Abstract

The purpose of this study was to determine if 100% O2 would enhance rat pulmonary alveolar macrophage (PAM) oxidative killing of conidia of the fungus Neurospora crassa. First, we found that incubation in 100% O2 had no effect on conidia viability in the absence of PAM. We obtained resident PAM from nonpretreated anesthetized male Sprague-Dawley rats by bronchoalveolar lavage. Compared with similar air exposures we found that 1 h in vitro exposure of PAM to 100% O2 (1.0 atmosphere absolute) increased their killing of opsonized phagocytized conidia by 52%, without altering phagocytosis. A reactive oxygen killing mechanism is suggested because 1) 100% O2 increased PAM chemiluminescence (CL) by 60% both at rest and during 1 h of phagocytosis, and 2) PAM in 100% O2 killed albino conidia (lacking free radical-quenching carotenoids) 2.9 times more readily than they killed wild-type conidia. Compared with air, 100% O2 delayed the PAM respiratory burst time to peak by 18% but did not alter the burst maximal acceleration. The latter and the similar 60% increase in PAM CL in 100% O2 both at rest and during 1 h of phagocytosis suggests a nonenzymatic O2 enhancement of the respiratory burst. Changed timing of burst events in 100% O2 suggests early O2 toxicity. We conclude that 1 h in 100% O2 increases PAM free radical production and fungicidal activity.

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