Jiang X Z, White R, Morgan K T
Neurotoxicology. 1985 Spring;6(1):93-103.
Female C57BL/6 mice were exposed for 6 h/day, 5 day/wk for 2 weeks, to 1,500 ppm methyl chloride. Focal and diffuse malacia, involving the cerebellar inner granular layer was found while renal lesions were minimal or absent. The cerebellar lesions were most frequently found in the ventral paraflocculus, and less often in other regions of the cerebellum. The earliest ultrastructural changes were seen in the nuclei of scattered cerebellar granule cells, with progression from slight confluence of heterochromatin, to complete nuclear condensation or karyorrhexis. More severely affected areas exhibited severe watery swelling and disruption of granule cell perikarya with less severe changes in other cell types. Blood vessels appeared normal, even in areas of severe malacia. It was concluded that the lesions in the mouse cerebellum closely resemble methyl chloride induced brain lesions previously described in guinea pigs, and that these lesions are not secondary to the renal toxicity of methyl chloride.
雌性C57BL/6小鼠每天暴露于1500 ppm的氯甲烷中，持续6小时，每周5天，共2周。发现局灶性和弥漫性软化灶，累及小脑内颗粒层，而肾脏病变轻微或无病变。小脑病变最常见于腹侧副绒球，较少见于小脑的其他区域。最早的超微结构变化见于散在的小脑颗粒细胞核，从异染色质轻度融合发展到完全核浓缩或核溶解。受影响更严重的区域表现为严重的水样肿胀和颗粒细胞胞体破裂，其他细胞类型的变化较轻。即使在严重软化灶区域，血管看起来也正常。得出的结论是，小鼠小脑的病变与先前在豚鼠中描述的氯甲烷诱导的脑病变非常相似，并且这些病变不是氯甲烷肾毒性的继发结果。
