AJP - Renal Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 263: F56-F61, 1992;
0363-6127/92 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baliga, R.
Right arrow Articles by Shah, S. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baliga, R.
Right arrow Articles by Shah, S. V.

AJP - Renal Physiology, Vol 263, Issue 1 56-F61, Copyright © 1992 by American Physiological Society

ARTICLES

Effect of selenium-deficient diet in experimental glomerular disease

R. Baliga, M. Baliga and S. V. Shah
Department of Pediatrics, Louisiana State University School of Medicine, New Orleans 70112.

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.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
J. B. de Haan, N. Stefanovic, D. Nikolic-Paterson, L. L. Scurr, K. D. Croft, T. A. Mori, P. Hertzog, I. Kola, R. C. Atkins, and G. H. Tesch
Kidney expression of glutathione peroxidase-1 is not protective against streptozotocin-induced diabetic nephropathy
Am J Physiol Renal Physiol, September 1, 2005; 289(3): F544 - F551.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
H. Liu, S. V. Shah, and R. Baliga
Cytochrome P-450 as a source of catalytic iron in minimal change nephrotic syndrome in rats
Am J Physiol Renal Physiol, January 1, 2001; 280(1): F88 - F94.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online