Faculty Collaboration Database

Hydroxyl radicals mediate injury to endothelium-dependent relaxation in diabetic rat. Mol Cell Biochem 1993 May 26;122(2):139-45

Date

05/26/1993

Pubmed ID

8232245

DOI

10.1007/BF01076098

Scopus ID

2-s2.0-0027328844 (requires institutional sign-in at Scopus site)   42 Citations

Abstract

The purpose of this study was to determine the radical species which mediates the toxic effects of exogenous oxygen-derived free radicals on endothelial function of chronic diabetic rat aorta. Endothelium-dependent relaxation to acetylcholine was impaired in diabetic vessels. Exposure to the exogenous free radical generating system of xanthine plus xanthine oxidase selectively impaired endothelium-dependent relaxation to acetylcholine in control and diabetic aorta with relaxations essentially abolished in diabetic aorta. The loss of relaxation to acetylcholine in diabetic aorta was prevented or attenuated by pretreatment with catalase, dimethylthiourea or desferrioxamine, but not by mannitol or superoxide dismutase. These results suggest that hydroxyl radicals play an important role in the endothelial injury produced by oxygen-derived free radicals in chronic diabetic rat aorta. Furthermore, the site of the injury is likely due to intracellular generation of hydroxyl radicals.

Author List

Pieper GM, Langenstroer P, Gross GJ

Author

Peter Langenstroer MD Professor in the Urologic Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Acetylcholine
Animals
Cell Death
Diabetes Mellitus, Experimental
Diabetic Angiopathies
Endothelium, Vascular
Free Radicals
Hydroxyl Radical
In Vitro Techniques
Male
Neutrophils
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species
Reference Values
Vasodilation