Biempica L, Rauch H, Quintana N, Sternlieb I
Department of Pathology, Albert Einstein College of Medicine, Bronx, New York.
Lab Invest. 1988 Oct;59(4):500-8.
The accumulation of excessive amounts of copper in the livers of toxic milk mice results in gross morphologic, histologic, and ultrastructural changes that are progressive with age even though the concentrations of copper tend to decrease in mice older than 6 months. Striking differences in morphologic integrity between regenerative nodules and the intervening parenchyma were observed. Profound changes in mitochondria, endoplasmic reticulum, and nuclei as well as accumulation of microvesicular lipid droplets were observed in injured hepatocytes. By contrast, the hepatocytes of regenerative nodules appeared well preserved. Comparisons with other inherited mammalian disorders associated with hepatic copper toxicosis indicate that copper causes species specific organelle injury.
在中毒性乳鼠的肝脏中，过量铜的积累会导致大体形态、组织学和超微结构的改变，这些改变会随着年龄的增长而逐渐加重，尽管在6个月以上的小鼠中铜的浓度往往会降低。观察到再生结节与周围实质在形态完整性上存在显著差异。在受损的肝细胞中观察到线粒体、内质网和细胞核的深刻变化以及微泡脂滴的积累。相比之下，再生结节的肝细胞似乎保存完好。与其他与肝铜中毒相关的遗传性哺乳动物疾病进行比较表明，铜会导致物种特异性的细胞器损伤。
