Abstract

Previously reported beneficial effects of dipyridamole on "damaged" mitochondria have not been confirmed in these experiments. Dipyridamole, in fact, has specific stimulatory or inhibitory effects on mitochondrial respiration depending on which segment of the electron transport chain is predominant. It is postulated that dipyridamole inhibits respiration by accepting electrons from NADH, thus competing with the main electron transport pathway for electrons. The drug is also capable of interacting with a highenergy intermediate when succinate is the substrate, resulting in an "uncoupling-like" action.