genetic account part for variation considered aspects human genetics, gut bacterial environmental exposures.