Villard P H, Seree E, Lacarelle B, Therene-Fenoglio M C, Barra Y, Attolini L, Bruguerole B, Durand A, Catalin J
EA 859, Laboratoire de Pharmacocinétique et de Toxicologie, Faculté de Pharmacie, Marseille, France.
Biochem Biophys Res Commun. 1994 Aug 15;202(3):1731-7. doi: 10.1006/bbrc.1994.2135.
Pulmonary and liver microsomes of male NMRI mice were used to study the inductive effect of cigarette smoke on various cytochrome P450 isoforms implicated in precarcinogen and premutagen bioactivation. The enzymatic activities catalyzed by CYP1A1, CYP2B, CYP2C, CYP2D, CYP2E1 and CYP3A were induced in liver microsomes. Immunoquantification of lung and liver CYP1A1, 2E1 and 3A demonstrated that 1) CYP1A1 was induced in lung and liver, 2) CYP3A subfamily was induced in liver and not detected in lung, 3) CYP2E1 was slightly induced in liver whereas its pulmonary expression was more largely increased (6.8 fold) than CYP1A1 (2.0 fold). This latter data suggests that CYP2E1, which is known to be expressed in human lung, could actively participate in pulmonary carcinogenesis induced by cigarette smoke.
利用雄性NMRI小鼠的肺微粒体和肝微粒体,研究香烟烟雾对参与前致癌物和前诱变剂生物活化的各种细胞色素P450同工型的诱导作用。肝微粒体中CYP1A1、CYP2B、CYP2C、CYP2D、CYP2E1和CYP3A催化的酶活性被诱导。肺和肝CYP1A1、2E1和3A的免疫定量分析表明:1)肺和肝中CYP1A1被诱导;2)CYP3A亚家族在肝中被诱导,在肺中未检测到;3)CYP2E1在肝中略有诱导,而其在肺中的表达比CYP1A1(2.0倍)增加得更多(6.8倍)。后一数据表明,已知在人肺中表达的CYP2E1可能积极参与香烟烟雾诱导的肺癌发生。