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 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.

Ozone/oxygen mixture modifies the subcellular redistribution of Bax protein in renal tissue from rats treated with cisplatin.

BACKGROUND: Cellular events in cisplatin-mediated nephrotoxicity include apoptosis induction, decreased protein synthesis, changes in the subcellular redistribution of Bax mitochondrial dysfunction, DNA injury, increased lipid peroxidation, depletion of glutathione and decrease in enzymatic activity of renal antioxidant enzymes. In previous papers we have shown that intra-rectal (i.r.) ozone/oxygen mixture protected and induced a significant recovery in cisplatin-induced renal damage and was related to a significant increase in the antioxidant system in renal tissue. METHODS: This study was undertaken to examine the effect of the ir applications of ozone/oxygen mixture in the renal expression pattern of Bax proteins in rats treated with cisplatin. A group of male Sprague-Dawley rats was pretreated with 15 i.r. applications of ozone/oxygen (1.1 mg/kg) before intraperitoneal injection of cisplatin (6 mg/kg). Another group was treated with five i.r. applications of ozone/oxygen mixture after cisplatin administration. Serum creatinine was measured thereafter. Subcellular distribution of Bax in renal tissue was analyzed by immunohistochemistry. RESULTS: Ozone pretreatment prevented the increase in serum creatinine levels and completely inhibited the acute tubular necrosis induced by cisplatin in renal tissue, diminishing the expression of Bax. Ozone treatment after cisplatin application reduced the increase in serum creatinine levels and the renal necrosis, inducing a lesser decrease of the Bax expression in cisplatin-treated kidneys. CONCLUSIONS: Expression of Bax in renal tissue seems to play an important role in the protection and recovery in cisplatin-nephrotoxicity achieved by ozone/oxygen mixture.