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Neurochem Res (2011) 36:19781983 DOI 10.1007/s11064-011-0521-3
ORIGINAL PAPER
Effects of Taurine on Nitric Oxide and 3-Nitrotyrosine Levels in Spleen During Endotoxemia
Filiz Sezen Bircan Barbaros Balabanli
Nurten Turkozkan Gonca Ozan
Accepted: 28 May 2011 / Published online: 15 June 2011 Springer Science+Business Media, LLC 2011
Abstract Taurine (2-aminoethanesulfonic acid) is a free sulfur-containing b-amino acid which has antioxidant, antiinammatory and detoxicant properties. In the present study, the role of endotoxemia on peroxynitrite formation via 3-nitrotyrosine (3-NT) detection, and the possible antioxidant effect of taurine in lipopolysaccharide (LPS)-treated guinea pigs were aimed. 40 adult male guinea pigs were divided into four groups; control, endotoxemia, taurine and taurine?endotoxemia. Animals were administered taurine (300 mg/kg), LPS (4 mg/kg) or taurine plus LPS intraperitoneally. After 6 h of incubation, when highest blood levels of taurine and endotoxin were attained, the animals were sacriced and spleen samples were collected. The amounts of 3-nitrotyrosine and taurine were measured by HPLC, and reactive nitrogen oxide species (NOx) which are stable end products of nitric oxide was measured spectrophotometrically in spleen tissues. LPS administration signicantly decreased the concentration of taurine whilst increased levels of 3-NT and NOx compared with control group. It was determined that taurine treatment decreased the levels of 3-nitrotyrosine and NOx in taurine?endotoxemia group. The group in which taurine was administered alone, contradiction to well-known antioxidant effect, taurine caused elevated concentration of 3-NT
and NOx. This data suggest that taurine protects spleen against oxidative damage in endotoxemic conditions. However, the effect of taurine is different when it is administered alone. In conclusion, taurine may act as an antioxidant during endotoxemia, and as a prooxidant in healthy subjects at this dose.
Keywords 3-Nitrotyrosine Endotoxin Peroxynitrite
Spleen Taurine
Introduction
Lipopolysaccharide (LPS) is a glycolipid component of the cell wall of gram-negative bacteria, and the administration of LPS can stimulate the development of the systemic inammatory response syndrome [1]. The main cellular targets for LPS are endothelial cells lining the vasculature and macrophages which found on high concentrations in the spleen [2,3]. Macrophages and endothelial cells are two major biological sources of nitric oxide (NO). It has been shown that released NO plays an important role in the development of LPS-mediated endotoxin shock [4]. Induction of NO synthesis during inammatory processes represents a...