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

Since the chronically cyanotic myocardium appears to be more susceptible to reperfusion injury after cardiac operations than the noncyanotic myocardium, we studied the association between the preoperative arterial oxygen tension and the myocardial superoxide dismutase, catalase, and glutathione peroxidase activities. Fourteen patients with tetralogy of Fallot scheduled for elective operations had baseline arterial blood gas measurements done before operation. During the operation right ventricular biopsy specimens were taken for enzyme analysis immediately before cold blood cardioplegic arrest and 20 minutes after crossclamp removal. The tissue antioxidant enzyme activities of the patients with tetralogy of Fallot were compared with the myocardial results in 15 adults with stable angina pectoris having elective aorta-coronary artery bypass graft operations. Myocardial tissues removed from two patients with hypertrophic obstructive cardiomyopathy who had corrective operations were analyzed for antioxidant activities. There were no changes in myocardial antioxidant enzyme activities during the operation in the patients with tetralogy of Fallot and coronary artery bypass graft. The myocardial superoxide dismutase, catalase, and glutathione peroxidase activities correlated (0.82, 0.68, and 0.89, respectively) significantly (p values were less than 0.01, 0.05, and 0.01, respectively) with the preoperative arterial oxygen tensions in the patients with tetralogy of Fallot. The myocardial glutathione peroxidase activities were at least four times higher in the myocardium of patients with coronary artery bypass graft and hypertrophic obstructive cardiomyopathy than in that of those with tetralogy of Fallot. This study provides putative evidence that the myocardium of patients with tetralogy of Fallot is a risk of oxygen-derived free radical injury during and immediately after corrective cardiovascular operations.
J Thorac Cardiovasc Surg 1992 Jul
PMID:Effect of oxygen tension and cardiovascular operations on the myocardial antioxidant enzyme activities in patients with tetralogy of Fallot and aorta-coronary bypass. 161 2

Amyloid beta-peptide (A beta) deposition has been associated with coronary heart disease and neurodegenerative diseases. A link between A beta and free radical generation has been explored in neuronal tissue. We report here on the effect of A beta on pressurized segments of coronary resistance arteries and the role of free radicals. A small oscillatory response to A beta (10[-6] M) that consisted of a relaxation followed by constriction and a return to the basal diameter was observed in all vessels. The thromboxane A2 analog U46619 produced a significantly greater constriction compared with the response before treatment with A beta. The presence of the antioxidant enzyme superoxide dismutase (SOD) reduced both the response to A beta alone and the enhanced response to U46619. Vasodilation responses to acetylcholine (10[-9]-10[-5] M) were virtually eliminated at all concentrations by A beta. We confirmed endothelial cell damage by A beta with electron microscopy. The results suggest that A beta deposition in coronary resistance arteries causes endothelial damage that is mediated through superoxide radicals.
J Cardiovasc Pharmacol 1997 Oct
PMID:Beta-amyloid-induced coronary artery vasoactivity and endothelial damage. 933 13

Although researchers in radiation and cancer biology have known about the existence of free radicals and their potential role in pathobiology for several decades, cardiac biologists only began to take notice of these noxious species in the 1970s. Exponential growth of free radical research occurred after the discovery of superoxide dismutase in 1969. This antioxidant enzyme is responsible for the dismutation of superoxide radical--a free radical chain initiator. A fine balance between free radicals and a variety of endogenous antioxidants is believed to exist. Any disturbance in this equilibrium in favour of free radicals causes an increase in oxidative stress and initiates subcellular changes leading to cardiomyopathy and heart failure. Our knowledge about the role of free radicals in the pathogenesis of cardiac dysfunction is fast approaching the point where newer therapies employing antioxidants are in sight.
Cardiovasc Res 1998 Dec
PMID:The role of oxidative stress in the genesis of heart disease. 1053 10

BACKGROUND: Cardiac dysfunction and tissue injury during endotoxemia may be caused by increased levels of oxygen free radicals. METHODS AND RESULTS: We therefore investigated the effects of endotoxic shock on cardiac function and contractility, plasma creatine kinase (CK) activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL) and white blood corpuscles, antioxidant reserve (cardiac chemiluminescence [LV-CL]), antioxidant enzyme activity (superoxide dismutase, catalase, glutathione peroxidase), cardiac malondialdehyde (MDA) concentration, a lipid peroxidation product, and hemodynamics in the absence or presence of flaxseed treatment in anesthetized dogs. Flaxseed contains lignans that have antioxidant activites and inhibit platelet-activating factor (PAF). The dogs were assigned to three groups: group I, sham control; group II, endotoxin (ET) treated (5 mg/kg intravenously); group III, ET + flaxseed (2 gm/kg/day orally) for 6 days. ET produced a decrease in cardiac function and contractility and antioxidant enzyme levels, and an increase in cardiac MDA and LV-CL, PMNL-CL, and plasma CK and lactate. Pretreatment with flaxseed attenuated the ET-induced cardiac dysfunction and cellular damage. Protection was incomplete for cardiovascular function, plasma CK, and lactate. CONCLUSIONS: These results suggest that oxyradicals and/or PAF may be involved in the deterioration of cardiovascular function and cellular integrity during ET shock and that antioxidant and anti-PAF agents may be effective in the treatment of ET shock.
J Cardiovasc Pharmacol Ther 1998 Oct
PMID:Oxygen Free Radicals and Endotoxic Shock: Effect of Flaxseed. 1068 13

Blood pressure, plasma NO(2) and NO(3) level, heart weight index, antioxidant enzyme activity, and vascular reactivity in rat intact aortic rings were assessed to investigate the effects of 8-week treatment with the hydroxy-methyl-glutaryl coenzyme A reductase inhibitor simvastatin (1 mg/kg per day) on endothelial dysfunction induced by chronic Nomega-nitro-l-arginine methyl ester (l-NAME 70 mg/kg per day). Results were compared with those obtained in rats receiving l-NAME, simvastatin or control animals. Coadministration of simvastatin did not restore l-NAME-increased blood pressure but normalized heart weight index (P < 0.05), endothelium-dependent relaxation to acetylcholine (P < 0.001), and plasma NO(2) and NO(3) concentration (P < 0.001) without affecting relaxation to sodium nitroprusside. Endothelium-dependent relaxation in these animals was abolished by acute incubation with l-NAME, unaffected by thromboxane synthetase inhibitor and TXA(2)/PGH(2) receptor antagonist, ridogrel, and decreased by indomethacin. Simvastatin treatment also increased plasma NO(2)+NO(3) without affecting endothelial function, heart weight index, and blood pressure of control rats. The presence of superoxide dismutase (SOD) and catalase improved endothelial relaxation only in l-NAME-treated rats, but O(2)- generated by hypoxanthine and xanthine oxidase inhibited the relaxant effect in both l-NAME and simvastatin plus l-NAME-treated rats. SOD activity was increased in all groups receiving simvastatin. Long-term treatment with simvastatin restored l-NAME-induced endothelial dysfunction, probably by preventing nitric oxide decrease. Other effects of simvastatin, including release of compensating vasodilatory cyclo-oxygenase products and increased SOD activity, could also be involved.
J Cardiovasc Pharmacol 2003 Aug
PMID:Effects of simvastatin on endothelial function after chronic inhibition of nitric oxide synthase by L-NAME. 1288 23

Chronic renal failure (CRF) is associated with oxidative stress that promotes production of reactive oxygen species. L-Carnitine is a cofactor required for transport of long-chain fatty acids into the mitochondrial matrix. Recent research has shown that some clinical conditions (i.e., anorexia, chronic fatigue, coronary heart disease, diphtheria, hypoglycemia, and male infertility) benefit from exogenous supplementation of L-carnitine. The aim of this study was to examine the role of L-carnitine in protecting the aorta, heart, corpus cavernosum, and kidney tissues against oxidative damage in a rat model of CRF. Male Wistar albino rats were randomly assigned to either the CRF group or the sham-operated control group, which had received saline or L-carnitine (500 mg/kg, i.p.) for 4 weeks. CRF was evaluated by BUN and serum creatinine measurements. Aorta and corporeal tissues were used for contractility studies or stored along with heart and kidney tissues for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels. Plasma MDA, GSH levels and erythrocyte superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were also studied. In the CRF group, the contraction and the relaxation of aorta and corpus cavernosum samples decreased significantly compared with controls and were partially reversed by L-carnitine treatment. In the CRF group, there were significant increases in tissue MDA with marked reductions in GSH levels in all tissues and plasma compared with controls. In the plasma SOD, CAT and GSH-Px activities were also reduced. All these effects were reversed by L-carnitine as well. The increase in MDA level and the concomitant decrease in GSH level of tissues and plasma and also suppression of the antioxidant enzyme activities in plasma demonstrate that oxidative mechanisms are involved in CRF-induced tissue damage. L-carnitine, possibly via its free radical scavenging and antioxidant properties, ameliorates oxidative organ injury and CRF-induced dysfunction of the aorta and corpus cavernosum. These results suggest that L-carnitine supplementation may have some benefit in CRF patients.
J Cardiovasc Pharmacol 2004 May
PMID:L-carnitine ameliorates oxidative damage due to chronic renal failure in rats. 1507 58

We investigated the effects of an isolated soy protein (ISP) diet offered over a 9-week period to rats in whom myocardial infarction (MI) had been induced, and a casein diet given as a control. Male Wistar rats were assigned to six groups after infarct size determination (n=8/group): Sham Casein (SC); Infarct Casein <25% (IC<25%); Infarct Casein >25% (IC>25%); Sham Soy (SS); Infarct Soy <25% (IS<25%); and Infarct Soy >25% (IS>25%). MI surgery was performed at the fifth week, and one month later, the animals were hemodynamically assessed to evaluate left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), contractility and relaxation indexes (+/-dP/dt). Lung and liver specimens were also collected for the estimation of organ congestion. Oxidative stress was evaluated in heart homogenates through chemiluminescence (CL), carbonyl groups, and antioxidant enzyme activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Infarcted groups treated with casein showed cardiac hypertrophy, lung and liver congestion, increased LVEDP and decreased LVSP and +/-dP/dt, all typical signals of heart failure. Ventricular dysfunction was correlated with increased myocardial oxidative damage as seen by CL and carbonyl groups data in the groups IC<25% and IC>25% (3 and 10-fold increase, respectively). The ISP diet was able to improve ventricular systolic and diastolic function in the groups IS<25% and IS>25% (LVEDP was reduced by 44% and 24%, respectively) and to decrease myocardial oxidative stress. The overall results confirm the preventive role of soy-derived products in terms of post-MI myocardial dysfunction probably by an antioxidant action.
Nutr Metab Cardiovasc Dis 2009 Feb
PMID:Diet with isolated soy protein reduces oxidative stress and preserves ventricular function in rats with myocardial infarction. 1857 92

Recent experimental and clinical studies have suggested that oxidative stress is enhanced in myocardial remodelling and failure. The production of oxygen radicals is increased in the failing heart, whereas normal antioxidant enzyme activities are preserved. Mitochondrial electron transport is an enzymatic source of oxygen radical generation and can be a therapeutic target against oxidant-induced damage in the failing myocardium. Chronic increases in oxygen radical production in the mitochondria can lead to a catastrophic cycle of mitochondrial DNA (mtDNA) damage as well as functional decline, further oxygen radical generation, and cellular injury. Reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis by activating matrix metalloproteinases. These cellular events play an important role in the development and progression of maladaptive myocardial remodelling and failure. Therefore, oxidative stress and mtDNA damage are good therapeutic targets. Overexpression of the genes for peroxiredoxin-3 (Prx-3), a mitochondrial antioxidant, or mitochondrial transcription factor A (TFAM), could ameliorate the decline in mtDNA copy number in failing hearts. Consistent with alterations in mtDNA, the decrease in mitochondrial function was also prevented. Therefore, the activation of Prx-3 or TFAM gene expression could ameliorate the pathophysiological processes seen in mitochondrial dysfunction and myocardial remodelling. Inhibition of oxidative stress and mtDNA damage could be novel and effective treatment strategies for heart failure.
Cardiovasc Res 2009 Feb 15
PMID:Mitochondrial oxidative stress and dysfunction in myocardial remodelling. 1885 81

Oxidative stress mediated by hyperglycaemia-induced generation of reactive oxygen species (ROS) contributes significantly to the development and progression of diabetes and related vascular complications. NAD(P)H oxidase has been implicated as the major source of ROS generation in the vasculature in response to high glucose and advanced glycation end-products. Sustained activation of NAD(P)H oxidase in diabetes may diminish intracellular levels of NADPH, an essential cofactor for endothelial NO synthase (eNOS) and several antioxidant systems. Recent evidence suggests that basal ROS production via NAD(P)H oxidase may upregulate antioxidant enzyme defenses via redox signalling. Thus, NAD(P)H oxidase may serve as a double-edged sword, with transient activation providing a feedback defense against excessive ROS generation through the activation of receptor tyrosine kinases and the redox-sensitive Nrf2-Keap1 signalling pathway. Overproduction of ROS leads to eNOS uncoupling, mitochondrial dysfunction, and impaired antioxidant defenses owing to depletion of intracellular NADPH. Given the largely negative outcome of antioxidant therapy in the treatment of diabetic complications, targeting the redox-sensitive transcription factor Nfr2 may provide an effective strategy to restore antioxidant defenses in diabetes.
Cardiovasc Res 2009 Apr 01
PMID:Vascular NAD(P)H oxidase activation in diabetes: a double-edged sword in redox signalling. 1917 52

The overproduction of reactive oxygen species plays an important role in the cascade of events during lung ischemia-reperfusion leading to graft failure. An evaluation of the peripheral markers of oxidative stress and antioxidant enzyme activities was carried out after reperfusion in a rat lung transplant model. The decrease in lipid peroxidation immediately after transplantation ( P < 0.05) may suggest an adaptative response and/or a protective effect of low potassium dextran against lipid peroxidation through natural scavenging mechanisms.
Thorac Cardiovasc Surg 2009 Aug
PMID:The potential protective effect of low potassium dextran against lipid peroxidation in a rat lung transplantation model. 1962 97


1 2 3 Next >>