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)

Postprandial lipemia has been recognized as a risk factor for atherosclerosis development. Consuming meals with suitable sources of antioxidants such as red wine reduces postprandial oxidative stress. However, information about the postprandial effects of wine ingestion outside meals on lipids and on in vivo low-density lipoprotein (LDL) oxidation in humans is scarce. The aim of this study was to investigate postprandial changes in lipids and in vivo LDL oxidation after moderate (250 ml) red wine ingestion, before and after sustained wine consumption of 250 ml/day for 4 days. After 4 days of sustained wine consumption a decrease in the LDL/high-density lipoprotein cholesterol ratio was observed after wine ingestion (p = 0.026). On day 4, a decrease in oxidized LDL levels and an increase in the antioxidant enzyme glutathione peroxidase activity (p = 0.025) were observed after wine ingestion. Our results show that consumption of red wine at moderate doses outside meals does not promote oxidative stress. Daily consumption of moderate doses of red wine can improve postprandial lipid profile and oxidative status when wine is ingested outside meals.
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PMID:Postprandial effects of wine consumption on lipids and oxidative stress biomarkers. 1513 77

Effects of ingesting garlic extract on plasma and erythrocyte antioxidant parameters of atherosclerotic patients were investigated in this study. Eleven patients with atherosclerosis participated in the study. They ingested a dose of 1 ml/kg body weight of garlic extract daily for 6 months (study period). Before and after this period, fasting blood samples were obtained, and oxidant (malondialdehyde, MDA and xanthine oxidase, XO) and antioxidant (superoxide dismutase, SOD and glutathione peroxidase, GSH-Px) parameters were studied in plasma and erythrocytes obtained from the patients. Blood samples obtained from 11 healthy subjects served as the controls. Plasma XO activity and MDA levels were higher, but plasma and erythrocyte GSH-Px activities were lower, in patients with atherosclerosis relative to those of the control group. Our results showed that ingestion of garlic extract leads to significantly lowered plasma and erythrocyte MDA levels in the patients even in the absence of changes in antioxidant enzyme activities. Our results also demonstrated the presence of oxidant stress in blood samples from patients with atherosclerosis, but ingesting garlic extract prevented oxidation reactions by eliminating this oxidant stress. Thus, it is possible that reduced peroxidation processes may play a part in some of the beneficial effects of garlic in atherosclerotic diseases.
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PMID:Effects of garlic extract consumption on plasma and erythrocyte antioxidant parameters in atherosclerotic patients. 1530 63

Oxidative stress is characterized by an overweight of pro-oxidants against antioxidant forces and is associated with atherosclerosis, aging, and reproductive complications. Placenta is the major source of pro-oxidant agents, antioxidant enzyme-systems, and hormones and is able to keep the lipid peroxidation under control in normal pregnancy. As oxidation processes are increased in pregnancy, we would expect a shortening of lag phase of low density lipoprotein (LDL)-oxidation. LDL oxidation assessed by measuring conjugated diene formation is a marker for the early part of lipid peroxidation process and the balance of pro-oxidants and antioxidants influences length of lag phase. Our results show that resistance of LDL oxidation is unchanged during normal pregnancy in the second and third trimester. Only antioxidants are able to protect LDL. Estriol is an antioxidant, increases the lag-phase of LDL-oxidation in vitro, and its serum concentration raises enormous during late pregnancy. Thus the biological role of high levels of estriol during pregnancy may be part of the self-protection to limit oxidative damages.
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PMID:Placental defence is considered sufficient to control lipid peroxidation in pregnancy. 1561 65

Many studies have shown the balance between the oxygen reactive species (ROS) and the antioxidant capacities, and that the massive ROS generation could lead to cell damage and diseases such as atherosclerosis, aging and cancer. Changes in antioxidant capacity like free radicals scavenging antioxidant agents such as vitamin E, C content, serum concentrations of bilirubin, uric acid, albumin and antioxidant enzyme systems like SOD, and GPx activities have been described to be related to many diseases. However, the research on chronic airway inflammatory disease and the antioxidant defence system is still not enough. Understanding of the antioxidant status and antioxidant enzymes in asthmatic patients is still unclear. In the present controlled study, we investigated the total antioxidant status (TAS) in serum and the antioxidant enzyme (total SOD and GPx) activities in 46 asthmatic children and 52 normal controls. The serum level of TAS in asthmatic children was significantly lower than the controls. The SOD concentration in asthmatic children was higher than the control, however the GPx was much lower than the control children, even though it was not statistical significance. In conclusion, these results suggested the existence of higher oxidative stress and reactive oxygen species (ROS) in asthmatic children, and that the antioxidant capacities in asthmatic children were altered. If the production of ROS was persistent, it would result in chronic inflammation and the imbalance of oxidative-reductive status in those patients.
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PMID:Evaluation of the serum antioxidant status in asthmatic children. 1562 67

Acrolein is a highly electrophilic alpha,beta-unsaturated aldehyde to which humans are exposed in a variety of environment situations and is also a product of lipid peroxidation. Increased unsaturated aldehyde levels and reduced antioxidant status play an important role in the pathogenesis of a number of human diseases such as Alzheimer's, atherosclerosis, and diabetes. Mammalian thioredoxin reductase (TR), a central antioxidant enzyme, is a selenoprotein that catalyzes the reduction of oxidized thioredoxin. The findings reported here show that low concentrations of acrolein rapidly inactivate TR, both in vitro and in vivo. These data suggest that acrolein may directly inactivate TR, resulting in an increase in oxidative cellular damage. In addition, we also found that the initial inactivation of TR molecules by acrolein triggers a compensatory signal for inducing TR gene expression in human umbilical vein endothelial cells (HUVEC). The results of the present study suggest that HUVEC may have a protective system against cell damage by acrolein via the upregulation of TR, which is an adaptive response to oxidative stress.
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PMID:Induction of thioredoxin reductase as an adaptive response to acrolein in human umbilical vein endothelial cells. 1565 4

Anthocyanin-rich beverages have shown beneficial effects on coronary heart disease in epidemiological and intervention studies. In the present study, we investigated the effect of black currant anthocyanins on atherosclerosis. Watanabe Heritable Hyperlipidemic rabbits (n = 61) were fed either a purified anthocyanin fraction from black currants, a black currant juice, probucol or control diet for 16 weeks. Purified anthocyanins significantly increased plasma cholesterol and low-density lipoprotein (LDL) cholesterol. Intake of black currant juice had no effect on total plasma cholesterol, but lowered very-low-density lipoprotein (VLDL) cholesterol significantly. There were no significant effects of either purified anthocyanins or black currant juice on aortic cholesterol or development of atherosclerosis after 16 weeks. Probucol had no effect on plasma cholesterol but significantly lowered VLDL-cholesterol and decreased aortic cholesterol accumulation. The erythrocyte antioxidant enzyme glutathione peroxidase was significantly increased by purified anthocyanins and superoxide dismutase was increased by both anthocyanin-containing treatments. Other markers of plasma antioxidant capacity, antioxidant enzymes, protein and lipid oxidation were not affected by any of the anthocyanin treatments. Adverse effects of purified anthocyanins were observed on plasma- and LDL-cholesterol. These effects were not observed with black currant juice, suggesting that black currants may contain components reducing the adverse effects of anthocyanins.
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PMID:Anthocyanins increase low-density lipoprotein and plasma cholesterol and do not reduce atherosclerosis in Watanabe Heritable Hyperlipidemic rabbits. 1575 6

Oxygen free radicals and related reactive species have been implicated in the etiology of many diseases, such as atherosclerosis, neurodegenerative disorders, and cancer. Antioxidant enzymes exist in cells to protect against the effects of these free radicals and other oxygen-derived species, which are produced during the oxidative stress. Tea (Camellia sinensis) is the most commonly consumed beverage worldwide. Both green and black tea are known to possess many pharmacological properties, including antioxidant, antipyretic, antibacterial, and antineoplastic effects. In the present study, the preventive effects of black tea extract (BTE) was evaluated in Swiss albino mice against 7,12-dimethyl benz(a)anthracene (DMBA)-induced oxidative stress. The animals were given 0.5%, 1%, and 1.5% BTE as the sole source of drinking solution for 1 week prior to the administration of DMBA, which was given orally as a single dose of 50 mg/kg body weight. At the end of the study period, the liver, kidney, and prostate tissues were dissected out for the determination of antioxidant enzyme levels (catalase, superoxide dismutase, glutathione reductase, glutathione-S-transferase), and lipid peroxidation. A dose-dependent protective effect of BTE against DMBA-induced depletion in enzymes activity was observed in all three tissues examined. Similarly, a significant dose-dependent inhibition of the lipid peroxidation caused by DMBA was observed in the BTE-administered animals in all three tissues examined. Our results revealed that BTE provides protection against oxidative damage induced by xenobiotics.
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PMID:Antioxidant potential of black tea against 7,12-dimethylbenz(a)anthracene- induced oxidative stress in Swiss albino mice. 1583 Oct 83

It is reported that the water extract of tea as well as tea polyphenols and tea pigments have strong antioxidant properties, which are considered as the major mechanism of the protective effects of tea on cancer and cardiovascular diseases. It has been shown that tea (including tea polyphenols and tea pigments) could induce the antioxidant enzyme activities, regulate phase I and II metabolic enzymes, inhibit the metabolic activation of carcinogens, reduce the formation of carcinogen DNA adducts, inhibit the expression and replication of oncogenes, directly affect the activity of transcription factors, and block the initiation of carcinogenesis, so as to eliminate and alleviate the damage to cellular communication caused by oxidative stress, and eventually prevent the abnormal proliferation of tumor cells. The mechanisms of the protective effects of tea on cardiovascular diseases are possibly related to its effects on the inhibition of lipid oxidation and quenching oxygen and hydroxy free radicals. It was demonstrated that tea pigments could inhibit the oxidation of LDL cholesterol and the adhesion of blood vessel endothelium cells, lower endothelin levels, enhance GSH-PX activities, prevent from blood coagulation and platelet aggregation, and facilitate fibrinogen dissolution, so as to prevent atherosclerosis of coronary arteries.
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PMID:[Studies on the antioxidant properties of tea]. 1595 73

Cardiovascular disease is the single leading cause of death and morbidity for Canadians. A universal feature of cardiovascular disease is dysfunction of the vascular endothelium, thus disrupting control of vasodilation, tissue perfusion, hemostasis, and thrombosis. Nitric oxide bioavailability, crucial for maintaining vascular endothelial health and function, depends on the processes controlling synthesis and destruction of nitric oxide as well as on the sensitivity of target tissue to nitric oxide. Evidence supports a major contribution by oxidative stress-induced destruction of nitric oxide to the endothelial dysfunction that accompanies a number of cardiovascular disease states including hypertension, diabetes, chronic heart failure, and atherosclerosis. Regular physical activity (exercise training) reduces cardiovascular disease risk. Numerous studies support the hypothesis that exercise training improves vascular endothelial function, especially when it has been impaired by preexisting risk factors. Evidence is emerging to support a role for improved nitric oxide bioavailability with training as a result of enhanced synthesis and reduced oxidative stress-mediated destruction. Molecular targets sensitive to the exercise training effect include the endothelial nitric oxide synthase and the antioxidant enzyme superoxide dismutase. However, many fundamental details of the cellular and molecular mechanisms linking exercise to altered molecular and functional endothelial phenotypes have yet to be discovered. The working hypothesis is that some of the cellular mechanisms contributing to endothelial dysfunction in cardiovascular disease can be targeted and reversed by signals associated with regular increases in physical activity. The capacity for exercise training to regulate vascular endothelial function, nitric oxide bioavailability, and oxidative stress is an example of how lifestyle can complement medicine and pharmacology in the prevention and management of cardiovascular disease.
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PMID:Vascular nitric oxide and oxidative stress: determinants of endothelial adaptations to cardiovascular disease and to physical activity. 1625 83

Glutathione is a vital intracellular antioxidant. The enzymes involved in its synthesis and utilisation are tightly regulated, but the importance of glutathione regulation in atherogenesis is poorly understood. Here, we establish that glutathione is severely (approximately 80%) depleted very early (10 weeks) in the atheroma-prone aortic arch of male apoprotein E-deficient (Apo-E(-/-)) mice compared to age-matched wild-type controls. Importantly, this event pre-empts lipid peroxidation and detectable atheroma by several months. Depletion of glutathione was associated with excessive oxidant burden and reduced transcription and activity of the rate-limiting enzyme for glutathione synthesis, gamma-glutamylcysteine ligase, together with the glutathione-dependent antioxidant enzyme, glutathione peroxidase. Depletion via reduced synthesis of glutathione precedes lipid peroxidation and atherogenesis in Apo-E(-/-) mice. We suggest that glutathione deficiency is central to the failure of the intracellular antioxidant defences and is causally implicated in the pathogenesis of atherosclerosis. Modification of the glutathione pathway may present a novel and important therapeutic target in the prevention and treatment of atherosclerosis.
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PMID:Depressed glutathione synthesis precedes oxidative stress and atherogenesis in Apo-E(-/-) mice. 1626 83


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