Karakashev P, Petrov L, Alexandrova A
Institute of Physiology, Bulgarian Academy of Sciences, Sofia.
Neoplasma. 2000;47(2):122-4.
The participation of lipid peroxidation products in the mechanisms of paraquat toxicity in Ehrlich ascites tumor (EAT) cells was observed. Paraquat in a concentration 0.5-1.0 mmol increased the level of lipid peroxidation according to the Ohakawa TBARS (thiobarbituric acid-reactive substances) method. These changes in TBARS production in EAT cells correlated with paraquat toxicity on the cells registered by using the method for cell injury, which is based on changes in lactate dehydrogenase activity. The metal chelator DTA removed the effect of paraquat on TBARS production and on cell injury. The present data suggested that the increased level of lipid peroxidation and cell injury is a result of the paraquat action in EAT cells depending on iron.
观察了脂质过氧化产物在艾氏腹水瘤（EAT）细胞百草枯毒性机制中的参与情况。根据大川TBARS（硫代巴比妥酸反应性物质）法，浓度为0.5 - 1.0 mmol的百草枯会增加脂质过氧化水平。EAT细胞中TBARS生成的这些变化与通过基于乳酸脱氢酶活性变化的细胞损伤方法所记录的百草枯对细胞的毒性相关。金属螯合剂DTA消除了百草枯对TBARS生成和细胞损伤的影响。目前的数据表明，脂质过氧化水平升高和细胞损伤是百草枯在EAT细胞中依赖铁的作用结果。
