Inhibition of nitric oxide synthase prevents energy failure and oxidative damage evoked in the brain by lipopolysaccharide.
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.
Czapski
G A
GA
Department of Cellular Signaling, Medical Research Centre, Polish Academy of Sciences, Pawińskiego 5, PL 02-106 Warszawa, Poland.
Cakała
M
M
Kopczuk
D
D
Kamińska
M
M
Strosznajder
J B
JB
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000201:enzymology*; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000633:toxicity*; D051379:Mice; D008810:Mice, Inbred C57BL; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*
D004791:Enzyme Inhibitors; D008070:Lipopolysaccharides; D019001:Nitric Oxide Synthase