Endotoxin Induces Glutathione Reductase Activity in Lungs of Mice

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Abstract
Glutathione reductase catalyzes the NADPH-dependent conversion of glutathione disulfide to glutathione and helps protect the lung from injury by reactive oxygen. In animals allowed to breathe nearly 100% oxygen, the activities of other antioxidants in the lung can be induced by treatment with endotoxin, and this induction is associated with increased tolerance to hyperoxia. The purpose of this study was to see whether glutathione reductase activity in the lungs of mice increased with endotoxin treatment alone. We studied 60 FVB mice (20 males and 40 females). Half received endotoxin (500 μg/kg) intraperitoneally at time 0 and 24 h, and the controls received an equal volume of saline. At 48 h we killed the mice and removed their lungs. Treatment of mice with endotoxin increased glutathione reductase activily in the lung 55% (0.035 ± 0.005 to 0.054 ± 0.010 μmo NADPH reduced/min/mg prolein; mean ± SD; endoloxin differenl from conlrol, p < 0.001). The increase in aclivily was Ihe same for male and female mice. We measured Ihe specific prolein for glutathione reductase by Weslern analysis and mRNA for glutathione reductase using a slol-blol analysis and found lhat both increased roughly 2-fold with endoloxin treatmenl. This suggesls lhat endotoxin Ireatment resulted in either increased rale of transcription of glulathione reductase mRNA or increased mRNA slabilily. We conclude that endoloxin treatment increases glutathione reductase aclivily in the lung and thai Ihis increase in activity may play a role in subsequent protection from hyperoxia.

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