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Single intraperitoneal injection of acrylonitrile, administered prior to the start, at the onset, or during oxygen exposure, respectively, in all cases significantly impaired the survival rate of rats exposed to 98% oxygen. Short periods of lung glutathione depletion by acrylonitrile accelerated the manifestation of O2 toxicity regardless of their timing with respect to the start of oxygen exposure, but in dependence on their intensity and duration. However, the effect of acrylonitrile was probably not solely glutathione-depletion-mediated, since O2 toxicity was enhanced even by acrylonitrile injection, given sufficiently in advance to allow the lung glutathione level to recover before the oxygen exposure started.
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