作者: A JEFFREY , G WILLIAMS
DOI: 10.1016/J.TAAP.2005.03.024
关键词:
摘要: Risk assessment of DNA-reactive carcinogens in food requires knowledge the extent DNA damage target organ which results from competition between adduct formation and repair. Estimates levels can be made by direct measurement or indirectly as a consequence their presence, for example, tumor animal models exposed populations epidemiologically. Food-borne are present variety sources. They generally not intrinsically but require bioactivation to metabolites process may modulated compound itself presence other xenobiotics. A single reactant form several distinct adducts each undergoing different rates Some reactants photochemically activated produce reactive oxygen species thus indirect oxidative damage. The arising exposures influenced variations doses, frequency with an individual is exposed, repair specific adducts. Each has characteristic efficiency it induces mutations. Based on experience well-studied carcinogen aflatoxin B(1) (AFB(1)), limit 20 ppb approximately 30 microg/day been set considered tolerable daily intake (TDI). Since AFB(1) potent carcinogen, doses <1.5 microg unknown compounds TDIs. Most DNA-reactants, including acrylamide, heterocyclic amines, alpha,beta-unsaturated carbonyl below this value. Above that value, actual either experimental animals risk assessment, or, when occurs, humans needed. number approaches undertake described immunological, mass spectrometric (32)P-postlabeling use surrogates such hemoglobin adducts, together evaluate results. discussion estimating possible threshold effects made.