24 research outputs found

    Impaired Relaxation in Aorta from Streptozotocin-diabetic Rats: Effect of Aminoguanidine (AMNG) Treatment

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    Aim The effect of 8 weeks′ streptozotocin (STZ)- induced diabetes and aminoguanidine (AMNG), the inhibitor of advanced glycosylation reaction, treatment on arteriolar reactivity to vasoactive substances was investigated in vitro

    Propargylglycine aggravates liver damage in LPS-treated rats: Possible relation of nitrosative stress with the inhibition of H2S formation

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    Background: Hydrogen sulfide (H2S) is a naturally occurring gaseous transmitter, which may play important roles in normal physiology and disease. Here, we investigated the effect of endogenously formed H2S in the endotoxemic organ injury

    Nitrergic, glutamatergic and gabaergic systems in lithium toxicity

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    We examined the role of nitrergic, glutamatergic and gamma-aminobutyric acid (GABA)-ergic systems in the mechanism(s) underlying lithium induced acute toxicity. With this aim, lithium (18 mEq/kg, i.p.) intoxicated rats were observed for 3 hr recording their clinical signs and death. Lithium exposure at the dose used produced central nervous system (CNS) depression. Pre-treatment of N-w-nitro-L-arginine methyl ester (L-NAME) a nonselective nitric oxide synthase inhibitor (10 mg/kg, i.p.), 7-nitroindazole (7-NI) a selective neuronal nitric oxide synthase inhibitor (25 mg/kg, i.p.), nitric oxide precursor L-arginine (1,000 mg/kg, i.p.) and MK-801 a noncompetitive antagonist of N-methyl-D-aspartic acid class of glutamate receptors (0.5 mg/kg, i.p.) all increased CNS depression and mortality in lithium group however, no change was seen in GABA receptor agonist GABA (1,000 mg/kg, i.p.) or D-arginine (1,000 mg/kg, i.p.) a biologically inactive enantiomer L-arginine pre-treated rats. Glutamic acid decarboxylase (GAD) enzyme activity was measured in hippocampus, cerebral cortex and cerebellum of the different groups of animals. GAD enzyme activity reduced in cerebral cortex but not altered in hippocampus or cerebellum by lithium as compared to the control (saline) group. We conclude that an interaction with nitrergic and glutamatergic systems may have a role in the acute toxicity of lithium in rats.The inhibition of glutamate metabolism may arise from this interaction and the involvement of GABA-ergic system should be further investigated in this toxicity

    High concentrations of asymmetric dimethylarginine are associated with ST-segment resolution failure after reperfusion for acute myocardial infarction

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    Background: Increased concentrations of asymmetric dimethylarginine (ADMA) have been detected in patients with cardiovascular risk factors. In addition, high baseline plasma concentrations of ADMA have been shown to be an independent predictor of adverse outcomes in various disorders. This study aimed to evaluate the impact of admission ADMA concentrations on microvascular flow after primary percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI)

    Serum levels of arginase I are associated with left ventricular function after myocardial infarction

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    Objectives: Upregulation of arginase redirects the arginine metabolism from nitric oxide (NO) synthesis to the formation of polyamine and proline, thus causing cardiac dysfunction. NO synthesis is also impaired by asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor. We aimed to evaluate the impact of arginase and ADMA levels on left ventricular function after myocardial infarction (MI)

    Dimethylarginines in patients with type 2 diabetes mellitus: Relation with the glycaemic control

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    We tested the relationship between plasma levels of dimethylarginines (ADMA and SDMA) and glycaemic control in 43 type 2 diabetic patients. Type 2 diabetics with poor glycaemic control (HbA1c > 6.5) had significantly lower SDMA and higher ADMA concentrations than those with well-controlled glycaemia (HbA1c < 6.5). (C) 2011 Elsevier Ireland Ltd. All rights reserved

    Effects of High Methionine Diet on Oxidative Stress in Serum, Apo-B Containing Lipoproteins, Heart, and Aorta in Rabbits

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    This study investigated in rabbits whether a high methionine (HM) diet influences oxidative stress parameters in serum, apo-B containing lipoproteins (LDL+VLDL), heart, and aorta. Rabbits received a normal commercial chow supplemented with 2% L-methionine (w/w) for 6 mo (approximately 1 g/kg body wt/day). Serum homocysteine (HCys), malondialdehyde (MDA), diene conjugate (DC), and cholesterol levels were found to be increased, but protein carbonyl (PC) and triglyceride levels remained unchanged in the HM group as compared to controls. Cholesterol, endogenous DC, and copper-induced MDA levels were significantly higher in the LDL+VLDL fraction of plasma lipoproteins in the HM group. MDA and DC levels were found to be increased in homogenates of heart and aorta in the HM group. The HM diet caused significant increases in cardiac glutathione peroxidase activity, but glutathione, vitamin E, and vitamin C levels and superoxide dismutase and glutathione transferase activities remained unchanged. There were no significant differences in the cholesterol levels and histopathological findings in the aortas of the control vs the HM group. This study demonstrates that a HM diet induces oxidative stress in serum, apo-B containing lipoproteins, heart, and aorta in rabbits

    Nitrergic, glutamatergic and gabaergic systems in lithium toxicity

    No full text
    We examined the role of nitrergic, glutamatergic and gamma-aminobutyric acid (GABA)-ergic systems in the mechanism(s) underlying lithium induced acute toxicity. With this aim, lithium (18 mEq/kg, i.p.) intoxicated rats were observed for 3 hr recording their clinical signs and death. Lithium exposure at the dose used produced central nervous system (CNS) depression. Pre-treatment of N-w-nitro-L-arginine methyl ester (L-NAME) a nonselective nitric oxide synthase inhibitor (10 mg/kg, i.p.), 7-nitroindazole (7-NI) a selective neuronal nitric oxide synthase inhibitor (25 mg/kg, i.p.), nitric oxide precursor L-arginine (1,000 mg/kg, i.p.) and MK-801 a noncompetitive antagonist of N-methyl-D-aspartic acid class of glutamate receptors (0.5 mg/kg, i.p.) all increased CNS depression and mortality in lithium group however, no change was seen in GABA receptor agonist GABA (1,000 mg/kg, i.p.) or D-arginine (1,000 mg/kg, i.p.) a biologically inactive enantiomer L-arginine pre-treated rats. Glutamic acid decarboxylase (GAD) enzyme activity was measured in hippocampus, cerebral cortex and cerebellum of the different groups of animals. GAD enzyme activity reduced in cerebral cortex but not altered in hippocampus or cerebellum by lithium as compared to the control (saline) group. We conclude that an interaction with nitrergic and glutamatergic systems may have a role in the acute toxicity of lithium in rats.The inhibition of glutamate metabolism may arise from this interaction and the involvement of GABA-ergic system should be further investigated in this toxicity

    Effect of post-polymerization heat-treatments on degree of conversion, leaching residual MMA and in vitro cytotoxicity of autopolymerizing acrylic repair resin

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    Objectives. This study evaluated the effect of post-polymerization heat-treatments on degree of conversion (DC), residual methyl methacrylate concentration (MMAr) and in vitro cytotoxicity of autopolymerizing acrylic repair resin
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