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Endotoxin protects selenium-deficient rats from hyperoxia.

S G Jenkinson, R J Long, R A Lawrence

    The Journal of Laboratory and Clinical Medicine
    |January 1, 1984
    PubMed
    Summary
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    Bacterial endotoxin protects rats from oxygen toxicity, even those with low antioxidant defenses. This protection occurs through mechanisms beyond the induction of key antioxidant enzymes like glutathione peroxidase (GSH-Px).

    Area of Science:

    • Biochemistry
    • Toxicology
    • Cellular Biology

    Background:

    • Bacterial endotoxin administration confers protection against hyperoxia (oxygen poisoning) in normobaric conditions.
    • Endotoxin treatment typically induces antioxidant enzymes, including glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT), in lung tissue.
    • GSH-Px is a selenoenzyme; selenium deficiency significantly reduces lung GSH-Px activity and heightens susceptibility to hyperoxic lung injury.

    Purpose of the Study:

    • To investigate if bacterial endotoxin can protect rats with compromised antioxidant defenses (specifically, selenium deficiency) from oxygen toxicity.
    • To determine the role of antioxidant enzyme induction in endotoxin-mediated protection in selenium-deficient rats.

    Main Methods:

    • Selenium-deficient and control rats were administered daily intraperitoneal injections of bacterial endotoxin (250 µg/kg) or phosphate-buffered saline (PBS).

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  • Animals were exposed to normobaric hyperoxia (greater than 95% O2).
  • Lung antioxidant enzyme activities (GSH-Px, SOD, CAT) were measured, and survival rates were monitored.

    • Main Results:

    • Bacterial endotoxin provided significant protection against hyperoxia in both selenium-deficient and control rats.
    • Protection was observed despite critically low lung GSH-Px activity in the selenium-deficient group.
    • Endotoxin did not induce GSH-Px, SOD, or CAT activities in selenium-deficient rats within the observed timeframe (48 hours), by which point PBS-treated selenium-deficient rats began to die.

    Conclusions:

    • Bacterial endotoxin confers protection against hyperoxia even in the absence of enhanced antioxidant enzyme activity.
    • In selenium-deficient rats, alternative protective mechanisms, not involving the induction of GSH-Px, SOD, or CAT, appear to mediate early protection from oxygen toxicity.