Effect of selenium-deficient diet in experimental glomerular disease

Abstract

We examined the effect of a selenium-deficient diet on two experimental models of glomerular disease, the puromycin aminonucleoside (PAN)-induced nephrotic syndrome, a model of minimal change disease, and passive Heymann nephritis, a complement-dependent and neutrophil-independent model that resembles membranous nephropathy. The specific activity of selenium-dependent glutathione peroxidase was markedly reduced in the liver, the kidney cortex, and in glomeruli in weanling male Sprague-Dawley rats placed on a selenium-deficient diet for 6 wk compared with rats fed a selenium-replete diet, with no significant differences in the specific activities of superoxide dismutase or catalase. PAN-injected selenium-deficient rats had a marked and significantly greater proteinuria throughout the course of the experiment compared with PAN-injected selenium-replete rats with no significant histological differences. In the passive Heymann nephritis model induced by injecting anti-Fx1A immunoglobulin G, rats fed a selenium-deficient diet had significantly higher urinary protein (day 5: 91 +/- 16 mg/24 h, n = 10) compared with rats fed a selenium-replete diet (52 +/- 5 mg/24 h, n = 11) with no differences in the amount of antibody deposited in the kidney. The most likely explanation for the effect of a selenium-deficient diet is that selenium deficiency resulted in a marked reduction of glutathione peroxidase, thus indicating an important role of glutathione peroxidase in these models of glomerular injury.

Serum selenium level and glutathione peroxidase activity in steroid-sensitive nephrotic syndrome

“…It is well known that an Se-deficient diet, both in humans and experimental animals, produces a reduction in GPX activity, and consequently decreases the antioxidant potential of tissues [14]. A diminished intake of Se in the diet of our patients seems unlikely.…”

Apoptosis and antioxidant defense in the nephrotic syndrome

“…A decreased TAS level may also be connected with either the abnormal intestinal absorption of these components or the low antioxidant diet of patients with NS, most of whom have a poor appetite, especially during the acute phase [19]. There are some data in the literature showing that diets deficient in selenium and vitamin E may lead to renal injury characterized by proteinuria and reduced glomerular filtration rate [20]. When endogenous GPX was experimentally depressed by a selenium-deficient diet in rats treated with puromycin aminonucleoside, the characteristic proteinuria was even more markedly augmented [21].…”

Therapeutic Effect of a Newly Developed Antioxidative Agent (OPC-15161) on Experimental Immune Complex Nephritis

“…Baliga et al [25] reported that puromycin-aminonucleoside-injected. selenium-deficient rats had marked proteinuria through out the course of these experiment as compared with puromycin-aminonucleoside-injected, selenium-replete rats.…”