作者: Paul Talalay , Robert P. Batzinger , Ann M. Benson , Ernest Bueding , Young-Nam Cha
DOI: 10.1016/0065-2571(79)90006-2
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摘要: Abstract The protection afforded by antioxidants against the induction of a variety experimental tumors in rodents phenomenon on great theoretical interest and potentially practical importance. possibility that exert their effects interacting directly with electrophilic species ultimate carcinogens cannot be excluded. However, at present most plausible mechanisms for protective invoke alteration balance between metabolic activation inactivation carcinogens. Dietary administration 2(3)- tert -butyl-4-hydroxyanisole (BHA) to mice results marked reduction levels mutagenic metabolites benzo(a)pyrene prevailing theurine peritoneal cavity. This dietary treatment is accompanied substantial elevations various glutathione S -transferase epoxide hydratase livers number other tissues rats. Direct addition certain purified -transferases mutagenicity assay system reduces activity urinary benzo(a)pyrene. Others have shown can function both this carcinogen. Other changes activities mouse hepatic enzymes associated feeding BHA include UDP-glucose dehydrogenase UDP-glucuronyl transferase suggesting an enhanced capacity glucuronide formation.