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Effect of selenium-deficient diet in experimental glomerular disease
1Department of Pediatrics, Louisiana State University School of Medicine, New Orleans 70112.
The American Journal of Physiology
|July 1, 1992
Summary
Selenium deficiency worsens kidney disease in rats by reducing glutathione peroxidase, an important antioxidant enzyme. This study highlights the protective role of selenium in glomerular injury models.
Area of Science:
- Nephrology
- Nutritional Science
- Biochemistry
Background:
- Glomerular diseases, including minimal change disease and membranous nephropathy, represent significant causes of kidney damage.
- Selenium is an essential trace element crucial for antioxidant defense, primarily through glutathione peroxidase enzymes.
Purpose of the Study:
- To investigate the impact of a selenium-deficient diet on two distinct experimental models of glomerular injury: puromycin aminonucleoside (PAN)-induced nephrotic syndrome and passive Heymann nephritis.
- To elucidate the role of selenium-dependent glutathione peroxidase in the pathogenesis of these kidney diseases.
Main Methods:
- Two experimental models of glomerular disease were utilized in Sprague-Dawley rats: PAN-induced nephrotic syndrome and passive Heymann nephritis.
- Rats were fed either a selenium-deficient or a selenium-replete diet for six weeks.
- Levels of selenium-dependent glutathione peroxidase, superoxide dismutase, and catalase activities were measured in liver, kidney cortex, and glomeruli.
- Proteinuria was quantified, and histological examination and antibody deposition were assessed in the kidney.
Main Results:
- Selenium deficiency significantly reduced glutathione peroxidase activity in the liver, kidney cortex, and glomeruli, without affecting superoxide dismutase or catalase.
- Rats on a selenium-deficient diet exhibited significantly higher proteinuria in both the PAN-induced nephrotic syndrome and passive Heymann nephritis models compared to selenium-replete controls.
- No significant differences in histological findings or antibody deposition were observed between the dietary groups in either model.
Conclusions:
- Selenium deficiency exacerbates proteinuria in experimental models of glomerular injury, likely due to the marked reduction in glutathione peroxidase activity.
- Glutathione peroxidase plays a critical role in protecting against glomerular injury, and its deficiency compromises renal function in these models.
- These findings underscore the importance of adequate selenium intake for maintaining kidney health and preventing or mitigating glomerular damage.