Effects of hypoxic hypoxia and reoxygenation on H2O2 production in rat brain in vivo.

The effects of hypoxic hypoxia and subsequent reoxygenation on hydrogen peroxide (H2O2) production was studied in the rat brain in vivo. Brain H2O2 production was measured by H2O2-dependent aminotriazole inactivation of endogenous brain catalase activity. Brain catalase activities of rats breathing air (0.2 ATA O2, control) were 168 +/- 5 (n = 10), 125 +/- 4 (n = 6), and 100 +/- 5 (n = 8) U/g brain (mean +/- SEM) at 0, 30, and 60 min after i.p. aminotriazole injection, respectively. Catalase activities after exposure to 5% O2 with N2 for 15 min, 10% O2 with N2 for 30 min, and 6% O2 with nitrous oxide (N2O) for 15 min were 131 +/- 4 (n = 7), 122 +/- 6 (n = 5), and 124 +/- 6 (n = 7) U/g brain, respectively, at 30 min after aminotriazole injection, and were not significantly different from each other or control. Reoxygenated on room air, 100% O2, and hyperbaric 3 ATA O2 for 30 min immediately after each period of hypoxia, brain catalase activity at 60 min after aminotriazole injection in the group of pre-exposure to 6% O2 with N2O was 67 +/- 3, 74 +/- 3, and 67 +/- 6 U/g brain with 0.2 ATA O2 (n = 6), 1.0 ATA O2 (n = 5), and 3.0 ATA O2 (n = 5), respectively. All of these were significantly different from control and other hypoxic pre-exposure groups with N2 (p <0.01) but not from each other. Reoxygenation of the brain after hypoxia with N2O could exacerbate cerebral damage by increasing oxygen free radical production.