Severe burn injuries cause functional impairment in distant internal organs. Although this mechanism is not clear, it is possible that free radical toxicity plays an important role. Research in animals and clinical studies have shown that there is a close relationship between a lipid peroxidative reaction and secondary pathological changes following thermal injury. It has been demonstrated that antioxidant treatment prevents oxidative tissue damage associated with thermal trauma. This study was designed to determine the possible protective effect of caffeic acid phenethyl ester (CAPE) treatment against oxidative damage in the kidney and lung induced by thermal injury. Rats were decapitated either 1, 3 or 7 days after burn injury. CAPE was administered intraperitoneally immediately after thermal injury. Kidney and lung tissues were taken for the determination of malondialdehyde (MDA) level, myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) and xanthine oxidase (XO) activities. Severe skin thermal injury caused a significant decrease in SOD and CAT activities, as well as significant increases in MDA level, XO and MPO activities in tissues during the postburn period. Treatment of rats with CAPE (10 mol/kg) significantly elevated the decreased SOD and CAT activities, while it decreased MDA levels and MPO as well as XO activity.
Carbon dioxide interacts both with reactive nitrogen species and reactive oxygen species. In the presence of superoxide, NO reacts to form peroxynitrite that reacts with CO2 to give nitrosoperoxycarbonate. This compound rearranges to nitrocarbonate which is prone to further reactions. In an aqueous environment, the most probable reaction is hydrolysis producing carbonate and nitrate. Thus the net effect of CO2 is scavenging of peroxynitrite and prevention of nitration and oxidative damage. However, in a nonpolar environment of membranes, nitrocarbonate undergoes other reactions leading to nitration of proteins and oxidative damage. When NO reacts with oxygen in the absence of superoxide, a nitrating species N2O3 is formed. CO2 interacts with N2O3 to produce a nitrosyl compound that, under physiological pH, is hydrolyzed to nitrous and carbonic acid. In this way, CO2 also prevents nitration reactions. CO2 protects superoxide dismutase against oxidative damage induced by hydrogen peroxide. However, in this reaction carbonate radicals are formed which can propagate the oxidative damage. It was found that hypercapnia in vivo protects against the damaging effects of ischemia or hypoxia. Several mechanisms have been suggested to explain the protective role of CO2 in vivo. The most significant appears to be stabilization of the iron-transferrin complex which prevents the involvement of iron ions in the initiation of free radical reactions., A. Veselá, J. Wilhelm., and Obsahuje bibliografii
Red wine polyphenols have been reported to possess beneficial properties for preventing cardiovascular diseases but their neuroprotective effects during chronic L-NAME treatment have not been elucidated. The aim of this study was to analyze a time course of Provinols
TM effects on brain NO synthase activity and oxidative damage in L-NAME-induced hypertension. Male Wistar rats, 12 weeks old, were divided into six groups: control groups, groups treated with N G-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg/day) for 4 or 7 weeks and groups receiving ProvinolsTM (40 mg/kg/day) plus L-NAME for 4 or 7 weeks. At the end of the treatment, marker of membrane oxidative damage – conjugated dienes (CD) in the brain and NO synthase activity in the cerebral cortex, cerebellum and brainstem were determined. L-NAME treatment for 4 or 7 weeks led to the increase in blood pressure, elevation of CD concentration and decrease of NO synthase activity in the brain parts investigated. ProvinolsTM partially prevented blood pressure rise and elevation of CD concentration. Comparing to the L-NAME treated group, ProvinolsTM increased NO synthase activity after 4 weeks of treatment. However, the prolonged ProvinolsTM treatment for 7 weeks had no effect on NO synthase activity decreased by L-NAME treatment. In conclusion, ProvinolsTM partially prevents L-NAME induced hypertension via
the different mechanisms depending on the duration of treatment. Prevention of oxidative damage in the brain with modulating effect on NO synthase activity is suggested.