CAJ | 학술논문

目的: 探讨氯化甲基汞(MMC)中毒大鼠小脑变性的病理改变及机制.方法:本研究在大鼠服用MMC 4 mg/(kg·d)所致的亚急性汞中毒模型上,分别在服用MMC后第11、15、18和21天断头,采用组织和免疫病理技术动态观察小脑的病理演变,并采用TUNEL染色观察细胞凋亡改变,同时在电镜下观察了超微结构改变.结果:在服用MMC第18天,TUNEL染色显示小脑颗粒细胞有散在的凋亡细胞,主要位于脑回深部近白质区的颗粒层.第21天,凋亡细胞明显增加,颗粒细胞减少.MRF-1染色可见大量的小胶质细胞反应,GFAP示胶质细胞增生明显,而Purkinje细胞则保留完整.服用MMC第18天的超微结构观察表明,细胞核皱缩,体积缩小,形态不规则,电子密度增高,可见密集深染的染色质,部分细胞核破碎,呈现为均一深染的泪珠状染色质,符合凋亡改变.结论:本研究结果表明汞中毒的小脑变性的病理机制为细胞凋亡,其病理变化符合人类汞中毒表现.
목적: 탐토록화갑기홍(MMC)중독대서소뇌변성적병리개변급궤제.방법:본연구재대서복용MMC 4 mg/(kg·d)소치적아급성홍중독모형상,분별재복용MMC후제11、15、18화21천단두,채용조직화면역병리기술동태관찰소뇌적병리연변,병채용TUNEL염색관찰세포조망개변,동시재전경하관찰료초미결구개변.결과:재복용MMC제18천,TUNEL염색현시소뇌과립세포유산재적조망세포,주요위우뇌회심부근백질구적과립층.제21천,조망세포명현증가,과립세포감소.MRF-1염색가견대량적소효질세포반응,GFAP시효질세포증생명현,이Purkinje세포칙보류완정.복용MMC제18천적초미결구관찰표명,세포핵추축,체적축소,형태불규칙,전자밀도증고,가견밀집심염적염색질,부분세포핵파쇄,정현위균일심염적루주상염색질,부합조망개변.결론:본연구결과표명홍중독적소뇌변성적병리궤제위세포조망,기병리변화부합인류홍중독표현.
Objective:To explore the pathology and pathogenesis of cerebellar injuries induced by methylmercury chloride(MMC) toxication in rats. Methods:Rats were given MMC(4 mg·kg-1·d-1) consecutively and sacrificed on days 11, 15, 18 and 21. Pathological changes of the cerebellum were observed by histo-immunopathology; in situ staining was performed for DNA strand breaks in cerebellar granule cells by TUNEL technique; and the ultrastructures were observed by electron microscope. Results:On day 18, sparse TUNEL positive granular cells were observed mainly in deep lamina adjacent to the white matter. On day 21, apoptotic cells markedly increased and granule cells decreased with well-preserved Purkinje cells. Immunostaining with MRF-1 and GFAP demonstrated severe microgliosis and astrocytosis. On day 18, electron microscopy demonstrated that the nuclei of MMC-treated animals were shrunken and displayed increased electron density, and some homogeneously dense nuclear chromatin with tear-drop features, which were compatible with the apoptotic changes. Conclusion:These results indicate that the pathological changes in the cerebellum in this subacute MMC intoxication model resemble human cases, and the degeneration of granule cells is apoptosis.