Publication de 4 numéros par an
ISSN Imprimer: 2155-014X
ISSN En ligne: 2155-0158
Effect of NaHS, Hydrogen Sulfide Donor, on the Functional State of the Respiratory Chain in the Rat Heart Mitochondria
RÉSUMÉ
In experiments on the mitochondria isolated from the heart tissue of adult rats, we studied the effects of NaHS, a hydrogen sulfide donor, on the respiratory chain of the organelles. We have found that NaHS (10−9 − 10−6 mol/l) causes a dose-dependent decrease in the rate of oxygen consumption both in the presence of succinate and ADP (state 3 by Chance), and in the absence of ADP (state 4). At that, a decrease in the oxygen consumption rate induced by NaHS in concentrations of 10−9 mol/l and 10−8 mol/l results in increased coupling of oxidation and phosphorylation, as evidenced by an increase in the respiratory control, while the efficiency of oxidative phosphorylation (ADP/O) remains unchanged. The study testifies to a protective effect of hydrogen sulfide donor on the functional state of the mitochondria. To elucidate other mechanisms of H2S protective action we also investigated the effect of hydrogen sulfide donor on the mitochondrial swelling. It has been found that NaHS in concentrations of 10−12 − 10−4 mol/l affects the level of mitochondria swelling of the rat hearts in a dose-dependent manner. A moderate swelling of the rat heart mitochondria is observed under the action of hydrogen sulfide donor in concentrations of 10−12 − 10−8 mol/l, exposed to Ca,2+, 1 nmol/mg protein in the medium. Under the NaHS action at a concentration of 10−9 mol/l, the mitochondria swelling was observed with the maximum change by 11%. 5-hydroxydecanoate (10−4 mol/l), an inhibitor of mitochondrial ATP-sensitive K+ channels (KATP-channels), partially reduces the mitochondrial swelling in the presence of NaHS (10−9 mol/l), which may indicate an activation of KATP-channels by the hydrogen sulfide donor. Our study indicates the contribution of KATP-channels to the mechanisms of hydrogen sulfide action on mitochondrial function.