The effect of DDT on K+ transport in mouse liver mitochondria.
This study describes DDT-induced changes in membrane permeability of mitochondria and erythrocytes to K+ as monitored by a K+-selective electrode. DDT is a strong inhibitor of valinomycin-mediated K+ uptake and the corresponding H+ efflux and an inducer of K+ leakage out of mitochondria but not to any significant extent out of erythrocytes. The inhibition of K+ uptake and H+ efflux was a function of (a) preincubation time between mitochondria and DDT, (b) mitochondrial concentration, (c) the nature of the carrier solvent and (d) temperature. The kinetics of inhibition of K+ uptake showed that DDT is an uncompetitive inhibitor with respect to valinomycin and a competitive inhibitor with respect to K+. The efflux of endogenous K+ showed a sigmoid dependency on DDT concentration and was reduced to endogenous rates when the temperature was lowered below the gel-liquid crystalline phase transition of the lipids. It is suggested that the DDT-induced changes in membrane permeability are due to perturbation of the lipid phase and that its toxicity may be due in part to hyperpolarization of subcellular membranes.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects*; D003634:DDT / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects; D005260:Female; D006801:Humans; D006859:Hydrogen / Q000378:metabolism; D066298:In Vitro Techniques; D051379:Mice; D008930:Mitochondria, Liver / Q000187:drug effects*; D011188:Potassium / Q000378:metabolism*; D014634:Valinomycin / Q000037:antagonists & inhibitors
D014634:Valinomycin; D006859:Hydrogen; D003634:DDT; D011188:Potassium