HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Welsh, N Articles by Sandler, S Search for Related Content PubMed PubMed Citation Articles by Welsh, N Articles by Sandler, S

The aim of the present investigation was to evaluate the putative involvement of oxygen free radicals in interleukin-1β (IL-1β)-induced suppression of islet glucose oxidation. Isolated adult rat pancreatic islets were exposed for 1 h to liposomally encapsulated superoxide dismutase (SOD; 10 mg/ml), catalase (CAT; 10 mg/ml) and glutathione peroxidase (GPX; 5 mg/ml), after which IL-1β (25 U/ml) or hydrogen peroxide (H₂O₂; 0·1 mM) was added, and the incubation was continued overnight. The following day, samples were taken from the incubation media for nitrite determinations, and islet glucose oxidation rates were measured. The CAT activity increased fourfold after addition of CAT-containing liposomes. It was found that IL-1β induced a marked increase in islet nitrite production, as an index of nitric oxide formation, and that this was paralleled by a decrease in islet glucose oxidation rates. H₂O₂-treated islets exhibited a modest decrease in glucose oxidation rates and a minor increase in the release of nitrite to the media. Treatment of islets with liposomes containing the antioxidant enzymes SOD, CAT and GPX, either alone or in combination, did not decrease the effect of IL-1β. However, the H₂O₂-induced decrease in glucose oxidation rates was counteracted by the combination of the antioxidants. It was concluded that, provided the intracellular delivery of the antioxidant enzymes to the islet cells was effective, oxygen free radicals probably do not play a decisive role in IL-1β suppression of islet glucose metabolism.

Journal of Endocrinology (1994) 143, 151–156

This article has been cited by other articles:

				X. Li, H. Chen, and P. N. Epstein Metallothionein and Catalase Sensitize to Diabetes in Nonobese Diabetic Mice: Reactive Oxygen Species May Have a Protective Role in Pancreatic {beta}-Cells Diabetes, June 1, 2006; 55(6): 1592 - 1604. [Abstract] [Full Text] [PDF]

				H. Chen, X. Li, and P. N. Epstein MnSOD and Catalase Transgenes Demonstrate That Protection of Islets From Oxidative Stress Does Not Alter Cytokine Toxicity Diabetes, May 1, 2005; 54(5): 1437 - 1446. [Abstract] [Full Text] [PDF]

				E. Gurgul, S. Lortz, M. Tiedge, A. Jorns, and S. Lenzen Mitochondrial Catalase Overexpression Protects Insulin-Producing Cells Against Toxicity of Reactive Oxygen Species and Proinflammatory Cytokines Diabetes, September 1, 2004; 53(9): 2271 - 2280. [Abstract] [Full Text] [PDF]