Hadler H I, Cook G L
J Environ Pathol Toxicol. 1979 Jul-Aug;2(6):1343-50.
Silicate substitutes for phosphate in the transitory uncoupling of rat liver mitochondria induced by hydrazine when beta-hydroxy-butyrate is the substrate. Uncoupling is blocked by rutamycin. Just as in the case when phosphate is combined with hydrazine, ATP, ADP, PPi, and Mg++ protect against hydrazine when silicate is combined with hydrazine. A high level of ADP in the absence of added phosphate, but in the presence of silicate, induces a pseudo state three of the mitochondria. Silicate, like sulfate and arsenate which have been reported previously, is activated by the enzymes which mediate oxidative phosphorylation. These results serve to explain a role for silicate in silicosis, black lung disease, and cancer. In addition, since there is suggestive evidence in the literature that lung tissue solubilizes asbestos fibers, these results not only expand the confluence between oxidative phosphorylation and chemical carcinogenesis but are correlated with the synergistic carcinogenicity of asbestos and smoking observed by epidemiologists.
当以β-羟基丁酸作为底物时，在肼诱导的大鼠肝线粒体瞬时解偶联过程中，硅酸盐可替代磷酸盐。解偶联被鱼藤霉素阻断。正如磷酸盐与肼结合的情况一样，当硅酸盐与肼结合时，ATP、ADP、焦磷酸（PPi）和镁离子（Mg++）可保护线粒体免受肼的影响。在未添加磷酸盐但存在硅酸盐的情况下，高水平的ADP会诱导线粒体进入假状态3。与先前报道的硫酸盐和砷酸盐一样，硅酸盐可被介导氧化磷酸化的酶激活。这些结果有助于解释硅酸盐在矽肺、黑肺病和癌症中的作用。此外，由于文献中有提示性证据表明肺组织可溶解石棉纤维，这些结果不仅扩展了氧化磷酸化与化学致癌作用之间的关联，而且与流行病学家观察到的石棉和吸烟的协同致癌性相关。
