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首页> 外文期刊>Mutation Research, C. Mutation Research Letters >EFFECT OF CIGARETTE SMOKE ON THE MUTAGENIC ACTIVATION OF VARIOUS CARCINOGENS IN HAMSTER
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EFFECT OF CIGARETTE SMOKE ON THE MUTAGENIC ACTIVATION OF VARIOUS CARCINOGENS IN HAMSTER

机译：香烟烟雾对仓鼠各种致癌物质突变激活的影响

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Male Syrian golden hamsters were exposed for 1 or 2 weeks to smoke produced by commercial non-filter cigarettes for 5 consecutive days in a Hamburg type II smoking machine. Postmitochondrial fractions (S9) prepared from the liver, lungs, and pancreas were used in the Ames liquid incubation assay, in order to assess the effect of cigarette smoke (CS) on the metabolic activation of four groups of procarcinogens. The mutagenic activities df five heterocyclic amines on strain TA98 in the presence of liver S9 mix were induced up to 3.7 times above controls including sham smoke control, while no significant alteration of mutagenicity was observed with. 3'-hydroxymethyl-N,N-dimethyl-4-aminoazobenzene and benzo[a]pyrene on TA98 or with N-nirosobis(2-oxopropyl)amine (BOP) on TA100. A similar stimulation of metabolic activation was also observed for 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) with S9 from the lungs but not from the pancreas. The mutagenic potential of 11 carcinogens including aflatoxin B-1 (AFB(1)) and two other heterocyclic amines was also examined using liver S9 from male hamsters pretreated with phenobarbital (PB) or 3-methylcholanthrene (MC). The numbers of revertant colonies were much higher (2-20-fold) in the presence of MC-treated liver S9 than in the presence of PB-treated liver S9, except in the case of AFB, which showed a higher mutagenicity with PB-induced S9. 7,8-Benzoflavone considerably inhibited the activities of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and Trp-P-l in the presence of either untreated, MC- or CS-treated liver S9, whereas metyrapone was totally lacking this effect, indicating that cytochrome P450(CYP)1A1/1A2 isoforms of hamster liver are predominantly involved in the metabolic activation of these carcinogens. CS exposure of hamsters might selectively induce hepatic CYP1A2 which cannot activate BOP. Consequently, the present findings could explain, in part, the anticarcinogenic effect of CS on BOP-induced pancreatic tumors in hamsters. The findings further support the idea that CS markedly stimulates the metabolic activation of food-derived carcinogens, which may contribute to the overall carcinogenic effects of cigarette smoking.
机译：在汉堡II型吸烟机中，将叙利亚雄性金仓鼠连续5天暴露于商用非过滤嘴香烟产生的烟雾中1或2周。为了评估香烟烟雾（CS）对四类致癌物代谢活化的影响，使用了从肝脏，肺脏和胰腺中制备的线粒体后级分（S9）进行Ames液体温育试验。在存在肝S9混合物的情况下，五种杂环胺对TA98菌株的诱变活性比对照（包括假烟控制）高3.7倍，而诱变活性未见明显变化。 TA98上的3'-羟甲基-N，N-二甲基-4-氨基偶氮苯和苯并[a] or或TA100上的N-硝基双（2-氧丙基）胺（BOP）。还观察到3-氨基-1,4-二甲基-5H-吡啶并[4,3-b]吲哚（Trp-P-1）具有类似的代谢活化刺激，S9来自肺部而非胰腺。还使用来自苯巴比妥（PB）或3-甲基胆甾（MC）预处理的雄性仓鼠的肝脏S9检验了11种致癌物（包括黄曲霉毒素B-1（AFB（1））和其他两种杂环胺）的诱变潜力。存在MC处理的肝脏S9的情况下，回复菌落的数量要比经过PB处理的肝脏S9的情况下的回复菌落数量高得多（2-20倍），而AFB的情况除外，后者显示出与PB-诱导S9。在未经治疗，经MC或CS处理的肝脏S9存在下，7,8-苄黄酮显着抑制2-氨基-3-甲基咪唑并[4,5-f]喹啉（IQ）和Trp-Pl的活性，而甲吡酮完全缺乏这种作用，表明仓鼠肝脏的细胞色素P450（CYP）1A1 / 1A2亚型主要参与这些致癌物的代谢活化。 CS暴露的仓鼠可能选择性地诱导肝脏CYP1A2不能激活BOP。因此，本研究结果可以部分解释CS对BOP诱导的仓鼠胰腺肿瘤的抗癌作用。这些发现进一步支持了CS明显刺激食物致癌物的代谢活化的想法，这可能有助于吸烟的总体致癌作用。

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