外来化合物对细胞膜上多价不饱和脂肪酸的过氧化是组织损害机理之一,如溴三氯乙烷、四氯化碳等对组织损害有明显作用。其他如paracetamol,溴化苯、adriamycin、石草枯等,其损害组织的重要性尚有争论和需进一步探讨。Mitchell综述了数种使肝致毒物后提出Paracetamol和溴化苯由于耗尽了肝细胞中谷胱甘肽而导致肝细胞坏死。这一现象与原发性肝细胞损害没关系,亦即测量到的脂质过氧化物并非细胞死亡的原因,而是其后果。但最近有作者报告发现在大白鼠肝细胞单层培养中,溴化苯能对细胞早期致毒。主要证据是加入抗氧化剂NN-二苯基-P-苯乙烯二胺(DPPD)只能延缓不能防止其对培养的肝细胞致毒。故溴化苯芳香 Exogenous compounds on the cell membrane polyunsaturated fatty acids peroxidation is one of the mechanisms of tissue damage, such as bromine trichloroethane, carbon tetrachloride and other organizations have a significant role in damage. Other such as paracetamol, benzene bromide, adriamycin, stone grass withered, its damage to the organization’s importance is still debated and needs further discussion. Mitchell reviewed several liver-toxin causing agents and proposed that Paracetamol and bromobenzene cause hepatocellular necrosis due to depletion of glutathione in hepatocytes. This phenomenon is not related to primary hepatocyte damage, ie, the measured lipid peroxides are not the cause of cell death but rather the consequence. However, a recent report by the authors found that brominated benzene can cause early toxicity to cells in rat hepatocyte monolayer culture. The main evidence is that the addition of the antioxidant NN-diphenyl-P-styrenediamine (DPPD) can only delay its inability to prevent its toxicity to cultured hepatocytes. It is brominated benzene aromatic