Nigar Yilmaz

Protective effects of thymoquinone on vancomycin-induced nephrotoxicity in rats

Aim: Oxidative stress has been implicated as a potential responsible mechanism in the pathogenesis of vancomycin (VCM)-induced renal toxicity. Therefore, we aimed to investigate the protective effect of thymoquinone (TQ) against VCM-induced nephrotoxicity by tissue oxidant/antioxidant parameters and histological changes in rats. Materials and methods: Wistar albino rats were randomly separated into four groups consisting of seven rats per group. The groups had normal saline (control group), VCM, VCM and TQ and TQ, respectively. VCM was injected intraperitoneally at a dose of 200 mg/kg and continued at 12-h intervals for 7 days. TQ was injected intraperitoneally at a dose of 10 mg/kg and continued at 24 h intervals for 8 days. Animals were killed and blood samples were analyzed for the levels of serum blood urea nitrogen (BUN) and creatinine (Cr). Kidney specimens were analyzed for levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as for histopathological changes. Results: We found that the levels of serum BUN, Cr and kidney tissue MDA were increased in the VCM group. Activities of SOD and GSH-Px in kidney tissue were decreased. TQ administration ameliorated significantly these changes. Conclusion: These results indicate that the TQ produces a protective mechanism against VCM-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

The protective effect of erythropoietin on renal injury induced by abdominal aortic-ischemia-reperfusion in rats.

BACKGROUND Renal injury induced by aortic ischemia-reperfusion (IR) is an important factor in the development of postoperative acute renal failure following abdominal aortic surgery. The purpose of this study is to examine the effect of erythropoietin on renal injury induced by aortic IR in rats. MATERIAL AND METHODS Twenty-four Wistar-Albino rats were randomized into 3 groups (8 per group). The control group underwent laparotomy and dissection of the infrarenal abdominal aorta without occlusion. The aortic IR group underwent clamping of the infrarenal abdominal aorta for 30 min followed by 60 min of reperfusion. The aortic IR + erythropoietin group underwent the same aortic IR periods and was pretreated with 1000 U/kg subcutaneous erythropoietin 5 min before ischemia. In rat kidney specimens, tissue levels of malondialdehyde (MDA), superoxide dismutase, catalase, and glutathione peroxidase were measured. Histological evaluation of the rat kidney tissues was also done. RESULTS Aortic IR significantly increased the levels of MDA and superoxide dismutase (P < 0.05 versus control). Erythropoietin significantly decreased the levels of MDA, superoxide dismutase, and catalase (P < 0.05 versus aortic IR). Histological evaluation showed that aortic IR significantly increased (P < 0.05 versus control), whereas erythropoietin significantly decreased (P < 0.05 versus aortic IR) the focal glomerular necrosis, dilation of Bowmans capsule, degeneration of tubular epithelium, necrosis in tubular epithelium, interstitial inflammatory infiltration, and congestion of blood vessels. CONCLUSIONS The results indicate that erythropoietin has protective effects on renal injury induced by aortic IR in rats.

Topiramate and vitamin e modulate antioxidant enzyme activities, nitric oxide and lipid peroxidation levels in pentylenetetrazol-induced nephrotoxicity in rats.

Previous studies have shown that generation of free radicals is increased following pentylenetetrazol kindling, due to increased cytosolic Ca2+ concentrations. Topiramate, a voltage-gated calcium channel inhibitor, has an evident effect in the treatment of childhood epilepsy; however, topiramate may cause nephrotoxicity. We investigated the effects of topiramate and vitamin E administration on pentylenetetrazol-induced nephrotoxicity in rats by evaluation of lipid peroxidation, nitric oxide, glutathione peroxidase, catalase and superoxide dismutase values. Forty male Wistar rats were randomly divided into five equal groups. Group 1 was used as control and group II received a single dose of pentylenetetrazol. Fifty and 100 mg/kg topiramate daily were intragastrically administered to rats in groups III and IV for 7 days, respectively. Intragastric 100 mg topiramate (daily for 7 days) and intraperitoneal vitamin E (150 mg/kg, daily for 3 days) combination were given to animals in group V before a single-dose pentylenetetrazol administration. Serum and kidney samples were taken after 3 hr of pentylenetetrazol administration. Pentylenetetrazol resulted in a significant increase in nitric oxide levels of serum and kidney, and lipid peroxidation levels of kidney although superoxide dismutase and catalase activities in the kidney was reduced by pentylenetetrazol administration. The lipid peroxidation levels in serum and kidneys and the nitric oxide levels in kidneys of groups III, IV and V were decreased by topiramate although the superoxide dismutase and catalase activities in the kidneys were increased. Lipid peroxidation and nitric oxide levels were reduced by the topiramate and vitamin E combination compared to only topiramate. Glutathione peroxidase activity was not affect by pentylenetetrazol, topiramate and vitamin E administrations. In conclusion, topiramate and vitamin E have protective effects on pentylenetetrazol-induced nephrotoxicity by inhibition of free radicals and by support of the antioxidant redox system.

Levels of lipid peroxidation, nitric oxide, and antioxidant vitamins in plasma of patients with fibromyalgia.

The etiology of fibromyalgia is not clearly understood. In recent years, a few studies have investigated the possible role of reactive oxygen species (ROS) in the etiology and pathogenesis of fibromyalgia. The aim of this study was to investigate plasma antioxidant vitamins, lipid peroxidation (LP), and nitric oxide (NO) levels in patients with fibromyalgia and controls. The study was performed on the blood plasma of 30 female patients and 30 age‐matched controls. After a fast of 12 h, blood samples were taken, and plasma samples were obtained for measurement of vitamins A, C, E, and β‐carotene concentrations and levels of LP and NO. Concentrations of vitamins A (p < 0.01) and E (p < 0.001) were significantly lower in patients with fibromyalgia than in controls, and LP levels were significantly (p < 0.05) higher in the plasma of the patients than in controls. Concentrations of vitamin C and β‐carotene and levels of NO did not change significantly. These results provide some evidence for a potential role of LP and fat‐soluble antioxidants in the patients with fibromyalgia. Copyright

Ghrelin and adiponectin levels in colostrum, cord blood and maternal serum

Background:  Ghrelin and adiponectin, which are considered to take part in the regulation of energy metabolism, have been found in breast milk and cord blood. The aims of this study were to determine ghrelin and adiponectin levels in colostrum, cord blood and maternal serum and to investigate the correlations between colostrum and cord blood levels of these peptides and the anthropometry of newborn infants and their mothers.

The Role of Arginine–Nitric Oxide Pathway in Patients with Alzheimer Disease

There is a reciprocal regulation of arginase and nitric oxide synthase in l-arginine-metabolizing pathways. There are various evidences of the role of nitric oxide in several neuropsychiatric disorders including Alzheimer’s disease. However, there is no study that has investigated the role of arginase as an important part of the arginine regulatory system affecting nitric oxide synthase activity in Alzheimer’s disease. This study aims to investigate arginase, manganese (a cofactor of arginase), and total nitrite levels (a metabolite of NO) and their relationship to the arginine–NO pathway in patients with Alzheimer’s disease. Arginase activities, Mn, and total nitrite levels were measured in plasma from 47 patients with Alzheimer’s disease and 43 healthy control subjects. Plasma arginase activities and manganese were found to be significantly lower and total nitrite level higher in patients with Alzheimer’s disease compared with controls. Our results suggest that the arginine–NO pathway is involved in the pathogenesis of Alzheimer’s disease.

Diazinon-induced brain toxicity and protection by vitamins E plus C

Diazinon (DI) is a widely used pesticide in agriculture, resulting in environmental deleterious effects on neural systems. The current study was performed to investigate the effects of treatment with vitamins E plus C on brain toxicity, which is possibly induced by DI. Twenty-one male rats were divided into three groups (n = 7/group) as follows: (1) control group (C); (2) DI-treated group (DI); (3) DI + vitamins E plus C-treated group (DI + Vit). In order to examine lipid peroxidation and antioxidant status in rats, the level of malondialdehyde (MDA), activities of two free radical scavanging enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) have been studied in brain of rat. The results showed that treatment with DI induced significant (p < 0.05) increases in the level of serum MDA in rat brain. The vitamins E plus C combination reduced lipid peroxidation in rat brain. The activity of SOD level was significantly higher in DI + Vit group, compared to the control group. GSH-Px, SOD and CAT values were not significantly different in the DI group than in control. Oxidative stress contributes to DI-induced brain toxicity. Our results suggested that vitamins E plus C combination may have a protective effect on DI-induced brain toxicity.

Vitamin D Concentrations are Decreased in Patients with Alopecia Areata

Vitamin D has been of increased interest in the role of maintaining immune system balance. Alopecia Areata (AA) is a T-cell mediated autoimmune disease which causes anagen-stage hair follicles. Low concentration of vitamin D may be a risk factor for AA. We aimed to determine vitamin D concentrations in patients with AA. 25-hydroxyvitamin D (25(OH)-D) concentrations and 1,25 dihydroxyvitamin D3 (1,25(OH)2D3) were determined from sera collected from patients with AA (n=42) and healthy controls (n=42). 25(OH)-D and 1,25(OH)2D3 concentrations were measured by ELISA method. The concentrations of both 25(OH)-D and 1,25(OH)2D3 were found to be significantly lower in patients with AA than control group (p<0.001 for each analysis). The results show that there is a significant difference between AA patients and normal subjects in terms of serum vitamin D concentrations. Therefore, it is suggested that vitamin D deficiency may have a role in the setting of AA.

Calorie restriction modulates hippocampal NMDA receptors in diet-induced obese rats

Calorie restriction (CR) has attracted increased interest since CR enhances lifespan and alters age-related decline in hippocampal-dependent cognitive functions. Obesity is associated with poor neurocognitive outcome including impaired hippocampal synaptic plasticity and cognitive abilities such as learning and memory. N-Methyl-d-aspartate receptors (NMDARs) are linked to hippocampal-dependent learning and memory, which may be stabilized by CR. In the present study, we aimed to establish the effects of CR on NMDARs in CA1 region of hippocampus in obese and non-obese rats. In addition, malondialdehyde (MDA) levels were determined as a marker for lipid peroxidation (LPO) in hippocampus. Four groups were constituted as control group (C, n = 9), obese group (OB, n = 10), obese calorie-restricted group (OCR, n = 9), and non-obese calorie-restricted group (NCR, n = 10). OCR and NCR were fed with a 60% CR diet for 10 weeks. After 10 weeks of CR, the MDA levels significantly decreased in the calorie-restricted groups. Obesity caused significant decreases in NR2A and NR2B subunit expressions in the hippocampus. The hippocampal NR2A and NR2B levels significantly increased in the OCR group compared with the OB group (P < 0.05). In contrast, the hippocampal NR2A and NR2B levels significantly decreased in the NCR group compared with the C group (P < 0.05). Oxidative stress can be prevented by CR, and these data may provide a molecular and cellular mechanism by which CR may regulate NMDAR-mediated response against obesity-induced changes in the hippocampus.

Oxidative stress markers in pregnant women who snore and fetal outcome: a case control study

Background. To determine the levels of oxidative stress markers in pregnant women who snore and compare with non‐snoring pregnant women. Fetal outcome of these 2 groups was also evaluated. Materials and methods. Prospective, case control study. Some 40 pregnant women who snored and 43 non‐snoring pregnant women were evaluated. The glutathione peroxidase (GSH‐Px), malondialdehyde (MDA) and myeloperoxidase (MPO) levels of the 2 groups were studied. Infant birthweight, Apgar scores, and other indicators of fetal outcome were obtained. Results. The mean level of GSH‐Px was significantly lower in the pregnant women who snored (p = 0.005), while the mean level of MDA was significantly higher in this group (p = 0.005). Levels of MPO were comparable between the groups (p > 0.05). The pregnant women who snored did not have infants with evidence of an increase in compromised outcome. Conclusion. Although the pregnant women who snored had high levels of MDA, they did not appear to be at increased risk for delivering infants with fetal compromise.