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Aysel Agar

Publications and source records attributed to Aysel Agar.

15 recordsLinked to original sources

Beneficial effects of docosahexaenoic acid on active avoidance performance in 1K-1C hypertensive rats.

The present study evaluated the role of chronic docosahexaenoic acid (DHA) supplementation on active avoidance learning task performance in experimental hypertension. Male Wistar rats were randomly divided into five experimental groups as follows: control, sham, DHA treated, 1K-1C hypertensive, and 1K-1C hypertensive+DHA treated. Hypertension was induced in 1K-1C rats via placing a silver clip (0.20-mm ID) around the left renal artery following a right uninephrectomy. DHA (36 mg/kg/day) was given to the treatment groups for 60 days by gastric gavage. Arterial blood pressure was measured by using the tail-cuff method. Active avoidance responses were determined by an automated shuttle-box. In brain (cerebrum) and hippocampus tissues, thiobarbituric acid reactive substances (TBARS) and nitrite levels were measured by fluorometric methods. DHA supplementation decreased blood pressure in hypertensive rats. Data from active avoidance training indicated that performance of active avoidance learning tasks were significantly impaired in 1K-1C hypertensive rats, but was completely restored by DHA supplementation. Increased cerebrum TBARS levels in 1K-1C rats were abolished by DHA administration. Cerebrum nitrite levels were lower in the DHA, 1K-1C and 1K-1C+DHA treated groups compared to controls. Hippocampus nitrite levels were lower in DHA treated and 1K-1C hypertensive rats compared to controls and higher in 1K-1C+DHA treated rats compared to the 1K-1C group. Our data indicates that DHA supplementation improves the performance of active avoidance learning tasks which is impaired in experimental hypertension. These affirmative changes might be due to a DHA-induced decrease in lipid peroxidation which may in turn limit the consumption of nitric oxide (NO) which promotes active avoidance learning.

Animals↗

Effect of chronic restraint stress and alpha-lipoic acid on lipid peroxidation and antioxidant enzyme activities in rat peripheral organs.

OBJECTIVES: The aim of this study was to evaluate the effect of chronic restraint stress and alpha-lipoic acid (LA) administration on lipid peroxidation and antioxidant enzyme activities in rat peripheral organs. METHODS: Forty male wistar rats, aged 3 months were randomized to one of the following groups: control, restraint stress, LA treated and restraint stress+LA treated. Chronic restraint stress was applied for 21 days (1h/day) and LA (100 mg/kg/day) was administered intraperitoneally for the same period. RESULTS: Restraint stress had no statistically significant effect on lipid peroxidation, copper/zinc superoxide dismutase (Cu/Zn SOD), catalase (CAT) and glutathione peroxidase (GPx) activity in rat liver and heart, when compared to the control group. Lipid peroxidation, determined by measuring malondialdehyde (MDA) levels, was found to be increased in the kidney of restraint stress treated rats, compared to controls. Restraint stress-induced lipid peroxidation in the kidney was significantly decreased via LA treatment. Administration of LA also enhanced GPx and decreased Cu/Zn SOD activity in rat kidney, liver and heart, compared to the control group. CONCLUSIONS: The presented data shows that LA is a protective agent against restraint stress--the inducer of lipid peroxidation in the kidney. These findings also suggest that LA-induced changes in antioxidant enzyme activities in rat peripheral organs may contribute to their versatile effects observed in vivo.

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Changes in visual evoked potentials, lipid peroxidation and antioxidant enzymes in rats exposed to restraint stress: effect of L-carnitine.

The purpose of our study was to investigate the effects of L-carnitine on lipid peroxidation, Visual Evoked Potentials (VEPs) and antioxidant enzyme activities such as superoxide dismutase and catalase in rats exposed to chronic restraint stress. Forty male Wistar rats, aged three months were used. They were equally divided into four groups: control (C), the group exposed to restraint stress (R), the group treated with L-carnitine(L) and the group exposed to stress and treated with L-carnitine (RL). Chronic restraint stress was applied for 21 days (1 h/day) and L-carnitine (50 mg/kg/day) was given by gavage to the L and RL groups for the same period. Brain and retina levels of thiobarbituric acid reactive substances (TBARS) were significantly increased in the R group and were not altered in the L group compared to the C group. Brain and retina TBARS levels were lower in the RL group than in the R group. Brain and retina superoxide dismutase and catalase activities were significantly decreased in the L and R groups compared to the C group. L-carnitine pretreatment had no significant effect on superoxide dismutase and catalase activity in the RL group. All latencies of VEP components were prolonged in the R and L groups with respect to the C group. L-carnitine increased the latencies of all VEP components in the L group whereas shortened them in the RL group compared to their control groups. L-carnitine may be a promising agent for the prevention of VEP and TBARS alterations caused by stress.

Analysis of Variance↗

The role of docosahexaenoic acid on visual evoked potentials in one kidney-one clip hypertension.

PURPOSE: To investigate the effects of polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) on visual evoked potentials (VEPs) in a one kidney-one clip (1K-1C) hypertension model in rats. METHODS: Five experimental groups were formed: a control group, a sham group, a group supplemented with DHA, a 1K-1C group, and a 1K-1C + DHA group. The DHA groups were treated for 60 days. In the 1K-1C groups, the right kidney was removed and a silver clip with a 0.2-mm gap was placed on the left renal artery. RESULTS: The DHA-supplemented rats had lower blood pressure than their respective controls (p < 0.01). The increased brain and retina thiobarbituric acid reactive substances (TBARS) levels in hypertensive rats were abolished by DHA administration. The brain nitrite levels were lower in the DHA, 1K-1C and 1K-1C + DHA groups compared with the control group (p < 0.01), and the retina nitrite level was higher in the 1K-1C + DHA group compared with the DHA and 1K-1C groups (p < 0.01). There was an improvement of P(2), N(2) and P(3) components following DHA supplementation in 1K-1C hypertensive rats compared with the 1K-1C group. CONCLUSION: The present study suggests that DHA supplementation has the potential to prevent VEP changes caused by an experimental model of hypertension. This state might be related to the lipid peroxidation lowering effect of DHA.

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The effect of sulfite and chronic restraint stress on brain lipid peroxidation and anti-oxidant enzyme activities.

Sulfites are used as anti-microbial and anti-oxidant agents in a variety of drugs, and function as a preservative in many food preparations. In addition to these effects, sulfites oxidize to sulfite radicals initiating lipid peroxidation. The objective of our study was to investigate the effect of restraint stress and sulfite on brain lipid peroxidation and anti-oxidant enzyme activities. Forty male Wistar rats, aged three months, were randomized to one of the following groups: control, restraint stress, sulfite-treated and restraint stress + sulfite-treated. Chronic restraint stress was applied for 21 days (1 h/day) and sodium metabisulfite (520 mg/kg per day) was given by gavage for the same period. Lipid peroxidation was measured using the thiobarbituric acid (TBA) fluorometric assay. TBA-reactive substances (TBARS) were found increased in all treatment groups when compared to the control group. Spectrophotometric measurement of copper/zinc superoxide dismutase (Cu/Zn SOD) and catalase (CAT) revealed decreased enzyme activities in rats exposed to restraint stress compared to control and sulfite-treated rats. GSH-Px activities were significantly decreased in the restraint stress and sulfite-treated rats compared with the control rats. GSH-Px activity measured in restraint stress + sulfite-treated rats was significantly lower than in the other groups. The presented data confirms the pro-oxidant activity of restraint stress and establishes that decreased anti-oxidant enzyme activities in restraint stress-treated rats enhances brain lipid peroxidation caused via the ingestion of sulfites.

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Effect of sulfite on red blood cell deformability ex vivo and in normal and sulfite oxidase-deficient rats in vivo.

The effect of sulfite, a widely used food additive, on red blood cell deformability ex vivo and in vivo was investigated. Ex vivo experiments were conducted in human blood exposed to sulfite (5, 10 and 20 mM). In vivo experiments were carried out in sulfite oxidase-competent (SOXC) and sulfite oxidase-deficient (SOXD) rats. In the in vivo experiments, sulfite was administered in the form of sodium metabisulfite (Na(2)S(2)O(5), 25 mg/kg/day) via drinking water. Vitamin E dissolved in olive oil at a dose of 50 mg/kg was administered by gastric gavages. Red blood cell (RBC) deformability was determined at various fluid shear stresses using an ektacytometer. Ex vivo sulfite exposure to RBC did not affect RBC deformability. In the in vivo experiments, although RBC deformability was not affected by sulfite treatment in SOXD rats, it was found to be significantly increased in SOXC rats. Vitamin E treatment in combination with sulfite caused impairment in RBC deformability in both SOXC and SOXD rats. We suggest that sulfite needs to be oxidized in order to improve RBC deformability.

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The prooxidant effect of sodium metabisulfite in rat liver and kidney.

Sodium metabisulfite (Na2S2O5) is used as an antioxidant and antimicrobial agent in a variety of drugs and functions as a preservative in many food preparations. In addition to their antioxidant activity, sulfites oxidize to sulfite radicals (SO3-) initiating lipid peroxidation. This study was performed to elucidate the effect of subchronic Na2S2O5 (520 mg/kg/day) ingestion on hepatic and renal antioxidant enzyme activities and lipid peroxidation in albino rats. The antioxidant effect of l-carnitine was also tested in rats treated with Na2S2O5. Plasma uric acid levels were monitored in all rats included in the study. Malondialdehyde (MDA) levels significantly increased in Na2S2O5 treated rats vs. controls, with kidney values of 2.21+/-0.21 vs. 1.22+/-0.35 and liver values of 79.85+/-19.5 vs. 31.36+/-5.0 nmol/mg protein, respectively. Selenium-glutathione peroxidase (GPx) activity was significantly increased in Na2S2O5 treated rats vs. controls, with kidney values of 38.22+/-2.21 vs. 8.09+/-0.76 and liver values of 31.11+/-6.37 vs. 11.70+/-1.02 U/g protein, respectively. Sodium metabisulfite treatment increased plasma uric acid levels in rats that were included in the study. No protective effect of l-carnitine was observed against lipid peroxidation in both liver and kidneys of rats treated with Na2S2O5. The presented data confirm the prooxidant activity of sulfites and suggest that increased GPx activity and plasma uric acid levels may partially reduce the observed renal and hepatocellular oxidative damage caused via the ingestion of sulfites.

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The effect of chronic restraint stress and sulfite on visual evoked potentials (VEPs): relation to lipid peroxidation.

Stress and sulfite can stimulate numerous pathways leading to an increased production of free radicals which generate a peroxidation cascade producing lipid peroxidation, protein oxidation, DNA damage and cell death, and contribute to the occurrence of pathologic conditions. The purpose of our study was to investigate the effects of stress and sulfite on visual evoked potentials (VEPs) and to examine the relationship between lipid peroxidation and VEP changes. Forty male wistar rats, aged three months were used. They were equally divided into four groups: control (C), the group exposed to restraint stress (R), the group treated with sulfite (S) and the group exposed to stress and treated with sulfite (RS). Chronic restraint stress was applied for 21 days (1h/day) and sodium metabisulfite (520 mg/kg/day) was given by gavage for the same period. All latencies of VEP components were prolonged in the R, S and RS groups with respect to the C group. Brain and retina TBARS levels were found to be increased in those groups compared to the C group. Our results strongly suggest that the latency prolongations of all VEP components may have resulted from the enhancement of lipid peroxidation. Correlation analysis between brain and retina TBARS levels and VEP latencies also support this conclusion. Our data in regard to latency prolongations of all VEP components in the stress group exposed to sulfite, reflected an additive effect of sulfite toxicity on VEP components. Therefore it could be suggested that chronic exposure to stress and sulfite together is associated with a considerable health risk.

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Effects of excess vitamin B6 intake on cerebral cortex neurons in rat: an ultrastructural study.

The aim of this study was to investigate whether excess of vitamin B6 leads to ultrastructural changes in cerebral cortex of forty-eight healthy albino rats which were included in the study. Saline solution was injected to to the control groups (CG-10, n = 12 for 10 days; CG-15, n = 12 for 15 days; CG-20, n=12 for 20 days). The three experimental groups (EG-10, n = 12; EG-15, n = 12; EG-20, n = 12) were treated with 5 mg/kg vitamin B6 daily for 10 days (EG-10), 15 days (EG-15) and 20 days (EG-20). Brain tissues were prepared by glutaraldehyde-osmium tetroxide double fixation for ultrastructural analysis. No significant changes were observed in the control groups. The ultrastructural analysis revealed that the numbers of damaged mitochondria, lipofuscin granules and vacuoles were significantly higher in all the experimental groups than in the control groups (p < 0.05). However, synaptic density was significantly decreased in the experimental groups as compared to the control groups (p < 0.05). The results suggest that the excess of vitamin B6 intake causes damage to the cerebral cortex due to cellular intoxication and decreased synaptic density. Thus, careful attention should be paid to the time and dose of vitamin B6 recommended for patients who are supplemented with this vitamin.

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The effect of chronic restraint stress on spatial learning and memory: relation to oxidant stress.

The aim of this study was to investigate the effect of chronic restraint stress (RS) on spatial learning and memory. Fifty healthy male Wistar rats, aged three months were used. They were equally divided into five groups--C: Control, W: Water Maze, CS-1: Restrained for 21 days (1 h/day) + water maze protocol following stress period, CS-2: Restrained for 28 days (1 h/day) + water maze protocol during last 7 days of stress period, CS-3: Restrained for 21 days and allowed to recovery for 7 days (1 h/day). Corticosterone levels were higher in all stress groups than in C and W groups. Nitrite levels of frontal cortex and hippocampus were found to be elevated in chronic stress groups with respect to C and W groups. Thiobarbituric acid reactive substances (TBARS) of both tissues were increased significantly in CS1 and CS2 groups compared with C, W, and CS3 groups. Escape latencies of CS1 and CS2 groups were longer than those of the W group on each day of acquisition. In transfer test, CS1 and CS2 groups stayed significantly shorter in target quadrant according to the W group. Significant correlations between corticosterone and either nitrite or TBARS of hippocampus and frontal cortex were found. Both acquisition and memory performances were negatively correlated with plasma corticosterone level, nitrite, and TBARS levels of hippocampus and frontal cortex. The results of this study suggest that stress-induced lipid peroxidation may affect the acquisition and memory performances.

Analysis of Variance↗

The effect of different hypertension models on active avoidance learning.

This study tested the effects of different hypertension models on active avoidance learning in rats. Three-month-old male Wistar rats were divided randomly into six groups as follows: control (C), sham operated (sham), two kidney-one clip (2K-1C), one kidney-one clip (1K-1C), deoxycorticosterone-salt (DOCA), and N-omega-nitro-L-arginine-methyl ester (L-NAME) groups. Mean arterial blood pressures were significantly higher in four hypertensive groups compared with control and sham groups. The active avoidance training results indicated that hypertension state is associated with learning impairment. Thiobarbituric acid-reactive substances (TBARS) were determined as an indicator of lipid peroxidation in brain and hippocampus. Additionally, brain and hippocampus nitrite levels were studied.

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Fiber structure of optic nerve in cadmium-exposed diabetic rats: an ultrastructural study.

This study aimed to show ultrastructural effects of diabetes and cadmium on the optic nerve. We used 52 healthy Swiss albino male rats. They were divided into four groups: control (C), diabetic (D), cadmium, (Cd), and diabetic with cadmium (D + Cd). The diabetic condition was created by intravenous injection of 5 mg alloxan/100 g. Intraperitoneal CdCl2(2 mg kg/week) was given to Cd and D + Cd groups for two months. At the end of the experimental period, animals were sacrificed and the optic nerves were dissected at the front level of chiasma opticum. The tissue samples were investigated by using light and electron microscopic techniques. It was found that both diabetes and Cd intoxication cause myelin disorganization and organelle destruction in axoplasm and cytoplasm of glia. The results suggested that Cd increases the oxidative stress induced by diabetes, by disturbing some enzymatic mechanisms.

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Effect of immobilization and cold stress on visual evoked potentials.

The main aim of our research was to study the effects of immobilization and/or cold stress on amplitudes and latencies of visual evoked potentials (VEPs) and thiobarbituric acid reactive substances (TBARS). Forty healthy male albino rats, aged three months, were used. The rats were equally divided into four groups: Control group (C), the group exposed to cold stress (CS), the group exposed to immobilization stress (IS), and the group exposed to both cold and immobilization stress (CIS). Plasma corticosterone concentrations were significantly increased in all stress groups. Lipid peroxidation was increased in brain and retina of all stress groups as indicated by the significant increase in TBARS levels compared to the C group. Glutathione peroxidase (GSH-Px) activity in brain and retina increased in the CS group, but decreased in the IS group relative to the C group. GSH-Px activity also increased in the brain, but not in the retina in the CIS group with respect to the C group. The mean latencies of P1, N1, P2, N2, and P3 components were significantly prolonged in all stress groups compared with the C group. The results suggest that stress induced lipid peroxidation may influence VEPs.

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Effect of cadmium on sciatic nerve in diabetic rats: an ultrastructural study.

The present study demonstrated the ultrastructural effects of diabetes and cadmium on the peripheral nervous system. In this study we used 52 healthy Swiss male albino rats. They were divided into four groups: control (C), diabetic (D), cadmium (Cd), and diabetic and cadmium (D + Cd). The diabetic condition was induced by intravenous injection of 5 mg alloxan/100 g body weight, via the caudal vein. Cd and D + Cd groups were injected with CdCl2 intraperitoneally (2 mg/Kg/week) for two months. At the end of the experimental period, animals were sacrificed and their sciatic nerves were dissected. The tissue samples were investigated by using light and electron microscopic techniques. Upon investigation, it was seen that myelinated axons in sciatic nerve of diabetic and Cd treatment groups had onion-bulb type myelin destruction, melting, and protrusion. Basal lamina of capillary endothelia of D, Cd, and D + Cd groups were thickened and the endothelial apical membrane was rough. In conclusion, Cd toxicity exacerbated the destructive effect of diabetes on the peripheral nervous system.

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The effect of different hypertension models on visual evoked potentials.

Even though there is an abundance of information about the complications of hypertension, studies of its influence on visual evoked potentials (VEPs) are rare. In previous studies, it was pointed out that hypertension induces changes on VEPs. However, it has not yet been clarified which models of hypertension are more effective on VEPs. The aim of this study was to investigate this subject in rats. Animals were divided equally into six groups: control group (C), sham operated (Sham), two kidney-one clip (2K-1C), one kidney-one clip (1K-1C), deoxycorticosterone-salt (DOCA), and N-omega-nitro-L-arginine-methyl ester (L-NAME) groups. Mean arterial pressure was significantly higher in four hypertensive groups compared with control and sham groups, but there were no significant differences either among hypertensive groups or between sham and control groups. At the end of the experimental period, flash visual evoked potentials were recorded. The mean latencies of P1, N1, P2, N2, and P3 components were significantly prolonged in all hypertensive groups compared with the control and sham groups. The mean latencies of all VEPs components in the L-NAME group were longer than in the other hypertensive groups. Thiobarbituric acid-reactive substances (TBARS) were determined as an indicator of lipid peroxidation. Our data showed that hypertension caused a significant increase of lipid peroxidation in brain and retinal tissues. Additionally, plasma renin activity (PRA) was highest in the 2K-1C group and lowest in the DOCA group.

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