Müller L, Wilhelm M
Toxicology. 1987 May;44(2):193-201. doi: 10.1016/0300-483x(87)90149-1.
The influence of aluminium (Al) chloride on toxic responses to cadmium (Cd) chloride of hepatocytes isolated from fed rats were investigated. Hepatocytes exposed to 50-200 microM Al took up the Al-ion more efficiently when the cells were simultaneously incubated with 50 microM Cd for 60 min. Aluminium (50-200 microM) could not prevent the release of about 50% of lactate dehydrogenase (LDH) from cells due to 50 microM Cd. Aluminium itself increased LDH leakage only to a moderate extent, indicating the low toxicity of Al to hepatocytes. Cadmium diminished the total hepatocellular thiols (protein + non-protein) and, even more pronounced, the acid soluble thiols after 60 min of incubation. However, this response to Cd was inhibited by simultaneous exposure to 50-200 microM Al in an Al concentration-dependent manner. Concomitantly, the Cd-dependent lipid peroxidation (LPO; measured as thiobarbituric acid reactants) at 60 min was decreased by Al, which itself did not enhance basal LPO in hepatocytes. These data show that Al partly protects hepatocytes from Cd-induced depletion of acid soluble thiols (i.e. reduced glutathione) and from stimulation of LPO. However, Al did not prevent the Cd-induced damage of the cell membrane.
研究了氯化铝(Al)对从喂食大鼠分离的肝细胞对氯化镉(Cd)毒性反应的影响。当细胞与50μM Cd同时孵育60分钟时,暴露于50 - 200μM Al的肝细胞更有效地摄取Al离子。50μM Cd会导致约50%的乳酸脱氢酶(LDH)从细胞中释放出来,而50 - 200μM的铝并不能阻止这种情况。铝本身仅在一定程度上增加LDH泄漏,表明铝对肝细胞的毒性较低。孵育60分钟后,镉会减少肝细胞总的硫醇(蛋白质 + 非蛋白质),更明显的是减少酸溶性硫醇。然而,同时暴露于50 - 200μM Al会以铝浓度依赖的方式抑制这种对镉的反应。同时,铝降低了60分钟时镉依赖的脂质过氧化(LPO;以硫代巴比妥酸反应物衡量),而铝本身并不会增强肝细胞的基础LPO。这些数据表明,铝部分保护肝细胞免受镉诱导的酸溶性硫醇(即还原型谷胱甘肽)耗竭以及脂质过氧化的刺激。然而,铝并不能阻止镉诱导的细胞膜损伤。