Memet Hanifi Emre

Effects of melatonin or acetylsalicylic acid on gastric oxidative stress after bile duct ligation in rats.

BackgroundAntioxidant enzyme activities decrease after bile duct ligation. The aim of this study was to assess the effect of melatonin and acetylsalicylic acid on antioxidant enzyme activities in gastric oxidative stress induced by bile duct ligation.MethodsSixty-four animals were divided into eight groups of eight rats each. Male Sprague-Dawley rats were subjected to either a sham operation or common bile duct ligation (BDL) before treatment with melatonin (MEL) or acetylsalicylic acid (ASA). Gastric superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and malondialdehyde (MDA) and nitric oxide (NO) levels were determined by spectrophotometers and evaluated.ResultsOur results indicated that BDL caused a significant increase in lipid peroxidation, whereas coadministration of MEL with ASA significantly decreased MDA and NO levels in BDL rats. Moreover, coadministration of MEL and ASA increased antioxidant enzyme activities after the BDL, and these increases were statistically significant for CAT and GPx. On the other hand, the increase in SOD activity was not significant.ConclusionsMelatonin administration, either alone or together with acetylsalicylic acid, decreases lipid peroxidation and increases antioxidant enzyme activities in gastric tissues of rats after bile duct ligation. ASA administration, however, either alone or with a vehicle, increases lipid peroxidation and decreases antioxidant enzyme activities.

Influence of dihydropyridine calcium antagonist nitrendipine on benzo(a)pyrene-induced oxidative stress

The aim of this study was to investigate the influence of nitrendipine (NIT), a dihydropyridine derived calcium channel antagonist, on polycyclic aromatic hydrocarbon benzo(a)pyrene (BAP)-induced oxidative stress. Male Sprague Dawley rats (155–220 g) were divided into four groups: Control (corn oil, i.p.); BAP (200 mg/kg, i.p.), BAP + NIT (200 mg/kg, i.p. + 50 mg/kg, i.p.), and NIT (50 mg/kg, i.p.) groups. Twenty-four hours after the injection of BAP, the rats were sacrificed and blood samples, liver, lung, and brain tissues were removed to determine serum alanine transaminase (ALT), aspartate transferase (AST), and gamma-glutamyltransferase (GGT) activities and tissue thiobarbituric acid reactive substances (TBARS), glutathione (GSH), and superoxide dismutase (SOD) levels. BAP significantly elevated serum ALT and TBARS levels in all tissues. However, NIT pre-treatment protected against increasing TBARS levels in lung and brain tissues. In addition, NIT pre-treatment significantly increased SOD levels in lung and liver tissues, as well as GSH levels in the lungs, compared to the BAP group. Thus, in conclusion, further studies are required to confirm the protective effects of calcium channel blockers, especially in liver tissue.

Renal Antioxidant Status in Rats with Hypertension Induced by N Sup Omega Nitro-L-Arginine Methyl Ester

Nitric oxide (NO) has a role in the etiopathogenesis of hypertension. Relaxation of vascular smooth muscles is failed when NO production is reduced leading to increased vascular peripheral resistance. N sup omega nitro-L-arginine methyl ester (L-NAME) is one of the inhibitors of NO production. The aim of this study was to investigate oxidant-antioxidant systems of renal tissue in rats with hypertension induced by L-NAME. Rats were divided into three groups: control group and study groups treated with 100 or 500 mg/l L-NAME in drinking water for 15 days. The activities of catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and NO were studied in the renal tissue after hypertension induction. Arterial blood pressure was increased in both L- NAME groups. CAT activity of 500-mg L-NAME group was higher than control. GSH-Px activity of 500-mg L-NAME group was decreased compared with 100-mg ones. NO level was lower in 500-mg L-NAME group than control. MDA levels in both L-NAME groups were decreased compared with control. In conclusion, hypertension was induced with oral L-NAME treatment. Increased CAT activity was compensated with decreased GSH-Px activity in 500-mg L-NAME group. Both study groups were protected from lipid peroxidation with NO inhibition.

Investigation of Propolis’ Effect on Thiobarbituric Acid Reactive Substances and Anti-Oxidant Enzyme Levels of Hippocampus in Diabetic Rats Induced by Streptozotocin

BACKGROUND: Propolis is an organic resinous viscous substance collected from flower bud and plant sprig by bees. Propolis has a potential treatment agent for oxidative damage caused by diabetes in hippocampus due to its flavonoid and phenolic content. AIM: In this study effect of propolis on thiobarbituric acid reactive substances and anti-oxidative enzyme levels of hippocampus in diabetic rats induced by streptozotocin was investigated. MATERIALS AND METHODS: The study involved measuring levels of SOD, CAT, GSH-Px and TBARs in hippocampus tissue of STZ-induced diabetic rats (Adult Male Sprague Dawley rats) after applying propolis for one month. The subjects of the study were composed of 51 rats randomly assigned to four groups (Control, STZ, P+STZ and STZ+P). For analysis of data, Kruskal Wallis Test was utilized. RESULTS: The findings of the study showed that there were no significant difference in the levels of TBARS, SOD, CAT and GSH-Px of hippocampus across the groups. CONCLUSION: Propolis application in four-week duration does not have effect on TBARS, SOD, CAT and GSH-Px levels of hippocampus of diabetic rats. These findings mean that more time for observing oxidative harms on hippocampus is needed.