Mechanisms of petroleum hydrocarbon toxicity: destruction of liver microsomal and mitochondrial calcium pump activities by a Prudhoe Bay crude oil.

S Khan, J F Payne, A D Rahimtula
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Abstract

Administration of Prudhoe Bay crude oil (PBCO) to rats resulted in an abrupt drop in liver mitochondrial and microsomal ATP-dependent calcium uptake activity. Also, in vitro incubations of either mitochondria or microsomes in the presence of a dimethyl sulfoxide (DMSO) extract of PBCO resulted in a dose-dependent inhibition of calcium influx. The release of calcium from calcium-loaded mitochondria and microsomes was also observed in the presence of the PBCO extract. At concentrations which effect calcium sequestration, the PBCO extract produced swelling of mitochondria. Microsomal ATPase activity in the presence or absence of calcium was unaffected by PBCO. The results indicate that increased permeability of the membranes to calcium is a contributory factor in the inhibition of calcium uptake by PBCO.

石油碳氢化合物毒性机制:普拉德霍湾原油对肝微粒体和线粒体钙泵活性的破坏。
大鼠服用普拉德霍湾原油(PBCO)导致肝脏线粒体和微粒体atp依赖性钙摄取活性突然下降。此外,线粒体或微粒体在PBCO的二甲亚砜(DMSO)提取物存在下的体外培养导致钙内流的剂量依赖性抑制。在PBCO提取物存在的情况下,还观察到钙从载钙的线粒体和微粒体中释放。在影响钙固存的浓度下,PBCO提取物产生线粒体肿胀。存在或不存在钙的微粒体atp酶活性不受PBCO的影响。结果表明,膜对钙的渗透性增加是PBCO抑制钙摄取的一个因素。
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