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.