Abstract
An increasing body of data shows that survival of mammalian cells is under the control of growth factors and autocrine survival factors (AF). We studied the effects of an AF deficit on the survival, intracellular ATP content and the transmembrane potential of mitochondria in IL-2-dependent CTLL-2 cells following oxidative stress. We show that cells cultivated under conditions of AF deficit became more susceptible to oxidative injury in comparison with CTLL-2 cells cultivated without an AF deficit (the control cells); their death occurred at lower H2O2 concentrations than in the case of control cells. The ATP content in CTLL-2 cells decreased under an AF deficit even without stress; treatment of these cells with hydrogen peroxide led to an additional significant decrease of ATP content, which was accompanied by injury of the cell membrane (blebbing) and by a sharp fall in mitochondrial potential. Cell death after oxidative stress under conditions of AF deficit was shown to proceed along both the apoptosis and necrosis pathways.
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