Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the mutual interaction between physical exercise and antioxidant systems in rats, we selected swimming as a model for exercise performance. Swimming belongs to the natural behavior of a rat, which under proper experimental conditions, primarily involves physical exercise with little emotional arousal. Therefore, we developed a swimming basin in which the intensity of exercise was manipulated by swimming speed and swimming duration. A laser beam interruption system enables recording of swimming patterns. For comparison we also used the basin to induce emotional arousal. Hereto the basin was transformed into a maze, in which unexpected blockade of a learned swimming route induced a panic-like emotional reaction. The antioxidant enzyme superoxide dismutase decreased in rat plasma after emotional arousal, not after physical exercise. Depletion of the antioxidant glutathione in the liver by diethyl maleate led to decrease of swimming performance. Noradrenaline but not adrenaline plasma levels increased in response to physical exercise. After emotional arousal the ratio noradrenaline/adrenaline did not change. In contrast, lactate only increased in response to emotional arousal. Plasma levels of glucose increased after both stress situations. Beta-adrenoceptor function, determined in the heart and in erythrocytes, only changed after physical exercise. The sensitivity to the beta-agonist (-)isoprenaline in the right atrium decreased and a downregulation of the beta-adrenoceptor density was observed in the erythrocyte.
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PMID:Control of physical exercise of rats in a swimming basin. 844 89

1. Oxidative mechanisms have been implicated in neonatal cardiomyocyte hypertrophy. We and others have shown that a HMG-CoA reductase inhibitor preserves endogenous antioxidant enzyme activity and inhibits cardiac hypertrophy in vivo. We therefore have examined whether noradrenaline (NA) induces the generation of reactive oxygen species (ROS) during its induction of neonatal cardiomyocyte hypertrophy and whether simvastatin, a HMG-CoA reductase inhibitor, attenuates ROS production and thus NA-induced hypertrophy of cardiomyocytes. 2. NA increased the intracellular ROS levels in a concentration-dependent manner. This increase of ROS was significantly inhibited by simvastatin and catalase. Prazosin partially suppressed NA-induced increase of ROS and beating, while preincubation with both prazosin and propranolol completely abolished NA-evoked increase of ROS and beating. Simvastatin did not affect NA-induced increase of beating. 3. The NA-induced increase of protein content was partially suppressed by prazosin and completely abolished by preincubation with both prazosin and propranolol. Simvastatin inhibited the increase of NA-induced increase of RNA content and [(3)H]-leucine incorporation in a concentration-dependent manner. Mevalonic acid (MVA) reversed the inhibition of NA-induced RNA and protein increase by simvastatin. Catalase also inhibited the NA-induced increase of RNA and protein. 4. We conclude that the inhibitory effects of simvastatin on myocyte hypertrophy were associated with its antioxidant effects and inhibition of MVA-metabolism pathway in neonatal rat cardiomyocytes. NA-induced increases of intracellular ROS and cardiomyocyte hypertrophy requires both alpha and beta adrenoceptors activation in neonatal rat cardiomyocytes. The increases of ROS induced by NA is required for hypertrophy.
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PMID:Simvastatin inhibits noradrenaline-induced hypertrophy of cultured neonatal rat cardiomyocytes. 1115 73

The occurrence and irreversibility of tardive dyskinesia (TD), a motor disorder of the orofacial region, resulting from chronic neuroleptic treatment has been considered a major clinical issue in the treatment of schizophrenia. The molecular mechanism underlying the pathophysiology of TD is not completely known. Several animal studies have demonstrated an enhancement of oxidative damage and increased glutamatergic transmission after chronic administration of neuroleptics. The present study investigated the effect of rutin, an antioxidant in haloperidol-induced orofacial dyskinesia by using different behavioural (orofacial dyskinetic movements, stereotypic rearing, locomotor activity, percent retention), biochemical [lipid peroxidation, reduced glutathione levels, antioxidant enzyme levels (SOD and catalase)] and neurochemical (neurotransmitter levels) parameters. Chronic administration of haloperidol (1 mg/kg i.p. for 21 days) significantly increased vacuous chewing movements, tongue protrusions and facial jerking in rats, which were significantly inhibited by rutin. Chronic administration of haloperidol also resulted in dopamine receptor sensitivity as evident by a well-shaped response (initial decrease followed by increase) in locomotor activity and stereotypic rearing and also decreased percent retention time on elevated plus maze paradigm. Pretreatment with rutin reversed these behavioural changes. Besides, haloperidol also induced oxidative damage in all regions of brain which was prevented by rutin, especially in the subcortical region containing striatum. Although turnover of dopamine and noradrenaline decreased in both cortical and subcortical regions after chronic administration of haloperidol, it was significantly reversed by high-dose rutin treatment. The findings of the present study suggested the involvement of free radicals in the development of neuroleptic-induced orofacial dyskinesia, a putative model of TD, and rutin as a possible therapeutic option to treat this hyperkinetic movement disorder.
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PMID:Protective effect of rutin, a polyphenolic flavonoid against haloperidol-induced orofacial dyskinesia and associated behavioural, biochemical and neurochemical changes. 1786 5

The status of nitric oxide (NO) in spontaneously hypertensive rats (SHR) is unclear and its bioavailability may be affected by imbalance with reactive oxygen species. We studied cardiovascular effects of an NO donor, pentaerythrityl tetranitrate (PETN) in SHR. We used Wistar rats, SHR and SHR treated with PETN (200 mg/kg/day). After six weeks, myocardium and aorta from each group were taken for biochemical and iliac artery for functional and morphological study. Long-term administration of PETN to SHR increased cGMP level in platelets and did not affect blood pressure. In myocardium, the therapy resulted in a decrease in cardiac hypertrophy and MDA level, and the increased antioxidant enzyme activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx). In aorta, PETN decreased the NO-synthase activity and had no affect on the enzyme activities of SOD and GPx or on MDA level. In the iliac artery, the endothelium-dependent relaxation to acetylcholine was slightly improved and the maximum vasoconstriction to noradrenaline was decreased. Wall thickness, cross-sectional area, inner diameter, and wall thickness/ inner diameter measured after perfusion fixation (120 mmHg) were not affected. The small effect of PETN on cardiovascular system suggests that NO deficiency is probably not the main cause of pathological alterations in SHR.
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PMID:The effect of an NO donor, pentaerythrityl tetranitrate, on biochemical, functional, and morphological attributes of cardiovascular system of spontaneously hypertensive rats. 1939 Jan 41

The aim of the present study was to explore the effects of continuous and intermittent exercise on the thoracic aortic vasoreactivity and free radical metabolism in rats fed with a high-fat diet (HD). Sprague-Dawley (SD) rats were randomly divided into four groups (n=8, each group): Conventional diet (CD), HD, HD with continuous exercise (HCE) and HD with intermittent exercise (HIE). HCE rats swam once/day for 90 min; HIE rats performed swimming exercises 3 times/day, 30 min each time with an interval of 4 h. In these two groups, the exercise was conducted 5 days a week for 8 weeks. Rats in the CD and HD groups were fed without swimming training. At the end of the exercise, all the rats were sacrificed and the blood, thoracic aorta and myocardium were collected immediately. The thoracic aortic vasoreactivity, the plasma total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), superoxide dismutase (SOD), malondialdehyde (MDA) and vascular endothelial nitric oxide synthase (eNOS) gene expression were measured. Compared to the control group, in the HD group the enhanced contractile response of the thoracic aortic rings to noradrenaline (NA) was observed (P<0.01). The levels of TC and LDL (P<0.01) were also increased in serum while the HDL level was reduced without statistical significance. In addition, the MDA content was upregulated in the myocardium, but the SOD level decreased (P<0.01). Furthermore, the expression of vascular eNOS mRNA was reduced (P<0.01). However, following the exercise the contraction of the thoracic aorta vascular rings to NA was reduced in the HCE and HIE groups (P<0.01), and the decreased contractile response was more evident in the HIE group compared to the HCE group (P<0.01). Additionally, in the HCE group the level of TG (P<0.01) was decreased, while the HDL (P<0.01) level was increased. Although the reduction of the TC and LDL level was also observed there was no significant difference compared to the HD group. In the HIE group, the TG, TC and LDL were downregulated while the HDL was enhanced (P<0.01). The TC and LDL levels were decreased more than those of the HCE group; however, there was no significant difference in the TG and HDL levels between these two groups; additionally, in these two exercise groups, the MDA level was decreased in the myocardium (P<0.01) while the SOD level was increased (P<0.01). Furthermore, the expression of eNOS was upregulated (P<0.01), but the increase was much more in the HIE group than that in the HCE group. In conclusion, exercise may attenuate the aggravated contraction induced by NA and improve the activity of the thoracic aorta in obese rats, which may be associated with enhanced antioxidant enzyme activity and reduced free radical generating. Additionally, intermittent exercise is better than the continuous exercise in improving the thoracic aorta vasoreactivity.
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PMID:Improvement of thoracic aortic vasoreactivity by continuous and intermittent exercise in high-fat diet-induced obese rats. 2617 Nov 60

The aim of present work is to assess the effects of bradykinin (Br) or noradrenaline (Nor) preconditioning to the levels of antioxidant enzymes: superoxide dismutase (SOD), copper, zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD) and catalase in ischemia/reperfusion (I/R) model in the rabbit spinal cord white matter as well as effect on glial fibrillary acidic protein (GFAP) and ubiquitin immunoreaction in glial cells. Rabbits were preconditioned by intraperitoneal single dose of Br or Nor 48 h prior to 20 min of ischemia followed by 24 or 48 h of reperfusion. White matter of L3-L6 spinal cord segments was used for comparison of antioxidant enzyme levels in sham control, ischemic groups and four preconditioned groups. The total SOD level in the Br or Nor preconditioned groups after 48 h of reperfusion was increased vs Br or Nor preconditioned groups after 24 h of reperfusion. The comparison among the ischemic group vs Br preconditioned (P<0.05), and Nor preconditioned (P<0.001) groups after 48 h of reperfusion, showed statistically significant decrease of Mn-SOD activity. Tissue catalase level activity was significantly decreased in the Br preconditioned group after 48 h of reperfusion (P<0.05) and Nor preconditioned groups after 24 h of reperfusion (P<0.001) and also after 48 h of reperfusion (P<0.001), in comparison to ischemic group after 48 h of reperfusion. Significantly decreased tissue catalase activity (P<0.05) in both Nor preconditioned groups after 24 or 48 h of reperfusion was measured vs Br preconditioned group after 48 h of reperfusion. According to our results, in the white matter, activation of stress proteins in glial cells, as well as antioxidant enzymes levels, were influenced by pharmacological preconditioning followed by 20 min of ischemia and 24 or 48 h of reperfusion. These changes contribute to ischemic tolerance acquisition and tissue protection from oxidative stress during reperfusion period.
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PMID:Bradykinin and noradrenaline preconditioning influences level of antioxidant enzymes SOD, CuZn-SOD, Mn-SOD and catalase in the white matter of spinal cord in rabbits after ischemia/reperfusion. 3163 45