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CYP1A1 levels in lung tissue of tobacco smokers and polymorphisms of CYP1A1 and aromatic hydrocarbon receptor.

机译：吸烟者肺组织中CYP1A1的水平及CYP1A1和芳香烃受体的多态性

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摘要

Induction of a polycyclic aromatic hydrocarbon-metabolizing cytochrome P450 isoform CYP1A1 is regulated by aromatic hydrocarbon receptor (AHR). High inducibility of CYP1A1, possibly due to genetic polymorphisms, has been considered to be a risk factor for lung cancer in tobacco smokers. The relationship between low or high pulmonary expression of CYP1A1 and polymorphic genotypes of CYP1A1 and AHR was investigated in 73 active smokers. CYP1A1 expression was determined in surgical lung samples by measuring ethoxyresorufin O-deethylase (EROD) activity and by immunostaining for CYP1A1 protein. The most common allelic variants of CYP1A1 and AHR in Finns, i.e. the MspI variant (CYP1A1*2A), I462V variant (CYP1A1*2B), and -459C to T variant of CYP1A1 and the R554K variant (AHR*2) of AHR were studied using polymerase chain reaction based methods. EROD activity correlated positively with the daily cigarette consumption (r = 0.45). There was additional variation in EROD activity independent of the amount of smoking e.g. among those who smoked one pack per day until the day of operation, EROD activity ranged from 4-142 (median 48) pmol/min/mg. The frequencies of the MspI, 462V, and -459T variant alleles of CYP1A1 and 554K variant allele of AHR were 0.158, 0.055, 0.055 and 0.075, respectively. No differences were observed in the frequencies of polymorphic genotypes between the smokers with low and those with high expression, when the relationship was studied using a regression analysis adjusted for cigarette consumption. Our results thus indicate that the interindividual variation of CYP1A1 levels in smokers' lung tissue is not attributable to genetic polymorphisms of CYP1A1 or AHR tested in this study.
机译：多环芳烃代谢细胞色素P450异构体CYP1A1的诱导受芳烃受体（AHR）的调节。 CYP1A1的高诱导性，可能是由于遗传多态性，已被认为是吸烟者肺癌的危险因素。在73名活跃吸烟者中研究了CYP1A1的低或高肺表达与CYP1A1和AHR的多态性基因型之间的关系。 CYP1A1的表达是通过测量乙氧基间苯二酚O-脱乙基酶（EROD）活性和对CYP1A1蛋白进行免疫染色来确定的。芬兰人中最常见的CYP1A1和AHR等位基因变体是MspI变体（CYP1A1 * 2A），I462V变体（CYP1A1 * 2B）和-459C至CYP1A1的T变体以及AHR的R554K变体（AHR * 2）使用基于聚合酶链反应的方法进行了研究。 EROD活性与每日吸烟量呈正相关（r = 0.45）。 EROD活性还有其他变化，与吸烟量无关，例如在每天抽一包直到手术当天的人群中，EROD活性范围为4-142（中位数48）pmol / min / mg。 CYP1A1的MspI，462V和-459T变异等位基因的频率和AHR的554K变异等位基因的频率分别为0.158、0.055、0.055和0.075。低烟民和高烟民吸烟者之间的多态性基因型频率没有差异，当使用针对卷烟消费量进行调整的回归分析研究这种关系时。因此，我们的结果表明，吸烟者肺组织中CYP1A1水平的个体差异并不归因于本研究中测试的CYP1A1或AHR的遗传多态性。

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