Curle D C, Ray M, Persaud T V, Bertalanffy F D
Department of Pediatrics and Child Health, University of Manitoba, Faculty of Medicine, Winnipeg, Canada.
Histol Histopathol. 1987 Jul;2(3):223-6.
Adult male mice of the ICR/Swiss Webster strain received a single intragastric administration of methylmercuric chloride 1,000 ppm, at dose levels of 5,10,15,20,25 and 30 mg/kg of body weight. The animals were killed six hours later. Tissue samples from the duodenum were fixed in 10% neutral buffered formalin for light microscopy. Chromosome clumping was observed in dividing cells at all dose levels, resembling a C-mitotic effect. It would lead to reduced mitotic cell formation on account of the subsequent lysis of the arrested metaphases. The cytostatic effect was brought about by the inactivation of the microtubule spindle fiber polymerization mechanism induced by methylmercuric chloride. There was a direct positive correlation between the varying dose levels of methylmercury and the proportion of cells arrested in metaphase in the crypts of the duodenum.
ICR/瑞士韦伯斯特品系的成年雄性小鼠接受了1000 ppm氯化甲基汞的单次胃内给药,剂量水平为5、10、15、20、25和30毫克/千克体重。六小时后处死动物。十二指肠组织样本用10%中性缓冲福尔马林固定用于光学显微镜检查。在所有剂量水平的分裂细胞中均观察到染色体聚集,类似于C有丝分裂效应。由于停滞中期随后的溶解,这将导致有丝分裂细胞形成减少。细胞抑制作用是由氯化甲基汞诱导的微管纺锤体纤维聚合机制失活引起的。甲基汞不同剂量水平与十二指肠隐窝中停滞在中期的细胞比例之间存在直接正相关。