In our research we studied the influence of mitochondrial H2S synthesis inhibition with o-carboxymethylhydroxylamine (50 mg/kg, in vivo) on oxidative stress indicators and respiratory chain function. It was found that the amount of hydrogen sulfide in the mitochondria and blood plasma of experimental animals was reduced by 25 and 45%, respectively. The rate of of (.)O2(-) and (.)OH-radicals generation increased both in mitochondria and plasma, indicating an intensification of free radicals formation process with a decrease in H2S content, which is a known antioxidant. In case of inhibition of the H2S enzyme production, the activity of the constitutive NO synthase in both mitochondria and blood plasma was decreased by 20 and 24%, respectively. In this case, the activity of inducible NOS in organelles increased by 3.27 times, indicating a significant increase in the formation of NO, which is likely to participate in the synthesis of peroxynitrite. The inhibition of the mitochondrial pathway to hydrogen sulfide synthesis impairs the functional capacity of the electron transport chain, which manifested itself in lowering the rate of oxygen consumption in the states V2, V3 and V4, as well as indicators of RCR and ADP / O. This, perhaps, is the main reason for the deterioration of functional functioning of the heart, because the efficiency of the energy supply of the myocardium, for which the mitochondria correspond, is crucial for the work of the heart.