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Öğe Effect Of Astaxanthin On Rat Brains Against Oxidative Stress Induced By Cadmium:Biochemical, Histopathological Evaluation(2018) Akkoyun, Hurrem Turan; Bengü, Aydın Şükrü; Ulucan, Aykut; Akkoyun, Mahire Bayramoğlu; Ekin, Suat; Temel, Yusuf; Çiftçi, MehmetAim of this study is to evaluate protective impact of Astaxanthin (AST) on rats with experimentalbrain injury induced with Cadmium (Cd). 32 male Wistar albino rats were divided into four groups as Control,Cadmium, Astaxanthin (AST), Cadmium (Cd)+Astaxanthin (AST). Rat brain tissues were obtained at the endof 30th day. Malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD) enzymeactivities were measured in brain homogenates and histopathological examination was performed. MDA levelswere improvement in cadmium administered group (p<0.01) as well as Cd+AST administered group (p<0.05)compared to control group. In addition a substantial reduction Cd+AST group was observed compared to cadmiumadministered group (p<0.01). GSH level shows a decrease in Cd and Cd+AST groups compared to control (p<0.05).SOD enzyme activity was found significantly lower in Cd and Cd+AST groups compared to control (p<0.01). Inaddition, increase of SOD in Cd+AST group compared to cadmium group was also found significant (p<0.05).Histopathological findings in the cerebral cortex and hippocampus were different between groups. In the controland AST administered groups, normal histological structure was observed in the brain, while severe lesions wereseen in the Cd administered group and in the Cd+AST group only mild degenerative lesions were observed.As a result, elevated MDA level due to Cd administration was attenuated with AST administration. Decreased GSHlevel and SOD enzyme activity due to Cd administration was increased with AST administration. In addition, ASTadministration decreased histopathological lesions. Consequently, it is thought that AST may be used for protectionagainst brain oxidative damage due to Cd.Öğe Investigation of Protecting Effect of Boric Acid against Mercury II Chloride Toxicity in Rat Brain Tissue(2020) Akkoyun, H. Turan; Bengü, Aydın Şükrü; Ulucan, Aykut; Akkoyun, Mahire Bayramoğlu; İzgi, Mehmet Sait; Şahin, Ömer; Ekin, SuatIn this study, the protective effects of boric acid (BA) in the prevention of brain damagecaused by mercury II chloride ( HgCl2) in rats were investigated. In the experiment, 24 adult andWistar albino male rats weighing roundly 200-300 g were used. Group I (Control, n=8): Isotonicsaline (i.p), Group II (HgCl2,n=8):(0.01g/kg)(oral), Group III (HgCl2 + (BA) (n:8): HgCl2(0.01g/kg)+ BA (3.25mg/kg/day i.p.) group were administered. The rats in all groups were sacrificed at theend of the 10th day and their brain tissues were taken. Biochemical parameters including theenzyme activities of SOD, CAT and GSH-Px were measured. The enzyme activity of SOD wasreduced in HgCl2 treated group in comparison to the control group (p<0.001). Activity of theenzyme was increased after BA administration (p?0.001). CAT enzyme activity decreased in HgCl2and HgCl2+BA administered groups with control (p?0.001). An increase in enzyme activity in BAgroup with HgCl2 administered group was observed. GSH-Px enzyme activity decreased in HgCl2(p?0.001) and HgCl2+BA (p?0.05) groups with control. However, an increase was found in BAadministered group with HgCl2 administered group (p?0.001). It is thought that antioxidant enzymeactivities such as SOD, CAT and GSH-Px are significantly changed and BA may have a protectiveeffect in the histopathological examination of brain tissue.Öğe Investigation of the Effects of Boric Acid on Preventing Lung Damage in the End of the Lower Extremity Ischemia Reperfusion in Rats(2020) Özcan, H. Cahit; Bengü, Aydın Şükrü; Akkoyun, H.Turan; Ulucan, Aykut; Akkoyun, Mahire BayramogluIn this study, the biochemical and histopathological changes in the lungs due to lower extremity ischemiareperfusioninjury and protective effect of boric acid to prevent them were investigated. The rats were divided into threegroups as Group 1 (Sham group, n=9), Group 2 (Ischemia-reperfusion group, I/R, n=9) and Group 3 (Ischemiareperfusion,(I/R) + boric acid (BA), n=9). Anaesthesia was applied to the first group of rats without any ischemiareperfusionprocess. Following a two-hour ischemia, two hours of reperfusion, with the help of left lower extremitiestourniquet, were applied to the second group. To the third group, 200 mg/kg (i.p.) boric acid application was performed10 minutes before the ischemia was initiated and two hours of ischemia and two hours of reperfusion application werecarried out. Some antioxidant enzymes in lung tissue (SOD, GSH-Px, CAT) were analyzed. In addition the lung tissuewas evaluated histopathologically. Boric acid application was found to significantly enhance the positive effect of antioxidantenzymes. Normal histological structure was better preserved, some of macrophages were non-activated, and aremarkable reduction of neutrophil infiltration was seen after treatment in boric acid given group.Öğe PROTECTIVE EFFECT OF ASTAXANTHIN AGAINST ALUMINUM INDUCED LIVER OXIDATIVE DAMAGE(Parlar Scientific Publications (P S P), 2017) Akkoyun, H. Turan; Bengu, Aydin Sukru; Akkoyun, Mahire Bayramoglu; Ulucan, Aykut; Arihan, OkanIn this study, protective effect of a potent antioxidant astaxanthine on preventing rat liver damage due to Al exposure was evaluated. In experimental design, 20 Wistar-albino rats were divided into four groups as Control, Aluminum (20 mg/kg/day i.p), Al + Astaxanthine (5 mg/kg/day AST orally, Al 20 mg/kg/day i.p) and AST (5 mg/kg/day). Study was conducted for 14 days. GSH was found significantly low in Al group compared to control and significantly high in AST and AST + Al administered groups compared to Al group(p<0.01). When MDA levels were investigated, an increase in Al administered group compared to control (p<0.01) and a decrease in Al + AST group compared to Al administered group (p<0.001) was found. In CAT enzyme activity level, a significant decrease in Al, AST and Al + AST administered groups compared to control (p<0.001), an increase in AST, Al + AST groups compared to Al administered group (p<0.001) and also an increase in CAT enzyme activity level in AST+Al administered group compared to AST group (p<0.001) was determined. Due to alterations in MDA and GSH levels and CAT enzyme activity in rat liver tissue as well as positive effects of AST in liver tissue histopathological assessments, it was concluded that AST has a protective role against such toxic molecules.Öğe PROTECTIVE EFFECT OF ELLAGIC ACID AGAINST CARBON TETRACHLORIDE (CCl4) - INDUCED OXIDATIVE BRAIN INJURY IN RATS(Parlar Scientific Publications (P S P), 2018) Akkoyun, H. Turan; Bengu, Aydin Sukru; Ulucan, Aykut; Bayramoglu-Akkoyun, Mahire; Arihan, OkanIn this study, it was aimed to investigate protective effects of Ellagic acid in rats which have brain damage formed with carbon tetrachloride (CCl4). 28 male Wistar albino rats were separated into 4 groups as Control, CCl4., Ellagic acid and CCl4+ Ellagic acid. From the brain tissue homogenate malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), gluthation peroxidase (GSH-Px), catalase (CAT) levels were measured and routine histopathological investigation was performed. An increase in MDA level (p<0.01) whereas a decrease in CAT, GSH-Px, SOD (p<0.01) and GSH (p<0.05) levels in CCl4 administered group compared to control was observed. In our study, in the control and Ellagic acid administered groups, no microscopic findings were observed in the brain, while severe lesions were seen in the CCl4 administered group and only mild congestion lesions were seen in the CCl4 + Ellagic acid group. Results of this study suggest a protection by ellagic acid against CCl4 induced brain damage. This protection is possibly via induction of antioxidant protective mechanism which is shown both by biochemical and histopathological methods.
