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Pulmonary effects of short term selenium deficiency
1Department of Anesthesiology, University of Wisconsin Clinical Science Center, Madison 53792-3272, USA.
Thorax
|May 1, 1996
Summary
Acute selenium deficiency in rats led to reduced lung glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity, increasing susceptibility to oxidant stress from hyperoxia.
Area of Science:
- Biochemistry
- Toxicology
- Nutritional Science
Background:
- Selenium-dependent glutathione peroxidase (GPx) is crucial for reducing peroxides.
- Chronic selenium deficiency impairs GPx, potentially compensated by glutathione-S-transferase (GST).
- Short-term effects of acute selenium deficiency on lung antioxidant enzymes are not well-described.
Purpose of the Study:
- To investigate the time course of GPx depletion in rat lungs during acute selenium deficiency.
- To assess the activity of various antioxidant enzymes and the localization of GPx and SOD.
- To determine the impact of acute selenium deficiency on susceptibility to hyperoxia.
Main Methods:
- Rats were fed a selenium-deficient diet, with lung GPx measured every five days.
- After 20 days, lung enzyme activities (GPx, catalase, SOD, GR, G-6-PD, GST) were quantified.
- Immunohistochemistry was used for GPx and SOD localization, and hyperoxia tolerance was tested.
Main Results:
- Selenium deficiency significantly reduced lung GPx activity by one-third after 20 days.
- Cyanide-inhibited SOD activity decreased by approximately 50% in deficient rat lungs.
- Selenium-deficient rats exhibited increased susceptibility to lethal hyperoxia compared to controls.
Conclusions:
- This study demonstrates the earliest observed moderate loss of GPx activity due to acute selenium deficiency.
- Reduced GPx and potentially SOD activity contribute to increased susceptibility to pulmonary oxidant stress.
- Elemental deficiencies can intricately interact with antioxidant responses during severe oxidative stress.