Figure 2.

The mitochondrial permeability transition pore is not required for hyperoxia-induced mortality. (A) Mice lacking cyclophilin D, a critical component of the mitochondrial permeability transition pore, or wild-type mice on an identical background were exposed to hyperoxia for measurement of survival. The median survival (LD₅₀) is in parentheses (n = 18 for Cyclophilin D^+/+; n = 12 for Cyclophilin D^−/−). The difference between wild-type and knockout mice was not significant (P = 0.79). The same mouse strains were exposed to hyperoxia for 84 hours for measurement of lung injury. Hematoxylin and eosin stained lung sections (original magnification ×100) (B), wet-to-dry weight ratios of the lung (C), and the percentage of TUNEL positive nuclei (D) (n >4 animals per group). *P < 0.05 for comparison with nomoxic controls. No significant differences were observed between the Cyclophilin D^+/+ and Cyclophilin D^−/− animals.