Oxidative stress is not associated with vascular dysfunction in a model of alloxan-induced diabetic rats

Arq Bras Endocrinol Metabol. 2010 Aug;54(6):530-9. doi: 10.1590/s0004-27302010000600004.

Abstract

Objectives: To verify if an experimental model of alloxan-diabetic rats promotes oxidative stress, reduces nitric oxide bioavailability and causes vascular dysfunction, and to evaluate the effect of N-acetylcysteine (NAC) on these parameters.

Methods: Alloxan-diabetic rats were treated or not with NAC for four weeks. Plasmatic levels of malondialdehyde (MDA) and nitrite/nitrate (NOx), the endothelial and inducible nitric oxide synthase (eNOS and iNOS) immunostaining and the vascular reactivity of aorta were compared among diabetic (D), treated diabetic (TD) and control (C) rats.

Results: MDA levels increased in D and TD. NOx levels did not differ among groups. Endothelial eNOS immunostaining reduced and adventitial iNOS increased in D and TD. The responsiveness of rings to acetylcholine, sodium nitroprusside, and phenylephrine did not differ among groups.

Conclusions: NAC had no effect on the evaluated parameters and this experimental model did not promote vascular dysfunction despite the development of oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcysteine / pharmacology*
  • Alloxan
  • Animals
  • Aorta, Thoracic / drug effects
  • Aorta, Thoracic / physiopathology
  • Diabetes Mellitus, Experimental / drug therapy
  • Diabetes Mellitus, Experimental / physiopathology*
  • Disease Models, Animal
  • Endothelium, Vascular / physiology*
  • Free Radical Scavengers / pharmacology*
  • Male
  • Malondialdehyde / blood
  • Nitric Oxide / physiology*
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III / blood
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology*
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Time Factors

Substances

  • Free Radical Scavengers
  • Nitric Oxide
  • Malondialdehyde
  • Alloxan
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III
  • Acetylcysteine