Turkish Journal of Biochemistry, cilt.41, sa.5, ss.316-321, 2016 (SCI-Expanded)
© 2016, Turkish Biochemistry Society. All rights reserved.Objective: Sepsis is a common cause of morbidity and mortality in the intensive care unit. Lipopolysaccharide (LPS)-induced excessive immune response is associated with multi-organ damage in sepsis. Excessive immune response causes multi-organ damage by increasing oxidative stress. Studies on the antioxidant effects of vitamin D demonstrated its protective role. In this study we aimed to investigate the effects of vitamin D on free radical metabolism in LPS injected rats. Methods: Twenty four wistar albino rats were separated into control, sepsis, sepsis+vitamin D and vitamin D groups. Sepsis was induced with single injection of LPS Esherichia coli (O111-b4) 16 mg/kg. Vitamin D was given 2 mg/kg 25 (OH) single dose via gavage for 3 days. Renal function tests were analyzed in serum. Tissue catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) activities were analyzed, and rat renal tissues were evaluated histopathologically. Results: SOD and GSH-Px activities were not significantly different between the groups. CAT activities were significantly decreased in all groups compared to control, this suppression was seen in the sepsis+vitamin D group versus sepsis group. GST activities were significantly decreased in sepsis and sepsis+vitamin D group compared to control, but GST activities were significantly elevated vitamin D group compare to sepsis and sepsis+vitamin D group. Blood urea nitrogen (BUN) and creatinine levels were significantly elevated in sepsis and sepsis+vitamin D group. Inflammation, expansion in bowman capsule were detected in sepsis and sepsis+vitamin D groups. Conclusion: Vitamin D treatment does not seem to have protective role against renal toxicity in sepsis.Nutrition with vitamin D in sepsis may have suppressive effect on antioxidant enzymes sush as CAT and GST due to reduced substrat level which use hydrogen peroxide (H2O2) and GSH as a substrate.