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    Antioxidant effect of sildenafil on cadmium-induced liver, lung and kidney injury
    (Society of Pharmaceutical Sciences of Ankara (FABAD), 2020) Baran A.H.; Berk A.; Kaymaz M.B.; Aktay G.
    The aim of this study is to investigate the protective effect of sildenafil against cadmium-induced liver, lung and kidney toxicity. In total of 28 Sprague Dawley female rats included in this study were divided into four groups: control, Sil, Cd, Sil+Cd groups. CdCl2 and Sil citrate were dissolved in distilled water, the injection volume adjusted to 0,5 ml / rat. On the 7th day, a single dose of 3,7 mg/kg Cd was injected ip in the morning and Sil was administered in drinking water for 10 days. On the 10th day of the experiment, 72 hours after Cd administration, the rats were sacrificed under anesthesia and the lungs, kidneys and livers of the rats were isolated and Thiobarbituric acid reactive substances (TBARs), GSH, total thiol (T-SH) levels in these tissues were evaluated. Tissue damage was assessed by serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, blood urea nitrogen (BUN) and creatine kinase (CK-MB). It was found that cadmium significantly increased AST, ALT, creatinine, BUN, CK-MB and TBARs levels compared to the control group, and significantly decreased GSH andT-SH levels. In sildenafil + cadmium administration, TBARs levels significantly decreased while GSH and T-SH levels significantly increased compared to cadmium group. The protective effect of sildenafil against multiple organ damage caused by cadmium may be due to its antioxidant properties. © 2020 Society of Pharmaceutical Sciences of Ankara (FABAD). All rights reserved.
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    Effect of cyclooxygenase-2 inhibition on nicotine-induced oxidative stress
    (University of Ankara, 2010) Ünüvar S.; Aktay G.
    We examined the tissue thiobarbituric acid reactive substances (TBARS), non-protein thiol (NP-SH) and total thiol (T-SH) group levels in order to deduce the role of cyclooxygenase-2 (COX-2) pathway on nicotine-induced oxidative tissue damage. Wistar Albino male rats were divided into three groups: Group I; 0.9% saline (ip), Group II; nicotine ditartarate (1.5 mg/kg, ip), Grup III; celecoxib (15 mg/kg, ip)+nicotine ditartarate (1.5 mg/kg ip). At the end of the 7th day, liver, lung, kidney, heart and brain tissues were removed. Nicotine treatment significantly increased TBARS, NP-SH and T-SH levels in all tissues. However, celecoxib treatment prior the nicotine injection, significantly decreased the TBARS levels and T-SH contents in all tissues in addition to NP-SH content in kidney, liver, lung and brain compared to nicotine group. Nicotine treatment caused excessive production of free radicals and evoked the antioxidant molecules. However, inhibition of cyclooxygenase-2 selectively prevented the nicotine-induced oxidative tissue damage dramatically. We concluded that, cyclooxygenase-2 pathway may be a notable mechanism of the nicotine toxicity.
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    Effects of nonsteroidal antiinflammatory drugs on the thiol groups and lipid peroxidation in ethanol-induced oxidative stress
    (2004) Aktay G.; Tozkoparan B.; Ertan M.
    The aim of this study was to investigate whether nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen (IBU), indomethacin (INDO), aspirin (ASP), and celecoxib (CEL) could enhance the susceptibility the oxidative stress caused by the acute intoxication with ethanol in gastric mucosa, liver and brain of mice. The results showed that only the IBU treatment contribute to the control of the lipid peroxidation (LPO) and thiol group levels in all tissues. However, CEL can be able to increase the susceptibility of gastric mucosa to ethanol-induced oxidative stress like classic NSAIDs. while it has a significant protective effect in brain tissue..