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Figure 1 | Journal of Biomedical Science

Figure 1

From: Nitric oxide protects the heart from ischemia-induced apoptosis and mitochondrial damage via protein kinase G mediated blockage of permeability transition and cytochrome c release

Figure 1

Perfusion of hearts with DETA/NO partially prevents the ischemia-induced decrease in respiratory chain activity and increase in proton leak of subsequently isolated mitochondria. (A): kinetics of the respiratory chain activity, and (B): kinetics of proton leak. Rat hearts were perfused for 3 min with 50 μM of DETA/NO, then ischemia was induced for 30 min. Isolated mitochondria were placed in a vessel with incubation buffer A (see Methods) and their oxygen consumption and membrane potential were measured simultaneously. 5 mM succinate (plus 1 μM rotenone) was used as respiratory substrate. Kinetics of the respiratory chain was determined as the dependence of the mitochondrial respiration rate on the membrane potential by titrating with carboxyatractyloside (0.4–8.0 nmol/mg mitochondrial protein). The kinetics of the proton leak was measured in the presence of excess oligomycin (1 μg/mg protein), mitochondrial respiration and membrane potential were titrated with malonate (0.33–6 mM). Means ± standard errors of 5 separate experiments are presented.

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