Tessitore L, Cecchini G, Curzio M, Zuretti M F, Baccino F M
Boll Soc Ital Biol Sper. 1979 Jan 15;55(1):65-8.
The AA in experiments performed on male rats treated with 0,5 mCi/kg of cycloheximide have observed an inhibition of liver protein degradation and have suggested two mechanism: 1) cycloheximide prevents the acute proteolytic response induced in fibroblast culture by exposure to serum-deficient media and in rat livers after perfusion probably by inhibiting the lysosomal - autophagic system, without modifications in total activity of lysosome proteinases. 2) It may be that protein degradation rate and level of lysosomal proteinases reinterrelated; the latter probably being a factor controlling the overall cell protein turnover rate.
在用0.5毫居里/千克放线菌酮处理的雄性大鼠身上进行的实验中,AA观察到肝脏蛋白质降解受到抑制,并提出了两种机制:1)放线菌酮可能通过抑制溶酶体-自噬系统,防止在成纤维细胞培养中因暴露于血清缺乏培养基而诱导的急性蛋白水解反应,以及在灌注后的大鼠肝脏中诱导的急性蛋白水解反应,而溶酶体蛋白酶的总活性没有改变。2)可能蛋白质降解速率与溶酶体蛋白酶水平相互关联;后者可能是控制整体细胞蛋白质周转率的一个因素。