Swelling and NAD(P)H depletion induced by different bacteriocins on rat heart mitochondria

ACUNA, L.; NIKLISON CHIROU, M. V.; BELLOMIO, A.; CARLOS JAVIER MINAHK; MORERO, R. D.

Villa Carlos Paz, Cordoba

Congreso; XLIV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2008

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular

Mitochondria are considered to play a central role in apoptotic cell death. The opening of the “mitochondrial permeability transitions pore” (MPT) is known to occur under conditions of oxidative stress and matrix calcium overload. Next, mitochondria swell and release cytochrome c from the intermembrane space which is a critical early event in mitochondrial mediated apoptosis. In the present work we studied the effect of different bacteriocins: microcin E492, microcin V and enterocin CRL35 on mitochondrial swelling and oxidation of NAD(P)H. The swelling was studied following the absorbance at 540 nm and NAD(P)H oxidation by measuring its intrinsic fluorescence at 450 nm. These experiments were performed with succinate “activated” mitochondria in the presence or absence of either rotenone (the complex I  inhibitor), cyclosporine A (a MPT inhibitor) or ascorbic acid as an antioxidant agent. We observed that all bacteriocins assayed, induced mitochondrial swelling and the oxidation of NAD(P)H, in a concentration dependent way. Effects that were inhibited by acid ascorbic and cyclosporine A. Our findings allow us to conclude that these peptides work through ROSgeneration.