The function of mitochondrial CYP1A1 in the lipid metabolism.

为了了解多环芳烃（PHAs）诱导的微粒体与线粒体CYP1A1的生理功能，它是微粒体而不是线粒体CYP1A1酶，保护免受口服BaP毒性。由于PHAs的代谢延迟导致转运体基因的异常表达，PHAs引起脂质代谢异常。我们的数据支持这样一种可能性，即是微粒体而不是线粒体CYP1A1酶防止pha诱导的线粒体功能障碍。

To understand the physiological functions of polycyclic aromatic hydrocarbons(PHAs) induced microsomal versus mitochondrial CYP1A1, it is the microsomal rather than mitochondrial CYP1A1 enzyme that protects against oral BaP toxicity. Because of metabolic delay of PHAs causes abnormal expression of transporter genes, PHAs is induced abnormal lipid metabolism. Our data support the likelihood that it is the microsomal rather than mitochondrial CYP1A1 enzyme that protects against PHAs induced mitochondrial dysfunction.