Inhibition of nitric oxide synthase prevents energy failure and oxidative damage evoked in the brain by lipopolysaccharide

Pol J Pharmacol. 2004 Sep-Oct;56(5):643-6.

Abstract

The inducible nitric oxide synthase (iNOS) plays an important role in endotoxic shock. However,little is known about the involvment of constitutive isoform(s) of NOS (cNOS). The aim of this study was to determine the role of cNOS in the mouse brain after lipopolysaccharide (LPS) injection. Concentrations of nicotinamide adenine dinucleotide (NAD(+)), carbonyl group and thiobarbituric acid reactive substances were determined spectrophotometrically, cNOS mRNA was evaluated by RT-PCR. Our data showed that LPS significantly decreased NAD(+) level, and enhanced protein and lipid oxidation, but had no effect on cNOS mRNA expression. Inhibitors of cNOS protected the cells against alterations evoked by LPS, suggesting involvement of cNOS isoforms in pathology.

Publication types

  • Comparative Study
  • Congress
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain / enzymology*
  • Energy Metabolism / drug effects
  • Energy Metabolism / physiology*
  • Enzyme Inhibitors / pharmacology
  • Lipopolysaccharides / toxicity*
  • Mice
  • Mice, Inbred C57BL
  • Nitric Oxide Synthase / antagonists & inhibitors*
  • Nitric Oxide Synthase / metabolism
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology*

Substances

  • Enzyme Inhibitors
  • Lipopolysaccharides
  • Nitric Oxide Synthase