Endotoxin protection of rats from pulmonary oxygen toxicity: possible cytokine involvement.
Treatment with endotoxin protects rats against lung injury during hyperoxia (greater than 98% oxygen at 1 atmosphere absolute for 60 h). This study demonstrates that serum from endotoxin-treated donor rats also protects recipients from oxygen toxicity. Rats treated with serum from saline-treated donors were not protected, and protection was not explained by residual endotoxin in protective sera. Unlike endotoxin-protected rats (where lung antioxidant enzyme activity is elevated after hyperoxia), postexposure superoxide dismutase (SOD) and catalase (CAT) activities in the lungs of serum-protected rats were not affected. Levels of tumor necrosis factor (TNF) and interleukin 1 (IL-1) in protective sera were increased. This study demonstrates that increases in lung SOD and CAT activity are not required for endotoxin protection from hyperoxia and suggests that TNF and IL-1 may participate in the mechanism of endotoxin protection.
Berg
J T
JT
Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688.
Allison
R C
RC
Prasad
V R
VR
Taylor
A E
AE
D000818:Animals; D002374:Catalase / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology*; D007375:Interleukin-1 / Q000502:physiology*; D008168:Lung / Q000187:drug effects / Q000201:enzymology; D055370:Lung Injury; D008297:Male; D010100:Oxygen / Q000633:toxicity*; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D004731:Endotoxins; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D002374:Catalase; D013482:Superoxide Dismutase; D010100:Oxygen