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. Author manuscript; available in PMC: 2012 Mar 23.
Published in final edited form as: FEBS Lett. 2011 Feb 25;585(6):921–926. doi: 10.1016/j.febslet.2011.02.029

Figure 2. The net release of H2O2 from isolated mitochondria in the presence and absence of ischemia.

Figure 2

Compared to SSM from time control hearts, ischemic damage to electron transport chain increases net H2O2 production from SSM using glutamate as complex I substrate and succinate+rotenone as a complex II substrate. In contrast, protection of SSM by blockade of electron transport during ischemia by amobarbital decreases the H2O2 generation compared to the untreated ischemia (upper panel). Ischemia also tends to increase H2O2 generation in IFM compared to time control (lower panel). (Mean±SEM; *p<0.05 vs. time control; † p<0.05 vs. untreated-ischemia).