Takano Hirohisa, Yanagisawa Rie, Ichinose Takamichi, Sadakane Kaori, Inoue Ken-ichiro, Yoshida Sei-ichi, Takeda Ken, Yoshino Shin, Yoshikawa Toshikazu, Morita Masatoshi
CREST, JST (Japan Science and Technology Corporation), Tokyo, Japan.
Arch Toxicol. 2002 Apr;76(3):146-51. doi: 10.1007/s00204-002-0323-0. Epub 2002 Feb 20.
Polycyclic aromatic hydrocarbons (PAH) and reactive oxygen species (ROS) derived from diesel exhaust particles (DEP) are implicated in the pathophysiology of respiratory diseases. Cytochrome P450 (Cyp) 1A1 can be induced by several kinds of PAH and produce ROS. We determined whether acute inhalation exposure to DEP induced the expression of Cyp 1A1 in murine lung. Intratracheal instillation of DEP dose-dependently increased the lung expression of Cyp 1A1 at the levels of both mRNA and protein, whereas DEP decreased expression in the lung of aryl hydrocarbon receptors in a dose-dependent manner. In contrast, charcoal particles as the control did not affect the expression of these molecules. These results suggest that the lung expression of Cyp 1A1 can be a biomarker of acute inhalation exposure to DEP and may be implicated in an accelerated production of ROS and the subsequent aggravation of lung injury.
柴油尾气颗粒（DEP）衍生的多环芳烃（PAH）和活性氧（ROS）与呼吸系统疾病的病理生理学有关。细胞色素P450（Cyp）1A1可被多种PAH诱导并产生活性氧。我们确定了急性吸入DEP是否会诱导小鼠肺中Cyp 1A1的表达。气管内滴注DEP在mRNA和蛋白质水平上均剂量依赖性地增加了肺中Cyp 1A1的表达，而DEP以剂量依赖性方式降低了芳烃受体在肺中的表达。相比之下，作为对照的木炭颗粒不影响这些分子的表达。这些结果表明，Cyp 1A1的肺表达可能是急性吸入DEP的生物标志物，并且可能与活性氧的加速产生以及随后的肺损伤加重有关。
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