Beales D, Hue D P, McLean A E
Biochem Pharmacol. 1985 Jan 1;34(1):19-23. doi: 10.1016/0006-2952(85)90094-2.
Hepatocytes from rats treated with phenobarbitone were exposed to 10 mM paracetamol for 1 hr and then incubated in buffered Ringer solution. Enzyme leakage and trypan blue entry became severe in the paracetamol treated cells some 2 hr after the end of exposure. These signs of cell injury could be blocked by 4 mM CaEDTA added during or after paracetamol exposure. CaEDTA did not alter covalent binding of [14C]paracetamol. Ca2+ free media did not prevent paracetamol injury. Lipid peroxidation was observed in cells but could be blocked without protecting the cells. Protein synthesis was depressed early on in cells previously exposed to paracetamol, CaEDTA did not protect against this inhibition. These observations suggest that an early cytoplasmic lesion develops into a later lethal lesion at the cell surface.
用苯巴比妥处理过的大鼠的肝细胞暴露于10 mM对乙酰氨基酚中1小时，然后在缓冲林格溶液中孵育。在暴露结束约2小时后，对乙酰氨基酚处理的细胞中酶泄漏和台盼蓝进入变得严重。在对乙酰氨基酚暴露期间或之后添加4 mM CaEDTA可以阻断这些细胞损伤的迹象。CaEDTA不会改变[14C]对乙酰氨基酚的共价结合。无钙培养基不能预防对乙酰氨基酚损伤。在细胞中观察到脂质过氧化，但可以在不保护细胞的情况下被阻断。先前暴露于对乙酰氨基酚的细胞中蛋白质合成早期受到抑制，CaEDTA不能防止这种抑制。这些观察结果表明，早期的细胞质损伤会发展为后期细胞表面的致命损伤。
