Figure 2. Deletion of p53 improved oxidative phosphorylation in mouse mitochondria following ischemia-reperfusion.

Ischemia-reperfusion decreased the dinitrophenol (DNP)-uncoupled rate of respiration in mitochondria isolated from wildtype mice oxidizing complex I and II substrates. The baseline rate of oxidation in wildtype [Mean ± SD: complex I (253 ± 57) and complex II (606 ± 41)] and in p53 deletion [Mean ± SD, complex I (243 ± 64) and complex II (562 ± 45)] mice is given. The percentage decrease in respiration during reperfusion was attenuated in p53 deletion mice (Panel A). Compared to wild type mice, H₂O₂ generation was decreased in p53 deletion before ischemia with complex I substrate (Panel B). The generation of H₂O₂ was increased in mitochondria isolated from both wild type and p53 deletion following reperfusion using complex I substrate (Panel B). Deletion of p53 decreased H₂O₂ generation during reperfusion when succinate + rotenone was used as complex II substrate compared to wild type mice (Panel C). Ischemia-reperfusion decreased the calcium retention capacity (CRC) in mitochondria isolated from both wild type and p53 deletion mice compared to mitochondria from non-ischemic hearts. Deletion of p53 did not significantly improve the CRC in mitochondria isolated following ischemia and 30 min. reperfusion compared to wild type controls (Panel D). Mean ± SD.

* p<0.05 vs. corresponding pre-ischemia. † p<0.05 vs. corresponding wild type hearts. n=6–8 in each group.