ACTION OF MITOCHONDRIAL ATPASE INHIBITOR PROTEIN (IF1) IN INTACT RAT THYMOCYTES AND EHRLICH ASCITES-CARCINOMA CELLS

The inhibition of mitochondrial ATPase in thymocytes and Ehrlich ascit es carcinoma cells after incubation of the cells with uncoupler, roten one, or cumene hydroperoxide was found to depend in a significant way on the action of the inhibitor protein IF1. Maximal inhibition of the oligomycin-sensitive ATPase activity (up to 70%) was found in the pres ence of uncoupler in the incubation medium. Even when the action of IF 1 was maximal, the residual ATPase activity caused marked ATP depletio n in thymocytes, while in Ehrlich ascites carcinoma (EAC) cells other ATP consuming processes prevailed. Our experiments suggest that there is no inactive ATPase-IF1 complex in intact thymocytes and EAC cells. The extent of inhibition of mitochondrial ATPase under oxidative stres s induced by cumene hydroperoxide was higher in thymocytes than in EAC cells and depended on cumene hydroperoxide concentration and duration of exposure. Cell death caused by uncoupler, rotenone, or oligomycin was related to the extent of ATP depletion in the cells. It is suggest ed that under certain experimental conditions IF1 can prevent cell dea th by slowing down the hydrolysis of ATP.