The SH-group reagent N-ethylmaleimide has become widely used as inhibitor of Pi transport in mitochondria. MalNEt decreases the ability of mitochondria to retain Ca2+ and evidence is provided that the Ca2+ efflux observed in MalNEt-treated mitochondria is not due to membrane damage. In contrast, N-ethylmaleimide-induced Ca2+ loss from mitochondria was accompanied by drastic alterations of e- flow and membrane permeability. We aim to clarify the mechanism of N-ethylmaleimide-induced Ca2+ release. It will be shown that N-ethylmaleimide does not alter per se the inner mitochondrial membrane but its effects are rather mediated by the rise of deltapH following divalent cation uptake. Thus, it appears that the rise of deltapH, and not N-ethylmaleimide per se, is responsible for the decreased e- transfer at site II and for the increased permeability to K+ and H+.
The Mechanism of Ca2+ Release Induced by N-Ethylmaleimide in Rat Liver Mitochondria
BERNARDI, PAOLO;
1981
Abstract
The SH-group reagent N-ethylmaleimide has become widely used as inhibitor of Pi transport in mitochondria. MalNEt decreases the ability of mitochondria to retain Ca2+ and evidence is provided that the Ca2+ efflux observed in MalNEt-treated mitochondria is not due to membrane damage. In contrast, N-ethylmaleimide-induced Ca2+ loss from mitochondria was accompanied by drastic alterations of e- flow and membrane permeability. We aim to clarify the mechanism of N-ethylmaleimide-induced Ca2+ release. It will be shown that N-ethylmaleimide does not alter per se the inner mitochondrial membrane but its effects are rather mediated by the rise of deltapH following divalent cation uptake. Thus, it appears that the rise of deltapH, and not N-ethylmaleimide per se, is responsible for the decreased e- transfer at site II and for the increased permeability to K+ and H+.
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