Anghileri L J, Heidbreder M, Weiler G, Dermietzel R
Exp Cell Biol. 1977;45(1-2):34-47. doi: 10.1159/000162856.
Hepatocarcinogenesis in rats produced by prolonged feeding of thioacetamide appears as a progressive phenomenon in which morphological changes are associated with important biochemical modifications. It seems most likely that changes in the permeability of cell membrane induced by the carcinogen are responsible for increased intracellular accumulation of Ca2+, and for the ensuring of cell injury produced by Ca2+ overloading of the mitochondria. This calcification of the mitochondria may play a role in the neoplastic transformation of the cell, especially as far as it concerns metabolic behavior and the genetic specification of the permeability characteristics of the transformed cell membrane. The increased synthesis of acid glycosaminoglycans suggests their involvement in calcium-mediated control of tumor development and growth.
通过长期喂食硫代乙酰胺诱导的大鼠肝癌发生呈现为一种渐进性现象，其中形态学变化与重要的生化改变相关。致癌物诱导的细胞膜通透性变化很可能是细胞内Ca2+积累增加的原因，也是线粒体Ca2+过载导致细胞损伤的原因。线粒体的这种钙化可能在细胞的肿瘤转化中起作用，特别是就其涉及代谢行为和转化细胞膜通透性特征的遗传特性而言。酸性糖胺聚糖合成的增加表明它们参与了钙介导的肿瘤发生和生长控制。
