Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Tipple, T.E. et al.

Trent E. Tipple, Stephen E. Welty, Lynette K. Rogers, Thomas N. Hansen, Young-Eun Choi, James P. Kehrer, Charles V. Smith,

Thioredoxin-related mechanisms in hyperoxic lung injury in mice.

Reduction of glutathione disulfide (GSSG) to glutathione (GSH) by glutathione reductase (GR) enhances the efficiency of GSH-dependent antioxidant activities. However, GR-deficient (a1Neu) mice are less susceptible to acute lung injury from continuous exposure to > 95% O(2) (96 h: 6.9 +/- 0.1 g right lung/kg body versus room air 3.6 +/- 0.3) than are C3H/HeN control mice (10.6 +/- 1.3 versus 4.2 +/- 0.3, P < 0.001). a1Neu mice have greater hepatic thioredoxin (Trx)1 and Trx2 levels than do C3H/HeN mice, suggesting compensation for the absence of GR. a1Neu mice exposed to hyperoxia for 96 hours showed lower levels of inflammatory infiltrates in lungs than did similarly exposed C3H/HeN mice. Pretreatment with aurothioglucose (ATG), a thioredoxin reductase (TrxR) inhibitor, exacerbated the effects of hyperoxia on lung injury in a1Neu mice (11.6 +/- 0.8, P < 0.001), but attenuated hyperoxic lung edema and inflammation in C3H/HeN mice (6.3 +/- 0.4, P < 0.001). No consistent alterations were observed in lung GSH contents or liver GSH or GSSG levels after ATG pretreatment. The data suggest that modulation of Trx/TrxR systems might provide therapeutically useful alterations of cellular resistance to oxidant stresses. The protective effects of ATG against hyperoxic lung injury could prove to be particularly useful therapeutically.[1]

References

Thioredoxin-related mechanisms in hyperoxic lung injury in mice. Tipple, T.E., Welty, S.E., Rogers, L.K., Hansen, T.N., Choi, Y.E., Kehrer, J.P., Smith, C.V. Am. J. Respir. Cell Mol. Biol. (2007) [Pubmed]

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