Müller L, Wilhelm M
Toxicology. 1987 May;44(2):203-12. doi: 10.1016/0300-483x(87)90150-8.
Aluminium (Al) chloride (10-200 microM) increased the Al content in hepatocytes isolated from fed male rats in a time- and concentration-dependent manner. After 60 min of incubation with 100 microM Al about 45% of cellular Al was found each in the mitochondrial and the postmitochondrial fraction of hepatocytes, whereas about 5% of Al sedimented with nuclei and cell debris. Concomitantly, the leakage of lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) increased in the presence of Al time- and concentration-dependently, but only to a moderate extent. Aluminium (10-200 microM) also accelerated the formation of lactate by hepatocytes. No significant differences were found in Al uptake and distribution and its effect on LDH leakage and lactate formation when the metal ion was given as AlCl3, Al(NO3)3 or Al(lactate)3. Al concentrations (AlCl3) exceeding 250 microM severely disturbed the determination of LDH, AST and lactate in a cell free system. The data suggest only a moderate toxicity of Al compounds to isolated hepatocytes, when given in amounts approximating (patho)physiological conditions.
氯化铝(10 - 200微摩尔)以时间和浓度依赖的方式增加了从喂食雄性大鼠分离的肝细胞中的铝含量。在用100微摩尔铝孵育60分钟后,肝细胞线粒体和线粒体后部分中各发现约45%的细胞铝,而约5%的铝与细胞核和细胞碎片一起沉淀。同时,乳酸脱氢酶(LDH)、丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)的泄漏在铝存在下随时间和浓度增加,但仅为中等程度。铝(10 - 200微摩尔)也加速了肝细胞乳酸的形成。当金属离子以氯化铝、硝酸铝或乳酸铝形式给予时,在铝摄取、分布及其对LDH泄漏和乳酸形成的影响方面未发现显著差异。超过250微摩尔的铝浓度(氯化铝)严重干扰了无细胞体系中LDH、AST和乳酸的测定。数据表明,当以接近(病理)生理条件的量给予时,铝化合物对分离的肝细胞仅具有中等毒性。