Lung

, Volume 163, Issue 1, pp 23–32

Oxidant lung injury: Intervention with sulfhydryl reagents

Authors

  • Carolyn E. Patterson
    • Department of Internal MedicineIndiana University School of Medicine
  • John A. Butler
    • Department of Internal MedicineIndiana University School of Medicine
  • Frank D. Byrne
    • Department of Internal MedicineIndiana University School of Medicine
  • Mitchell L. Rhodes
    • Department of Internal MedicineIndiana University School of Medicine
Article

DOI: 10.1007/BF02713803

Cite this article as:
Patterson, C.E., Butler, J.A., Byrne, F.D. et al. Lung (1985) 163: 23. doi:10.1007/BF02713803

Abstract

Intracellular pools of reduced sulfhydryl compounds are taxed in protective and repair processes during oxidant lung injury. To determine the efficacy of exogenous sulfhydryl compounds in preventing the toxic effects of high oxygen exposure on lung, the cell permeable sulfhydryl compounds, cysteamine (CYS) or N-acetylcysteine (NaC), were infused continuously in rats during exposure to 1 atm O2. CYS caused a reduction in mortality compared to vehicle treated-oxygen exposed rats at seven days (56% vs 78% respectively). At 48 hours, CYS reduced oxidant-induced pulmonary edema, measured by wet to dry weight ratios, and prevented oxidation of lung nonprotein sulfhydryls. NaC was even more effective in reducing mortality compared to vehicle treated-oxygen exposed rats (28% vs 78% respectively). In contrast to this beneficial effect of sulfhydryl compounds in oxygen toxicity, oxidant injury due to paraquat poisoning was exacerbated. Mortality increased in mice and rats given paraquat and treated with CYS. We speculate that this effect may be due to the ability of paraquat to accept reducing equivalents directly from CYS, thereby increasing reactive oxygen generated from reduced paraquat.

Key words

Oxygen toxicityParaquat toxicitySulfhydryl treatment

Copyright information

© Springer-Verlag New York, Inc 1985