Oktay Hasan Ozturk

High plasma nesfatin-1 level in patients with major depressive disorder

AIM In the present study, our aim was to determine the changes in the plasma concentrations of a recently discovered peptide hormone nesfatin-1 in patients with major depressive disorder and then to make a comparison with the control group. METHOD Subjects in the patient group were randomly selected from Mustafa Kemal University, Medical School, Research and Training Hospital, Psychiatry Department, Outpatient Clinic and subjects in the control group were selected from healthy volunteers. Healthy control subjects were matched in terms of weight and body mass index. Hamilton Depression Rating Scale (HAM-D) was applied to both groups. ELISA method was used for measurement of plasma nesfatin-1 levels. RESULTS The average nesfatin-1 level was statistically higher in patients with major depressive disorder than in the control group (p<0.001). A positive correlation was observed between plasma nesfatin-1 levels and HAM-D scores both in the patient group (r=0.59, p<0.001) and in the control group (r=0.58, p<0.001). CONCLUSION Our findings suggest a possible relationship between major depressive disorder and high plasma nesfatin-1 level.

Prognostic Significance of Neutrophil Gelatinase–Associated Lipocalin in ST-Segment Elevation Myocardial Infarction

Objectives This study investigated the prognostic value of neutrophil gelatinase–associated lipocalin (NGAL) in patients with ST-segment elevation myocardial infarction (STEMI). Background Neutrophil gelatinase–associated lipocalin is a promising biomarker for acute kidney injury. Recently, it was concluded that NGAL may be used beyond the boundaries of renal physiopathology. It was found to be an important factor indirectly contributing to the inflammatory processes. Little is known regarding its predictive role in STEMI. Methods One hundred six consecutive patients who underwent percutaneous coronary intervention (PCI) for STEMI and control group consisted of age- and sex-matched 60 consecutive patients with chest pain admitted to the hospital for elective PCI. According to median NGAL level, patients were classified into high- and low-NGAL groups. Results Neutrophil gelatinase–associated lipocalin levels were higher in patients with STEMI compared to the elective PCI group subjects. Inhospital and 1-year mortality rates were found to be significantly greater in patients with high NGAL. In addition, inhospital and 1-year major adverse cardiovascular event rates were significantly greater in the high-NGAL group, compared to the low NGAL group. High NGAL level on admission was a significant predictor for long-term mortality and major adverse cardiovascular events. The receiver operating characteristics curve analysis further illustrated that NGAL level on admission is a strong indicator of mortality, with an area under the curve of 0.76 (95% confidence interval, 0.62–0.89). Conclusions High NGAL levels may be associated with poor prognosis after PCI in patients with STEMI. However, further studies with larger numbers of patients and longer follow-up are required to evaluate the usefulness of plasma NGAL level for predicting prognosis of STEMI.

Frequency of MEFV gene mutations in Hatay province, Mediterranean region of Turkey and report of a novel missense mutation (I247V)

In the present study, 1000 patients with clinical suspicion of FMF were retrospectively reviewed to determine the spectrum of MEFV gene mutations by using DNA sequence analysis between September, 2008 and April, 2012. Sixteen different mutations and 55 different genotypes were detected in 618 of 1000 patients. Among 16 different mutations, R202Q (21.35%) was the most frequently observed mutation; followed by E148Q (8.85%), M694V (7.95%), M680I (2.40%), V726A (1.85%), M694I (0.95%), A744S (0.80%), R761H (0.55%), P283L (0.35%), K695R (0.20%), E230K (0.15%), L110P (0.10%), I247V (0.05%), G196W (0.05%) and G304R (0.05%). In the present study, a novel missense mutation (I247V) and a silent variant (G150G) were identified in the MEFV gene. On the other hand, P238L, G632A and G304R mutations are the first cases reported from Turkey. Our results indicated that MEFV mutations are highly heterogeneous in our study population as in other regions of Turkey and mutation screening techniques such as PCR-RFLP, amplification refractory mutation system or reverse hybridization do not adequately detect uncommon or novel mutations. Therefore, it was proven that sequence analysis of the MEFV gene could be useful for detection of rare or unknown mutations.

Beneficial effect of erdosteine on methotrexate-induced testicular toxicity in mice.

Methotrexate is used to treat certain types of cancer of the breast, skin, head and neck, or lung. Methotrexate can cause serious or life-threatening side effects on liver, lungs, kidneys, and immune system. Methotrexate chemotherapy causes testicular damage in humans. The aim of this study was to investigate the possible protective role of erdosteine on testicular toxicity of methotrexate in mice. Twenty-six male mice were divided into four groups as follows: group 1, control; group 2, erdosteine-treated; group 3, methotrexate-treated; and group 4, methotrexate + erdosteine treated. On the first day of experiment, a single dose of methotrexate was intraperitoneally administered to groups 3 and 4, although a daily single dose of erdosteine was orally administered to group 2 and 4 for 7 days. At the end of the experiment, the testes of the animals were removed and weighed. The levels of total antioxidant capacity and total oxidative stress, and myeloperoxidase activity in the methotrexate group were higher than the control group (p<0.05). Lipid peroxidation levels were not changed in methotrexate group compared with control group. In conclusion, erdosteine could effectively protect the testes in methotrexate-induced toxicity.

Direct and indirect effects of kisspeptin on liver oxidant and antioxidant systems in young male rats

Kisspeptin is a recently discovered hypothalamic peptide which plays an important role in the central control of reproductive functions. We have investigated direct and indirect effects of kisspeptin on the liver oxidative stress in young male rats. Twenty‐four rats were divided into four groups (n = 6/group). First group served as control and received saline. Kisspeptin‐10 was administered to the animals in the second group (20 nmol/rat/day), for a period of 7 days. Rats were given only one dose gosereline (0.9 mg/rat), a GnRH agonist in the third group. The last group received kisspeptin‐10 with gosereline. The activities of catalase, superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (AD) and level of malondialdehyde were studied in liver tissue. Serum samples were separated for total antioxidant capacity (TAC), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, blood urea nitrogen (BUN), colesterol, high‐density lipoprotein (HDL) and triglyceride. Kisspeptin increased the activities of SOD and catalase (p < 0.05). When compared to the control group, the levels of malondialdehyde, TOS and AST were lower, but levels of BUN, cholesterole, HDL and AD were higher in the other three groups (p < 0.05). In conclusion, our findings suggest that kisspeptin may have antioxidant and thus protective effects on the liver tissue. Copyright

Protective Effects of Edaravone on Experimental Spinal Cord Injury in Rats

Background: Spinal cord injury (SCI) is a leading cause of morbidity and mortality among youth and adults. Secondary injury mechanisms within the spinal cord (SC) are well known to cause deterioration after an acute impact. Free radical scavengers are among the most studied agents in animal models of SCI. Edaravone is a scavenger of hydroxyl radicals. Methods: We aimed to measure and compare the effects of both methylprednisolone and edaravone on tissue and on serum concentrations of nitric oxide (NO), malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and tissue total antioxidant capacity (TAC) in rats with SCI. SCI was induced in four groups of Wistar albino rats by a weight-drop method. The neurological function of the rats was periodically tested. At the end of the experiment, blood samples were collected, and SC tissue samples were harvested for biochemical evaluation. Results: The tissue level of NO was decreased in the edaravone-treated group compared with the no-treatment group (p < 0.05). The tissue levels of SOD and GSH-Px were higher in the edaravone-treated group than in the no-treatment group (p < 0.05). The serum levels of NO were lower in the edaravone-treated and methylprednisolone-treated groups than in the no-treatment group (p < 0.05). The serum levels of SOD in the edaravone-treated group did not differ from those of any other group. The serum levels of MDA in the edaravone-treated and no-treatment groups were higher than in the two other groups (p < 0.05). Tissue levels of MDA in the edaravone-treated group were lower than in the no-treatment group (p < 0.05). Tissue levels of TAC in the edaravone-treated group were higher than in the no-treatment and methylprednisolone-treated groups (p < 0.05). The neurological outcome scores of the animals in treatment groups did not depict any statistically significant improvement in motor functions. However, edaravone seemed to prevent further worsening of the immediate post-SCI neurological status. Conclusion: Our biochemical analyses indicate that edaravone is capable of blunting the increased oxidative stress that follows SCI. We show, for the first time, that edaravone enhances the TAC in SC tissue. This beneficial effect of edaravone on antioxidant status may act to minimize the secondary neurological damage that occurs during the acute phase after SCI.

Serum adiponectin and resistin levels in patients with obsessive compulsive disorder

We aimed to investigate the changes in serum adiponectin and resistin levels in patients with obsessive compulsive disorder and control groups. The serum adiponectin and resistin levels of 29 patients (16 females, 13 males) with obsessive compulsive disorder and weight, age and sex-matched 31 healthy controls (17 females, 14 males) were determined. Yale-Brown Obsessive Compulsive Scale (Y-BOCS) was applied to all groups. ELISA method was used to measure adiponectin and resistin levels. The mean adiponectin level was 11.92±2.04 ng/ml and resistin level was 13.23±2.78 ng/ml in obsessive compulsive disorder group, while it was 18.81±5.24 ng/ml and 8.17±2.53 ng/ml in control group. Changes in plasma adiponectin and resistin levels in obsessive compulsive disorder may have implications about possible cardiovascular and metabolic abnormalities seen in obsessive compulsive patients.

The protective effects of omega-3 fatty acid against toluene-induced neurotoxicity in prefrontal cortex of rats.

Objective: Toluene is used as an organic solvent, and it has neurotoxic effects. Omega-3 is an essential fatty acid required for brain development. The aim of this study was to investigate the protective effects of omega-3 fatty acid against toluene-induced neurotoxicity in prefrontal cortex of rats. Materials and methods: A total of 21 male Wistar rats were divided into three groups with seven rats in each group. Rats in group I were the controls. Toluene was intraperitoneally injected into the rats of group II with a dose of 0.5 ml/kg. Rats in group III received omega-3 fatty acid with a dose of 0.4 g/kg/day while exposed to toluene. After 14 days, all the rats were killed by decapitation. Enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the level of malondialdehyde (MDA) were spectrophotometrically studied in the prefrontal cortex of rats. Results: Enzymatic activities of SOD and GSH-Px were decreased, and MDA levels were significantly increased in rats treated with toluene compared with the controls. However, the increased SOD and decreased GSH-Px enzymatic activities and MDA levels were detected in the rats administered with omega-3 fatty acid while exposed to toluene. Conclusion: The results of this experimental study indicate that omega-3 fatty acid treatment can prevent toluene-induced neuronal damage in the prefrontal cortex of rats.

Effect of Thymoquinone on Oxidative Stress in Escherichia coli–Induced Pyelonephritis in Rats

BACKGROUND Recurrent urinary tract infections are important in children and adults with diabetes mellitus and/or incontinence due to risk of pyelonephritis (PYN) and renal damage. There is a positive correlation released free radicals during PYN and renal damage. Experimental studies showed that antioxidant agents improve renal damage when used immediately after bacterial inoculation. OBJECTIVE The aim of the present study was to evaluate whether treatment by thymoquinone (TQ) before or during Escherichia coli inoculation prevents oxidative damage in acute pyelonephritis (PYN) in an ascending obstructive rat model. METHODS In this study, 42 Wistar rats were grouped as follows: control, PYN (24, 48, and 72 hours), and TQ-PYN (24, 48, and 72 hours). E. coli (1 ×10(9) colony forming units) was inoculated into the bladder via urethral catheterization in both the PYN and TQ groups. TQ injections were performed 24 hours before bacteria inoculation and repeated at 24-hour intervals during the indicated time at a dose of 10 mg/kg body weight intraperitoneally in TQ groups. RESULTS Superoxide dismutase activity was statistically lower in the TQ-PYN-48 and -72 groups than the PYN-48 and -72 groups (P < 0.001, P = 0.004, respectively). Catalase activity was significantly higher in PYN-24, -48, and -72 groups than the control group (P < 0.001). In addition, there was a significant difference between the TQ-PYN-24, -48, and -72 groups and PYN groups in terms of glutathione peroxidase activity (P < 0.001, P = 0.026, P = 0.046, respectively). When the TQ-PYN-72 group was compared with the PYN-72 group, malondialdehyde levels were significantly lower in the TQ-PYN-72 group than in the PYN-72 group (P = 0.033). A histologic examination also confirmed the protective effect of TQ. In statistical analysis of histopathologic findings, there were significant differences between the PYN-24 and TQ-PYN-24, PYN-48 and TQ-PYN-48, and PYN-72 and TQ-PYN-72 groups (P = 0.008, P < 0.001, P < 0.001, respectively). CONCLUSIONS The results indicate that TQ administration attenuated the oxidative damage that occurred in PYN and, therefore, could be used as a supportive agent to protect the kidneys from oxidative damage caused by PYN.

Effects of β-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats.

BACKGROUND NSAIDs have been found to induce gastrointestinal tract damage. Recently, it has been suggested that this might be mediated by lipid peroxidation. OBJECTIVE The aim of this study was to assess the potential protective effects of β-glucan against acetylsalicylic acid (ASA-induced gastric damage by means of its antioxidant capacity in an experimental rat model. METHODS Thirty-two male Wistar albino rats (200-250 g) were randomized into 4 groups consisting of 8 rats each. The β-glucan group received 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. The ASA group received saline once a day for 10 days and 300 mg/kg (20 mg/mL) ASA as a single dose, 4 hours before anesthesia. The ASA+β-glucan group was administered 50 mg/kg β-glucan once a day for 10 days and 30 minutes before anesthesia. Additionally, 300 mg/kg (20 mg/mL) ASA was administered as a single dose, 4 hours before anesthesia. The control group received saline once a day for 10 days and 30 minutes before anesthesia. All medications were administered by intragastric gavage. The stomach from each rat was dissected and divided into 2 parts for histologic and biochemical analysis. Gastric tissue malondialdehyde (MDA), nitric oxide (NO) levels, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were determined for oxidative parameter analysis. RESULTS The gastroprotective and antioxidant effects of β-glucan appeared to attenuate the ASA-induced gastric tissue damage. Compared with the control group, MDA and NO levels and CAT and GSH-Px activities were significantly increased in the stomachs of ASA-treated rats (MDA, 4.12 [0.44] to 13.41 [1.05] μmol/L; NO, 8.04 [7.25-9.10] vs 30.35 [22.34-37.95] μmol/g protein; CAT, 0.050 [0.004] to 0.083 [0.003] k/g protein; GSH-Px, 0.57 [0.42-0.66] to 1.55 [1.19-1.76] U/L; all, P < 0.001), whereas SOD activity was significantly decreased in the same group (291 [29] to 124 [6] U/mL; P < 0.001). In the ASA+β-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P < 0.001). CONCLUSION β-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.