Bondy S C, McKee M
Department of Community and Environmental Medicine, University of California, Irvine 92717.
Toxicol Lett. 1991 Sep;58(1):13-21. doi: 10.1016/0378-4274(91)90185-9.
The effect of a neurotoxic organo-metal, methyl mercuric iodide, and an aromatic solvent, toluene, upon the transmembrane potential (psi), across both the limiting membrane of isolated nerve terminals and their mitochondria, has been studied. Exposure of nerve endings to either of these toxicants in vitro resulted in a dose-dependent diminution of psi that was especially pronounced in the case of mitochondria. This was not prevented by a concurrent exposure to an antioxidant (alpha-tocopherol), or an iron chelator (deferoxamine), or ganglioside GM1. No significant changes were detected in synaptosomal potentials derived from cortices of rats exposed to methyl mercury or toluene at levels known to increase the rate of formation of reactive oxygen species within this region. The special vulnerability of mitochondrial psi to these agents may be due to the disruption of oxidative phosphorylation and may be related to the increase in intrasynaptosomal free ionic calcium that both of these chemicals can induce.
研究了神经毒性有机金属甲基碘化汞和芳香族溶剂甲苯对分离的神经末梢及其线粒体的跨膜电位（ψ）的影响。在体外将神经末梢暴露于这些毒物中的任何一种都会导致ψ呈剂量依赖性降低，这在 mitochondria 的情况下尤为明显。同时暴露于抗氧化剂（α-生育酚）、铁螯合剂（去铁胺）或神经节苷脂 GM1 并不能阻止这种情况。在暴露于已知会增加该区域活性氧形成速率的甲基汞或甲苯水平的大鼠皮质中提取的突触体电位未检测到显著变化。线粒体 ψ 对这些药物的特殊易感性可能是由于氧化磷酸化的破坏，并且可能与这两种化学物质均可诱导的突触体内游离离子钙的增加有关。
