Abstract
Mitochondria scavenge extramitochondrial superoxide anion via a respiration-dependent (i.e., non- enzymatic) mechanism. This study reports that hyperoxia exposure (>95% O2for 48 h) reduced (P< 0.05) lung mitochondrial respiration-dependent superoxide scavenging by 56% compared to lung mitochondria from untreated control rats. In comparison, endotoxin treatment (5 μg insufflated intratracheally 24 h earlier) increased (P< 0.05) lung mitochondrial respiration-dependent superoxide scavenging by 57% compared to mitochondria from untreated control rats. Further, lung mitochondria from rats given endotoxin 24 h prior to hyperoxia exposure had more than twice the respiration-dependent superoxide scavenging capacity as compared to mitochondria from untreated rats exposed to hyperoxia (P< 0.05). In contrast, endotoxin treatment did not increase (P> 0.05) lung mitochondrial enzymatic (i.e., superoxide dismutase) scavenging activity when corrected for mitochondrial protein content in either hyperoxia-exposed or air-exposed rats. Therefore, hyperoxia exposure decreased, whereas endotoxin treatment increased, respiration-dependent lung mitochondrial scavenging of extramitochondrial superoxide. This recently identified cellular antioxidant defense appears to be an early target in hyperoxia but its induction provides an important component of endotoxin-induced tolerance to hyperoxic lung damage.
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