In the present study, we also evaluated the effect of ECGg supplementation on biomarkers related to the antioxidant defence system and antioxidant enzymes in animals exposed to sevoflurane. It is well known free radical species (FRS) are constantly produced as a normal consequence of aerobic metabolism. Oxidative stress results from an imbalance between radical-generating and radical-scavenging systems, leading to cell membrane impairment or DNA damage. MDA is a reflection of lipid peroxidation. Protein carbonyl content is evaluated as an index of protein oxidation. Protein SH groups are important antioxidant defenses
19. Increased lipid peroxidation and decreased antioxidant protection may lead to cytotoxicity, allergy, mutagenicity, and carcinogenicity
20. MDA is a reflection of lipid peroxidation, whereas SOD and GSH-Px are important antioxidant defenses. These enzymes are involved in the clearance of superoxide and H2O2 to maintain the structure and function of biological membranes
19. SOD dismutases superoxide H2O2 and this compound is catabolized by catalase and GSH-Px. In higher organisms, GSH-Px appears to have largely supplanted the need for catalase membranes
19. Thus, our findings support the existence of a local and systemic oxidative stress from spontaneous ventilated animals during exposure to sevoflurane. Moreover, anesthesia conducted with propofol reduced oxidative stress and enhanced antioxidant defense mechanisms expressed by larger concentrations of free radical scavengers. Sivaci and et al showed that antioxidant activity is affected after sevoflurane anesthesia whereas antioxidant activity is reduced significantly after desflurane anesthesia
21.
In a recent study 22 demonstrates that endothelium-dependent vasorelaxation induced by the tea-derived catechin EGCg occurs in response to a potent, dose-dependent activation of eNOS in endothelial cells. The resulting increase in eNOS activity is observed within a few minutes, suggesting posttranslational regulation of eNOS as an underlying mechanism. In agree with this study, we also found that level of NO in kidney tissue incresed with EGCg supplementation. It has been showed that catechins chelating properties could also have a fundamental role in preventing peroxidation 23.
Dikmen et al 24 observed an elevation of SOD, GSH-Px and CAT levels in anasthesic groups they reported that elevation of SOD, CAT and GSH-Px activities due to increased production of free radicals. In the present study, our results show that animals exposed to sevoflurane had increased MDA, NO, SOD and GSH-Px concentrations in kidney tissue, but the increased level of GSH-Px was not statically significant. Conversely, EGCg supplementation decreased MDA, SOD and GSH-Px levels in animals exposed to sevoflurane. We could not find any previous report on the effects of EGCg supplementation on kidney tissue levels of MDA, NO and antioxidant enzymes in rats exposed to anasthesic agents and to compare with our results. Against all the protective enzymatic mechanisms, cellular damage that supports the elevation of lipid peroxidation was observed in group 1. Histopathological findings in group 1, there was severe degeneration with moderate cortical necrosis in kidney tissue. Administration of sevoflurane plus EGCg in rats, decreased degeneration in histopatological findings.
In conclusion, the amount of lipid peroxidation and antioxidant enzyme activities were more increased in following sevoflurane administration in the 3% concentration. The administration of EGCg (40 mg/kg/d) significantly protected kidney tissue. These conclusions were supported by the improved reduced levels of MDA.