Gebhart A M, Brabec M J
Toxicol Lett. 1985 Jan;24(1):71-8. doi: 10.1016/0378-4274(85)90142-0.
40 h after an acute dose of CCl4 (11.3 mmol/kg), the incorporation of [1-3H]ethanolamine into rat hepatic microsomal phospholipids was inhibited to 70% of control. Incorporation into phospholipids of the inner and outer mitochondrial membranes was 30-35% of control. Rates of incorporation were equal to or above normal rates in all membranes 65 h after dosage. The activity of methyltransferase in microsomal fractions isolated from rats 10 to 66 h after dosage was depressed. These data suggest that the alteration of mitochondrial phospholipids that parallels mitochondrial dysfunction after acute CCl4 dosage could be attributed to a CCl4-induced inhibition of the microsomal phospholipid biosynthetic pathways.
给予大鼠急性剂量的四氯化碳(11.3 mmol/kg)40小时后,[1-3H]乙醇胺掺入大鼠肝微粒体磷脂的量被抑制至对照的70%。掺入线粒体内外膜磷脂的量为对照的30 - 35%。给药65小时后,所有膜中的掺入速率等于或高于正常速率。给药后10至66小时从大鼠分离的微粒体组分中甲基转移酶的活性降低。这些数据表明,急性四氯化碳给药后与线粒体功能障碍平行的线粒体磷脂改变可能归因于四氯化碳诱导的微粒体磷脂生物合成途径的抑制。