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本文报告了焦炉尾气飘尘及几种多环芳烃(PAH)与苯并(a)芘(BaP)对鼠伤寒沙门氏菌/微粒体系统的联合致突变作用及其机理的研究。 沙门氏菌致突变试验的结果发现高剂量尾气飘尘提取物(相当于1.1m~3尾气飘尘)与BaP(40μM)联合时,致突变作用呈拮抗现象。用3-甲基胆蒽诱导大鼠肝微粒体BaP代谢产物为指标所进行的高压液相色谱分析表明,这四种PAH抑制了BaP近致癌物7,8-二氢二羟和灭活代谢产物的生成。四种PAH都抑制了芳烃羟化酶的活性,这最可能是由于不同的PAH在细胞色素P-450同一结合部位的竞争。而且,四种PAH经代谢后还抑制了环氧化物水化酶的活性。
This paper reports the combined mutagenicity and mechanism of coke oven exhaust fly ash and several polycyclic aromatic hydrocarbons (PAHs) and benzo (a) pyrene (BaP) against S. Typhimurium / microsomal system. Salmonella mutagenicity test results showed that high-dose exhaust fly dust extract (equivalent to 1.1m ~ 3 exhaust gas fly) and BaP (40μM), the mutagenicity was antagonistic phenomenon. High-pressure liquid chromatography analysis using 3-methylcholanthrene-induced BaP metabolites of rat liver microsomes showed that these four PAHs inhibited BaP near-carcinogen 7,8-dihydroxy dihydroxy and inactivation metabolism Product generation. All four PAHs inhibited aromatase hydroxylase activity, most likely due to competition of different PAHs at the same binding site of cytochrome P-450. Moreover, four PAHs also inhibit epoxide hydratase activity after metabolism.