Aysel Agar

Akdeniz University, Satalia, Antalya, Turkey

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Publications (92)165.64 Total impact

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    ABSTRACT: This study aimed to elucidate locomotor activity changes in 6-hydroxydopamine (6-OHDA) induced Parkinson's disease (PD) and investigate the possible beneficial effects of melatonin on altered levels of locomotor activity, cyclooxygenase (COX), prostaglandin E2 (PGE2), nuclear factor kappa B (NF-κB), nitrite/nitrate and apoptosis. Male Wistar rats were divided into five groups: vehicle (V), melatonin-treated (M), 6-OHDA-injected (6-OHDA), 6-OHDA-injected + melatonin-treated (6-OHDA-Mel) and melatonin treated + 6-OHDA-injected (Mel-6-OHDA). Melatonin was administered intraperitoneally at a dose of 10 mg/kg/day for 30 days in M and Mel-6-OHDA groups, for 7 days in 6-OHDA-Mel group. Experimental PD was created stereotactically via unilateral infusion of 6-OHDA into the medial forebrain bundle (MFB). The 6-OHDA-Mel group started receiving melatonin when experimental PD was created and treatment was continued for 7 days (post-treatment). In the Mel-6-OHDA group, experimental PD was created on the 23rd day of melatonin treatment and continued for the remaining 7 days (pre- and post-treatment). Locomotor activity performance decreased in 6-OHDA group compared with vehicle; however melatonin treatment did not improve this impairment. Nuclear factor kappa Bp65 and bcl-2 levels were significantly decreased while COX, PGE2 and caspase-3 levels were significantly increased in 6-OHDA group. Melatonin treatment significantly decreased COX, PGE2 and caspase-3 activity, increased bcl-2 and had no effect on NF-κB levels in PD. 6-OHDA injection caused an obvious reduction in TH positive dopaminergic neuron viability as determined by immunohistochemistry. Melatonin supplementation decreased dopaminergic neuron death in 6-OHDA-Mel and Mel-6-OHDA groups compared with 6-OHDA group. Melatonin also protected against 6-OHDA-induced apoptosis, as identified by increment in Bcl-2 levels in dopaminergic neurons. The protective effect of melatonin was more prominent for most parameter following 30 days treatment (pre- and post-) than 7 days post-treatment. In summary, melatonin treatment decreased domaninergic neuron death in experimental Parkinson model by increasing bcl-2 protein level and decreasing caspase-3 activity.
    Neurochemistry International 09/2014; · 2.66 Impact Factor
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    ABSTRACT: We aimed to define the influence of different hypertension models on lipid peroxidation markers [conjugated dienes (CD) and thiobarbituric acid-reactive substances (TBARS)], antioxidant protection [paraoxonase-1 (PON1) activity] and visual evoked potential (VEP) changes in rats.
    09/2014; 14(6):498-504.
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    ABSTRACT: The effects of extremely low frequency electric fields (ELF-EFs, 3-300 Hz) on lipid peroxidation levels and antioxidant enzyme activities have been shown in many tissues and plasma after exposure to 50 Hz AC electric fields. However, similar studies investigating brain lipid peroxidation status are limited. Moreover and as far as we know, no study has been conducted to examine mismatch negativity (MMN) response in rats following exposure to 50 Hz AC electric field. Therefore, the purpose of the study was to investigate different intensity and exposure duration of ELF-EFs on MMN component of event related potentials (ERPs) as well as apoptosis and oxidative brain damage in rats. Ninety male rats, aged 3 months were used in our study. A total of six groups, composed of 15 animals each, was formed as follows: sham exposed rats for 2 weeks (C2), sham exposed rats for 4 weeks (C4), rats exposed to 12 kV/m and 18kV/m electric fields for 2 weeks (E12-2 and E18-2), rats exposed to 12 kV/m and 18kV/m electric fields for 4 weeks (E12-4 and E18-4). At the end of the experimental period, MMN responses were recorded in urethane-anesthetized rats by electrodes positioned stereotaxically to the surface of the dura. After MMN recordings, animals were killed by exsanguination and their brain tissues were removed for 4-hydroxy-2-nonenal (4-HNE), protein carbonyl and TUNEL analysis. In the current study, different change patterns in ERP parameters were observed dependent on the intensity and exposure duration of ELF-EFs. There were differences in the amplitudes of ERP between the responses to the standard and the deviant tones in all groups. When peak-to-peak amplitude of the difference curves were evaluated, MMN amplitude was significantly decreased in the E18-4 group compared with the C4 group. Additionally, the amount of 4-HNE was increased in all experimental groups compared with the control group. Consequently, it could be concluded that electric field decreased MMN amplitudes possibly induced by lipid peroxidation.
    Neuroscience 05/2014; · 3.12 Impact Factor
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    ABSTRACT: The present study aimed to elucidate visual evoked potentials (VEP) changes in MPTP induced Parkinson's Disease (PD) and investigate the possible benefical effects of neuronal (n) and inducible (i) nitric oxide synthase (NOS) inhibitors on altered VEPs, lipid peroxidation and apoptosis. 3 months old C57BL/6 mice were randomly divided into 6 groups which included control (C), 7-nitra indazole treated (7-NI), S-methylisothiourea (SMT) treated, 1, 2, 3, 6-tetrahydropyridine (MPTP) treated, 7-NI+MPTP treated and SMT+MPTP treated. Motor activity of mice was evaluated via the pole test. At the end of the experimental period VEPs were recorded, brain and retina tissues were removed for biochemical analysis. Dopaminergic neuron death at substantia nigra (SN) was determined by immunohistochemical analysis of tyrosine hydroxylase (TH). Immunohistochemical staining was also performed to determine iNOS and nNOS in all tissue sections. Mice with experimental PD exhibited decreased motor activity. Dopaminergic cell death at pars compacta of SN (SNpc) was significantly increased in MPTP treated group compared to control. Diminished Parkinsonism symptoms were observed in 7-NI+MPTP and SMT+MPTP groups. Treatment with 7-NI and SMT decreased dopaminergic cell death in MPTP treated mice. Caspase-3 activity, nitrite/ nitrate and 4-hydroxynonenal (4-HNE) levels were significantly increased in SN of MPTP treated mice compared to control. Treatment with 7-NI and SMT significantly decreased elevated caspase-3 activity, nitrite/nitrate and 4-HNE levels in SN of MPTP treated mice. No significant difference in above parameters were observed in the retina. VEP latencies were significantly prolonged in MPTP group compared to control group. 7-NI and SMT treatment caused a significant decrease in VEP latencies in MPTP treated mice compared to none treated MPTP group. This data shows that 7-NI and SMT improves prolonged VEP latencies. The protective effects of 7-NI and SMT on VEP alterations can be related to decreased dopaminergic cell death and reduced lipid peroxidation.
    Neurochemistry International 04/2014; · 2.66 Impact Factor
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    ABSTRACT: The effects of extremely low-frequency electric fields (ELF-EFs, 3–300 Hz) on lipid peroxidation levels and antioxidant enzyme activities have been shown in many tissues and plasma after exposure to 50-Hz alternating current (AC) electric fields. However, similar studies investigating brain lipid peroxidation status are limited. Moreover and as far as we know, no study has been conducted to examine mismatch negativity (MMN) response in rats following exposure to a 50-Hz AC electric field. Therefore, the purpose of the study was to investigate different intensities and exposure durations of ELF-EFs on MMN component of event-related potentials (ERPs) as well as apoptosis and oxidative brain damage in rats. Ninety male rats, aged 3 months were used in our study. A total of six groups, composed of 15 animals each, was formed as follows: sham-exposed rats for 2 weeks (C2), sham-exposed rats for 4 weeks (C4), rats exposed to 12-kV/m and 18-kV/m electric fields for 2 weeks (E12-2 and E18-2), rats exposed to 12- and 18-kV/m electric fields for 4 weeks (E12-4 and E18-4). At the end of the experimental period, MMN responses were recorded in urethane-anesthetized rats by electrodes positioned stereotaxically to the surface of the dura. After MMN recordings, animals were killed by exsanguination and their brain tissues were removed for 4-hydroxy-2-nonenal (4-HNE), protein carbonyl and TUNEL analysis. In the current study, different change patterns in ERP parameters were observed dependent on the intensity and exposure duration of ELF-EFs. There were differences in the amplitudes of ERP between the responses to the standard and the deviant tones in all groups. When peak-to-peak amplitude of the difference curves was evaluated, MMN amplitude was significantly decreased in the E18-4 group compared with the C4 group. Additionally, the amount of 4-HNE was increased in all experimental groups compared with the control group. Consequently, it could be concluded that electric field decreased MMN amplitudes possibly induced by lipid peroxidation.
    Neuroscience 01/2014; 272:154–166. · 3.12 Impact Factor
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    ABSTRACT: The present study aimed to elucidate visual evoked potentials (VEP) changes in MPTP induced Parkinson’s Disease (PD) and investigate the possible benefical effects of neuronal (n) and inducible (i) nitric oxide synthase (NOS) inhibitors on altered VEPs, lipid peroxidation and apoptosis. 3 months old C57BL/6 mice were randomly divided into 6 groups which included control (C), 7-nitra indazole treated (7-NI), S-methylisothiourea (SMT) treated, 1, 2, 3, 6-tetrahydropyridine (MPTP) treated, 7-NI+MPTP treated and SMT+MPTP treated. Motor activity of mice was evaluated via the pole test. At the end of the experimental period VEPs were recorded, brain and retina tissues were removed for biochemical analysis. Dopaminergic neuron death at substantia nigra (SN) was determined by immunohistochemical analysis of tyrosine hydroxylase (TH). Immunohistochemical staining was also performed to determine iNOS and nNOS in all tissue sections. Mice with experimental PD exhibited decreased motor activity. Dopaminergic cell death at pars compacta of SN (SNpc) was significantly increased in MPTP treated group compared to control. Diminished Parkinsonism symptoms were observed in 7-NI+MPTP and SMT+MPTP groups. Treatment with 7-NI and SMT decreased dopaminergic cell death in MPTP treated mice. Caspase-3 activity, nitrite/ nitrate and 4-hydroxynonenal (4-HNE) levels were significantly increased in SN of MPTP treated mice compared to control. Treatment with 7-NI and SMT significantly decreased elevated caspase-3 activity, nitrite/nitrate and 4-HNE levels in SN of MPTP treated mice. No significant difference in above parameters were observed in the retina. VEP latencies were significantly prolonged in MPTP group compared to control group. 7-NI and SMT treatment caused a significant decrease in VEP latencies in MPTP treated mice compared to none treated MPTP group. This data shows that 7-NI and SMT improves prolonged VEP latencies. The protective effects of 7-NI and SMT on VEP alterations can be related to decreased dopaminergic cell death and reduced lipid peroxidation.
    Neurochemistry International 01/2014; · 2.66 Impact Factor
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    ABSTRACT: We aimed at investigating the effects of sulfite-induced lipid peroxidation and apoptosis mediated by secretory phospholipase A2 (sPLA2) on somatosensory evoked potentials (SEP) alterations in rats. Thirty male albino Wistar rats were randomized into three experimental groups as follows; control (C), sodium metabisulfite treated (S), sodium metabisulfite + Quinacrine treated (SQ). Sodium metabisulfite (100 mg/kg/day) was given by gastric gavage for 5 weeks and 10 mg/kg/day quinacrine was applied as a single dose of intraperitoneal injection for the same period. The latencies of SEP components were significantly prolonged in the S group and returned to control levels following quinacrine administration. Plasma-S-sulfonate level was increased in S and SQ groups. TBARS levels in the S group were significantly higher than those detected in controls. Quinacrine significantly decreased brain TBARS levels in the SQ group compared with the S group. Quinacrine treatment didn't have an effect on the increased sPLA2 level of the sulfite administered group. Immunohistochemistry showed that sulfite caused an increase in Caspase-3 and TUNEL positive cells, restored to control levels via quinacrine administration. This study showed that sPLA2 might play a role in ingested sulfiteinduced SEP alterations, oxidative stress, apoptotic cell death and DNA damage in the brain.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 11/2012; · 2.99 Impact Factor
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    ABSTRACT: The aim of the study was to investigate the effects of extremely low-frequency electric field (ELF EF) on visual evoked potential (VEP), thiobarbituric acid reactive substances (TBARS), total antioxidant status (TAS), total oxidant status (TOS), and oxidant stress index (OSI). Thirty female Wistar rats, aged 3 months, were divided into three equal groups: Control (C), the group exposed to EF at 12 kV/m strength (E12), and the group exposed to EF at 18 kV/m strength (E18). Electric field was applied to the E12 and E18 groups for 14 days (1 h/day). Brain and retina TBARS, TOS, and OSI were significantly increased in the E12 and E18 groups with respect to the control group. Also, TBARS levels were significantly increased in the E18 group compared with the E12 group. Electric fields significantly decreased TAS levels in both brain and retina in E12 and E18 groups with respect to the control group. All VEP components were significantly prolonged in rats exposed to electric fields compared to control group. In addition, all latencies of VEP components were increased in the E18 group with respect to the E12 group. It is conceivable to suggest that EF-induced lipid peroxidation may play an important role in changes of VEP parameters.
    Electromagnetic Biology and Medicine 10/2012; · 0.81 Impact Factor
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    ABSTRACT: Docosahexaenoic acid (DHA), a major polyunsaturated fatty acid (PUFA) in the phospholipid fraction of the brain, is essential for normal cellular function. Neurodegenerative disorders such as Parkinson's disease (PD) often exhibit significant declines in PUFAs. The aim of this study was to observe the effects of DHA supplementation in an experimental rat model of PD created with '1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine' (MPTP). Adult male Wistar rats were divided into four groups: (1) Control; (2) DHA-treated; (3) MPTP-induced; and (4) MPTP-induced + DHA-treated. Motor activity was investigated using the 'vertical pole' and 'vertical wire' tests. The dopaminergic lesion was determined by immunohistochemical analysis for tyrosine hydroxylase (TH)-immunopositive cells in substantia nigra (SN). Immunoreactivities of Bcl-2, Akt and phosphorylated-Akt (p-Akt) in SN were evaluated by immunohistochemistry. MPTP-induced animals exhibited decreased locomotor activity, motor coordination and loss of equilibrium. Diminished Parkinsonism symptoms and decreased dopaminergic neuron death were detected in the MPTP-induced + DHA-treated group compared to the MPTP-induced group. Moderate decreases in Akt staining were found in the MPTP-induced and MPTP-induced + DHA-treated groups compared to controls. p-Akt immunoreactivity decreased dramatically in the MPTP-induced group compared to the control; however, it was increased in the MPTP-induced + DHA-treated group compared to the MPTP-induced group. The staining intensity for Bcl-2 decreased prominently in the MPTP-induced group compared to the control, while it was stronger in the MPTP-induced + DHA-treated group compared to the MPTP-induced group. In conclusion, DHA significantly protects dopaminergic neurons against cell death in an experimental PD model. Akt/p-Akt and Bcl-2 pathways are related to this protective effect of DHA in experimental PD.
    Folia Histochemica et Cytobiologica 07/2012; 50(2):228-38. · 1.10 Impact Factor
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    ABSTRACT: This study aimed to investigate the effects of docosahexaenoic acid (DHA) on the oxidative stress that occurs in an experimental mouse model of Parkinson's disease (PD). An experimental model of PD was created by four intraperitoneal injections of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (4 × 20 mg/kg, at 12h intervals). Docosahexaenoic acid was given daily by gavage for 4 weeks (36 mg/kg/day). The motor activity of the mice was evaluated via the pole test, and the dopaminergic lesion was determined by immunohistochemical analysis for tyrosine hydroxylase (TH)-immunopositive cells. The activity of antioxidant enzymes in the brain were determined by spectrophotometric assays and the concentration of thiobarbituric acid-reactive substances (TBARS) were measured as an index of oxidative damage. The number of apoptotic dopaminergic cells significantly increased in MPTP-treated mice compared to controls. Although DHA significantly diminished the number of cell deaths in MPTP-treated mice, it did not improve the decreased motor activity observed in the experimental PD model. Docosahexaenoic acid significantly diminished the amount of cell death in the MPTP+DHA group as compared to the MPTP group. TBARS levels in the brain were significantly increased following MPTP treatment. Glutathione peroxidase (GPx) and catalase (CAT) activities of brain were unaltered in all groups. The activity of brain superoxide dismutase (SOD) was decreased in the MPTP-treated group compared to the control group, but DHA treatment did not have an effect on SOD activity in the MPTP+DHA group. Our current data show that DHA treatment exerts neuroprotective actions on an experimental mouse model of PD. There was a decrease tendency in brain lipid oxidation of MPTP mice but it did not significantly.
    Neurochemistry International 06/2011; 59(5):664-70. · 2.66 Impact Factor
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    ABSTRACT: This study aimed to investigate the effects of hypercholesterolemia on visual evoked potentials (VEPs) and sulfite additional effects. Rats were assigned as follows: control (C), sulfite (S), hypercholesterolemia (H), vitamin E (E), sulfite + vitamin E (SE), hypercholesterolemia + sulfite (HS), hypercholesterolemia + vitamin E (HE), and hypercholesterolemia + sulfite + vitamin E (HSE). Hypercholesterolemic diet led significant increase in plasma cholesterol levels of rats. Brain thiobarbituric acid reactive substances (TBARS) levels were significantly increased in S, E, SE, HE and HSE groups compared with C. TBARS levels were increased in HE and HSE groups as compared to HS group. Nitrite levels were decreased in S, SE, H, HS and HSE groups compared with C. Nitrite level was notably increased in the HE group compared with H group. Sulfite exposure prolonged N1 and P3 latencies of VEP in group S compared with C. Prolonged VEP latencies by sulfite were significantly decreased by vitamin E in SE group. Cholesterol rich diet increased VEP latencies in comparison with control latencies. Sulfite gave rise to an additional increase in P3 latency in HS group compared with H group. Vitamin E-treated animals had notably shortened latencies of VEP components in HE and HSE groups according to the H and HS groups, respectively.
    Toxicology mechanisms and methods 04/2011; 21(6):479-86. · 1.37 Impact Factor
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    ABSTRACT: This study aimed to investigate the effect of docosahexaenoic acid (DHA) on visual evoked potentials (VEPs) in a mice model of Parkinson's disease (PD). Mice model was created by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and DHA was given by gavage. Cyclooxygenase-2 (COX-2), caspase-3 activities, nuclear factor kappa-B (NF-κB) and prostaglandin E2 (PGE2) levels were determined in substantia nigra (SN) and retina. Cyclooxygenase-2 intensities were also determined immunohistochemically. The tyrosine hydroxylase (TH) immunolabelling was significantly decreased in MPTP group compared to control. Docosahexaenoic acid decreased dopaminergic neuron death in MPTP + DHA group when compared to MPTP group. Mice treated with MPTP showed motor deficits as compared to control. Significant improvement was observed in MPTP + DHA group when compared to MPTP group. Treatment with MPTP significantly increased the activity of COX-2 and total COX in SN when compared to the control group. Docosahexaenoic acid caused a significant decrease in total COX and COX-2 activity in SN of mice given MPTP. Cyclooxygenase-2 showed strong immunostaining in MPTP group when compared to other groups in SN. Levels of PGE2 increased in MPTP group when compared to control in SN. Docosahexaenoic acid treatment in MPTP group reduced PGE2 in SN. Nuclear factor kappa-B levels were found to be decreased in SN of MPTP group. The mean latencies of P1, N1, P2, N2, P3, N3, P4, N4, and P5 VEP components were significantly prolonged in MPTP group when compared to control. In MPTP + DHA group, the mean latencies of all components except P5 returned to control values. Current data shows that DHA treatment improves prolonged VEPs latencies and locomotor activity.
    Neurotoxicity Research 01/2011; 20(3):250-62. · 2.87 Impact Factor
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    ABSTRACT: Times Cited: 0
    01/2011; 28:132-141.
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    ABSTRACT: Parkinson's disease (PD) is the second most common neurodegenerative disorder marked by cell death in the Substantia nigra (SN). Docosahexaenoic acid (DHA) is the major polyunsaturated fatty acid (PUFA) in the phospholipid fraction of the brain and is required for normal cellular function. Glial cell line derived neurotrophic factor (GDNF) and neurturin (NTN) are very potent trophic factors for PD. The aim of the study was to evaluate the neuroprotective effects of GDNF and NTN by investigating their immunostaining levels after administration of DHA in a model of PD. For this reason we hypothesized that DHA administration of PD might alter GDNF, NTN expression in SN. MPTP neurotoxin that induces dopaminergic neurodegeneration was used to create the experimental Parkinsonism model. Rats were divided into; control, DHA-treated (DHA), MPTP-induced (MPTP), MPTP-induced+DHA-treated (MPTP+DHA) groups. Dopaminergic neuron numbers were clearly decreased in MPTP, but showed an increase in MPTP+DHA group. As a result of this, DHA administration protected dopaminergic neurons as shown by tyrosine hydroxylase immunohistochemistry. In the MPTP+DHA group, GDNF, NTN immunoreactions in dopaminergic neurons were higher than that of the MPTP group. In conclusion, the characterization of GDNF and NTN will certainly help elucidate the mechanism of DHA action, and lead to better strategies for the use of DHA to treat neurodegenerative diseases.
    Folia Histochemica et Cytobiologica 11/2010; 48(3):434-41. · 1.10 Impact Factor
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    ABSTRACT: The purpose of this study was to investigate the effects of hypercholesterolemia and sulphite on active avoidance learning. Male Wistar rats were divided into eight groups as follows: Control (C), Sulphite (S), Vitamin E (E), Sulphite + Vitamin E (SE), Hypercholesterolemia (H), Hypercholesterolemia + Sulphite (HS), Hypercholesterolemia + Vitamin E (HE), and Hypercholesterolemia + Sulphite + Vitamin E (HSE). At the end of the experimental period, the serum cholesterol level (mean ± SD) was significantly higher in H group (111.5 ± 11.11 mg dL(-1) ) as compared to C group (63.5 ± 4.9 mg dL(-1) ). Levels of thiobarbituric acid reactive substances (TBARS) were increased in HS group as compared to C, H, and S groups. Vitamin E reduced TBARS levels in HSE group compared with HS group. Active avoidance results indicated that hypercholesterolemia was associated with learning impairment. Our data clearly revealed that the combination of hypercholesterolemia and sulphite results in exaggerated impairment of active avoidance. Vitamin E improved active avoidance in HSE group compared with HS group. Therefore, the synergistic effect of hypercholesterolemia and sulphite may be associated with a considerable health risk.
    Environmental Toxicology 09/2010; 27(8):453-60. · 2.71 Impact Factor
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    ABSTRACT: The aim of this study was to clarify the dose-dependent effect of sulfite (SO₃²⁻) ingestion on brain and retina by means of electrophysiological and biochemical parameters. Fifty two male Wistar rats, aged 3 months, were randomized into four experimental groups of 13 rats as follows; control (C), sulfite treated groups (S(1); 10 mg/kg/day, S₂; 100mg/kg/day, S₃; 260 mg/kg/day). Control rats were administered distilled water, while the other three groups were given sodium metabisulfite (Na₂S₂O₅) of amounts mentioned above, via gavage for a period of 35 days. All components of visual evoked potential (VEP) were prolonged in S₂ and S₃ groups compared with S₁ and C groups. Plasma-S-sulfonate levels, which are an indicator of sulfur dioxide (SO₂) exposure, were increased in Na₂S₂O₅ treated groups in a dose-dependent manner. Furthermore, the significant increments in thiobarbituric acid reactive substances (TBARS) and 4-hydroxy-2-nonenal (4-HNE) levels occurred with increasing intake of Na₂S₂O₅. Though not significant, glutathione (GSH) and oxidized glutathione (GSSG) levels were observed to decrease with increasing doses of Na₂S₂O₅. In conclusion, Na₂S₂O₅ treatment in rats caused a dose-dependent increase in lipid peroxidation and all VEP latencies. The data indicate that lipid peroxidation could play an important role in sulfite toxicity.
    Neurotoxicology and Teratology 09/2010; 33(2):244-54. · 3.18 Impact Factor
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    ABSTRACT: Growing data report memory and other cognitive problems among individuals with diabetes mellitus. Nitric oxide may play a key role in many physiological and pathological situations. The aim was to investigate the role of NO in diabetes-induced changes in learning and lipid peroxidation. Six groups of 10 rats each were formed: control (C), diabetic (D), control+L-arginine (CA), diabetic+L-arginine (DA), control+L-NAME (CN), and diabetic+L-NAME (DN) groups. Experimental diabetes mellitus was induced by injection of streptozotocin (60 mg/kg body weight). 160 mg/kg/day L-arginine or 10 mg/kg/day L-NAME were injected intraperitoneally to the relevant groups for eight weeks. Active avoidance behavior was studied in the middle of the eighth week using an automated shuttle box. Brain and hippocampal nitrite levels were measured by a fluorometric method. TBARS levels were measured fluorometrically using 1,1,3,3-tetramethoxypropane as a standard. The active avoidance training indicated that diabetes was associated with learning impairment. Administration of L-NAME and L-arginine significantly impaired active avoidance performance compared with the control group. They also decreased glucose level in group DA compared with the diabetic group. Brain nitrite level was significantly different in the diabetic group; hippocampus nitrite level tended to be lower in the L-NAME groups than the diabetic and control groups, although L-arginine increased hippocampal and brain nitrite values in the CA group compared with control groups. Brain and hippocampal TBARS levels were significantly higher in diabetic than in control rats. Imbalance related to nitric oxide production may contribute to cognitive dysfunction in diabetes mellitus.
    Medical science monitor: international medical journal of experimental and clinical research 03/2009; 15(3):BR88-93. · 1.22 Impact Factor
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    ABSTRACT: This study investigated the effect of heme oxygenase (HO) inhibition on visual evoked potentials (VEPs). HO catalyzes the oxidative degradation of heme. Products of HO reaction are biliverdin, ferrous iron, and carbon monoxide (CO). CO is a signal molecule and is an endogenous modulator in the soluble guanylate cyclase/cyclic guanosine monophosphate signaling pathway. Rats were treated with HO inhibitors tin protoporphyrin IX (SnPP IX) or zinc protoporphyrin IX (ZnPP IX) or HO inducer sodium arsenite (Na-arsenite). Soluble guanylate cyclase is inhibited by 1H-[1,2,3]oxydiazolo[4,3-a]quinoxalin-1-one (ODQ) and induced by 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1). VEPs were recorded under mild ether anesthesia with the help of stainless steel subdermal electrodes and a photic stimulator. SnPP IX, ODQ or SnPP IX + YC-1 injections significantly prolonged latencies of P3; however, Na-arsenite shortened latency of P3. It has been shown that HO affects VEPs.
    The International journal of neuroscience 01/2009; 119(9):1384-98. · 0.86 Impact Factor
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    ABSTRACT: ISI Document Delivery No.: 434MY
    Med. Sci. Monitor. 01/2009; 15:BR88-BR93.
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    ABSTRACT: This study aimed to investigate the effect of alpha-lipoic acid (LA) administration on sulfite-induced alterations in visual evoked potentials (VEPs). Fifty two male albino Wistar rats were randomized into four experimental groups as follows; control (C), LA treated (L), sodium metabisulfite (Na(2)S(2)O(5)) treated (S), Na(2)S(2)O(5)+LA treated (SL). Na(2)S(2)O(5) (260 mg/kg/day) and LA (100 mg/kg/day) were given by intragastric intubation for 5 weeks. The latencies of VEP components were significantly prolonged in the S group and returned to control levels following LA administration. Thiobarbituric acid reactive substances (TBARS) levels in the S group were significantly higher than those detected in controls. LA significantly decreased brain and retina TBARS levels in the SL group compared with the S group. Sulfite caused a significant decrease in retina and brain glutathione peroxidase (GPx) activities which was restored to control levels via LA administration. Brain glutathione (GSH):glutathione disulfide (GSSG) ratio was significantly increased in rats jointly treated with sulfite and LA compared to rats treated with sulfite alone. Though not significant, a similar increase in GSH:GSSG ratio was also observed in the retina of SL group. This study showed that LA is protective against sulfite-induced VEP alterations and oxidative stress in the brain and retina.
    Neurotoxicology and Teratology 09/2008; 31(1):34-9. · 3.18 Impact Factor

Publication Stats

580 Citations
165.64 Total Impact Points

Institutions

  • 1991–2014
    • Akdeniz University
      • • Department of Physiology
      • • Faculty of Medicine
      • • Department of Histology and Embryology
      • • Department of Ophthalmology
      Satalia, Antalya, Turkey
  • 2006–2009
    • Pamukkale University
      • Department of Phsiology
      Denisli, Denizli, Turkey