Endotoxin protects selenium-deficient rats from hyperoxia.
Rats treated with low doses of bacterial endotoxin have been shown to be protected from oxygen poisoning under normobaric conditions. Induction of lung activity of the antioxidant enzymes glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) has been reported to occur with endotoxin administration. GSH-Px is a selenoenzyme and selenium-deficient rats have decreased lung GSH-Px activity and enhanced lung toxicity during a hyperoxic exposure. To determine whether bacterial endotoxin administration can provide protection for animals with decreased antioxidant defenses, selenium-deficient and control rats received daily intraperitoneal injections of 250 micrograms/kg bacterial endotoxin or phosphate-buffered saline (PBS) during normobaric exposure to greater than 95% O2. Both groups of animals were protected from hyperoxia by bacterial endotoxin administration despite the extremely low lung GSH-Px activity in the selenium-deficient rats. GSH-Px, SOD, or CAT activities were not induced in the selenium-deficient rats by 48 hr (the time when the selenium-deficient rats treated with PBS began to die). In the selenium-deficient rat, mechanisms other than enzyme induction appear to be providing early protection from hyperoxia.
D000818:Animals; D002374:Catalase / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D008297:Male; D010100:Oxygen / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000172:deficiency*; D013482:Superoxide Dismutase / Q000378:metabolism
D004731:Endotoxins; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D012643:Selenium; D010100:Oxygen