Ozone oxidative preconditioning reduces nitrite levels in blood serum in LPS: induced endotoxic shock in mice

Objective and design Reactive oxygen species, and also reactive species of nitrogen such as nitric oxide, play an important role in the pathogenesis of peritonitis and septic shock. Ozone oxidative preconditioning (OOP) has shown protective effects in various experimental models of peritonitis in ra...

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Veröffentlicht in:Inflammation research 2009-08, Vol.58 (8), p.441-443
Hauptverfasser: Alvarez, Ricardo González, Zamora, Zullyt Barbara, Borrego, Aluet, Delgado, René, Schulz, Siegfried, Alonso, Yaima
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Sprache:eng
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Zusammenfassung:Objective and design Reactive oxygen species, and also reactive species of nitrogen such as nitric oxide, play an important role in the pathogenesis of peritonitis and septic shock. Ozone oxidative preconditioning (OOP) has shown protective effects in various experimental models of peritonitis in rats and endotoxic shock in mice. Currently, strong evidence is available that this protective effect of OOP is due to its action on the balance between endogenous antioxidants and pro-oxidants, which is favorable for anti-oxidant defense. The aim of this research was to elucidate whether or not OOP is able to reduce nitrite levels in blood serum of mice treated with lipopolysaccharide (LPS). We used an experimental model of endotoxic shock induced by LPS in mice in which the animals were pre-treated with ozone/oxygen mixture for 5 days (once daily), with injection of LPS 24 h thereafter to induce endotoxic shock. Results Mice pretreated with OOP showed a significant decrease in nitrite levels with all three doses tested [0.2 mg/kg (50.91%), 0.4 mg/kg (47.3%) and 1.2 mg/kg (34.6%)]. Conclusions Ozone oxidative preconditioning significantly reduced nitrite levels in blood serum of mice with endotoxic shock induced by LPS. We propose that OOP merits further testing in studies as a potential alternative treatment to reduce nitrite levels in patients with sepsis syndrome and septic shock.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-009-0055-1