Kunimoto M
Environmental Health Sciences Division, National Institute for Environmental Studies, Ibaraki, Japan.
Biochem Biophys Res Commun. 1994 Oct 14;204(1):310-7. doi: 10.1006/bbrc.1994.2461.
Cerebellar neurons in primary culture were exposed to methylmercury, a well-established neurotoxicant known as a cause of Minamata disease, at 0.1-1.0 microM for up to 72 hours and compared with the neurons undergoing apoptosis induced by withdrawing K+ from the medium. Cerebellar neurons treated with methylmercury at up to 0.3 microM showed morphological changes characteristic to apoptosis, depending on methylmercury dose; formation of apoptotic vesicles, disappearance of neurites and condensation of nuclear chromatin. In addition, soluble DNA prepared from the methylmercury-treated cells exhibited the typical DNA fragmentation pattern similar to that in cells undergoing apoptosis induced by K+ withdrawal. At higher concentration of methylmercury, however, a non-apoptotic pathway of cell death started to predominate over the apoptotic pathway. These results indicate that the death of cerebellar granule neurons induced by methylmercury is, at least at lower doses, apoptotic.
将原代培养的小脑神经元暴露于甲基汞（一种公认为水俣病病因的神经毒素）中，浓度为0.1 - 1.0微摩尔，持续72小时，并与通过从培养基中去除钾离子诱导凋亡的神经元进行比较。用高达0.3微摩尔的甲基汞处理的小脑神经元表现出凋亡特有的形态学变化，这取决于甲基汞的剂量；凋亡小泡的形成、神经突的消失和核染色质的凝聚。此外，从经甲基汞处理的细胞中制备的可溶性DNA呈现出与因钾离子去除诱导凋亡的细胞中典型的DNA片段化模式相似。然而，在较高浓度的甲基汞作用下，一种非凋亡性细胞死亡途径开始比凋亡途径占主导地位。这些结果表明，至少在较低剂量下，甲基汞诱导的小脑颗粒神经元死亡是凋亡性的。
