16 research outputs found
N–(p–amylcinnamoyl) anthranilic acid attenuates remedial effects of memantine on memory deficits following intracerebroventricular streptozotocin administration in rats
Investigation of the association between ROCK1 gene Lys222Glu ve Arg1262Gln polymorphisms and breast cancer
THE BIDIRECTIONAL EFFECT OF CREATINE SUPPORTS THE MAINTENANCE OF OXIDANT-ANTIOXIDANT HOMEOSTASIS DURING EXERCISE
The importance of supplements used with exercise is increasing day by day. In this study, it was aimed to evaluate the effects of creatine monohydrate (CrM) supplementation with different intensities of exercise on oxidative stress through dynamic thiol disulfide homeostasis. Fourty two BALB/c mice were used and randomly divided into 6 groups; control (C), low-intensity exercise (LIE), high-intensity exercise (HIE), C+CrM (4% of daily diet), LIE+CrM, and HIE+CrM groups. Exercise groups were performed low-intensity (8m/min/30min/day) and high-intensity (24m/min/30min/day) exercise on a mouse treadmill for 8 weeks. At the end of the experimental period, the thiol disulfide homeostasis levels analyzed by using a new automated measurement technique. When the native thiol and total thiol values were examined the difference between the groups was statistically significant (respectively, p=0.029, p=0,035). Creatine intake with exercise decreased native thiol and total thiol levels. However, serum disulfide levels were lower in LIE+CrM compared to other study groups, but there was no statistically significant difference. It is thought that creatine supplementation with exercise reduces the thiol-disulfide homeostasis burden of the organism, and that after the depletion of creatine stores, the sustainability of oxidant-antioxidant homeostasis can be extended, thus prolonging the duration of antioxidant resistance.</jats:p
Protective effects of Y-27632 on acute dichlorvos poisoning in rats
Anticholinesterase poisoning is an important health problem in developing countries, and understanding of its underlying mechanisms is essential for the effective treatment. This study is designed to examine the effects of Y-27632, a selective Rho-kinase inhibitor, on organophosphate-induced cardiac toxicity and mortality in rats. Rats were randomly divided into 4 groups: control (corn oil), dichlorvos (30 mg/kg intraperitoneally), and 1- and 10-mg/kg Y-27632 + dichlorvos groups. After 6 hours of intraperitoneal injection, venous blood and cardiac samples were obtained, biochemical or immunohistochemical analyses were performed, and the intensity of muscle fasciculation was recorded. Serum cholinesterase activities were suppressed with dichlorvos, and these reductions were inhibited with Y-27632 pretreatment. Serum creatine kinase, creatine kinase-MB activities, and myoglobin and N-terminal probrain natriuretic peptide concentrations were not markedly affected with poisoning or Y-27632. Although serum nitric oxide concentrations did not change with dichlorvos, cardiac nitric oxide levels were markedly increased with Y-27632 pretreatment. Cardiac glutathione levels also increased with 1 mg/kg Y-27632. There was no staining for apoptosis, and immunohistochemical analyses of inducible nitric oxide synthase showed no change in cardiac tissue for all of the groups. Both doses of Y-27632 abolished mortality in rats with acute dichlorvos exposure (100% survival). These results show that administration of Rho-kinase inhibitor can produce protective effects against dichlorvos intoxication in rats. These findings may provide new possibilities for the treatment of organophosphate poisoning. © 2010 Elsevier Inc. All rights reserved
CYP gene expressions in obesity-associated metabolic syndrome
Purpose: The contribution of cytochrome P450 (CYP) gene expressions in metabolic syndrome (MetS) has not been elucidated, and was the aim of this study
Cardiac Effects of Magnesium Sulfate Pretreatment on Acute Dichlorvos-Induced Organophosphate Poisoning: An Experimental Study in Rats
Serum vitamin D, vitamin D binding protein levels and leukocyte vitamin D receptor gene expression in patients with ischaemic stroke
Objective: To investigate the possible contributions of serum 25-hydroxyvitamin D and vitamin D binding protein levels along with leukocyte vitamin D receptor gene expression in patients with ischaemic stroke
Cardiac effects of magnesium sulfate pretreatment on acute dichlorvos-induced organophosphate poisoning: An experimental study in rats
Although atropine and oximes are traditionally used in the management of organophosphate poisoning, investigations have been directed to finding additional therapeutic approaches. Thus, the aim of this study was to evaluate the cardiac effects of magnesium sulfate pretreatment on dichlorvos intoxication in rats. Rats were randomly divided into three groups as control, dichlorvos, and magnesium sulfate groups. After 6 h of dichlorvos or corn oil (as a vehicle) injection, venous blood samples were collected, and cardiac tissue samples were obtained. Biochemical analyses were performed to measure some parameters on serum and cardiac tissue. Immunohistochemical analyses of apoptosis and inducible nitric oxide (NO) synthase showed no change in cardiac tissue. Serum cholinesterase levels were markedly depressed with dichlorvos, and further suppressed markedly with magnesium sulfate pretreatment. Although we have demonstrated that serum NO levels in dichlorvos and magnesium sulfate groups were lower than the control group, cardiac tissue NO levels in magnesium sulfate group were higher than the other two groups. Mortality was not significantly affected with magnesium sulfate pretreatment. Uncertainty still persists on the right strategies for the treatment of organophosphate acute poisoning; however, it was concluded that our results do not suggest that magnesium sulfate therapy is beneficial in the management of acute dichlorvos-induced organophosphate poisoning, and also further studies are required. © Springer Science+Business Media, LLC 2009
Association between the 196G > A (VAL66 MET) and -1360C > T (C-270T) polymorphisms of the brain-derived neurotrophic factor gene and bipolar disorder
Backgrounds: Bipolar disorder is a severe psychiatric disease, characterized by recurrent manic and depressive episodes, and is believed to have a strong genetic component. Several data suggest that the brain-derived neurotrophic factor (BDNF) gene is a potential candidate gene for this affective disease. The aim of this study was to test a possible association between the BDNF gene polymorphisms and bipolar disorder in a Turkish population
