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)

Effects of benidipine hydrochloride or triple therapy (hydralazine, reserpine, and hydrochlorothiazide) on renal cortical and medullary intrinsic antioxidant enzyme (AOE) activity were evaluated in stroke-prone spontaneously hypertensive rats (SHR-SP) as an animal model for human essential hypertension with cerebral stroke. This study showed a significant decrease of renal intrinsic glutathione peroxidase (GSH-Px) activity in untreated SHR-SP. Renal GSH-Px activity in untreated SHR-SP was significantly lower than that in Wister Kyoto rats (WKY) as a normotensive reference strain. GSH-Px activity in SHR-SP was significantly improved after benidipine hydrochloride therapy. Levels of urinary albumin excretion or creatinine clearance (Ccr) in SHR-SP were also improved after the therapy. Glomerular sclerosis index was slightly improved in SHR-SP treated with benidipine hydrochloride according to light microscopic analysis. It appears that hypertension may influence the renal intrinsic GSH-Px activity, albuminuria, and Ccr in SHR-SP. Thus it is indicated that control of blood pressure may improve the GSH-Px activity in SHR-SP.
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PMID:Effects of benidipine hydrochloride on antioxidant enzyme activity in stroke-prone spontaneous hypertensive rats (SHR-SP). 913 5

Several lines of evidence suggest that patients with essential hypertension have impaired endothelial nitric oxide activity and increased superoxide anion production. However, the mechanisms underlying these abnormalities remain unknown. We measured enzymatic superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities in erythrocytes and whole blood, respectively, in 30 newly-diagnosed, normolipidaemic untreated mild hypertensive patients and in 164 age-matched healthy controls. SOD and GPX activities in hypertensive patients (806 +/- 225 U/Hb.g and 5491 +/- 2073 U/L, respectively) were significantly lower than in the control group (931 +/- 202 U/Hb.g and 6669 +/- 1560 U/L, respectively) (P < 0.005). No significant association was found between these antioxidant enzyme activities and blood pressure in normotensive controls. In the hypertensives, only log-transformed SOD activity showed a significant negative correlation with systolic and diastolic blood pressure (r = 0.37, P < 0.05; r = 0.64, P < 0.0001, respectively). The low endogenous antioxidant enzyme activities observed may in turn result in decreased superoxide anion removal leading to nitric oxide inactivation. Journal of Human Hypertension (2000) 14, 343-345
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PMID:Decreased endogenous antioxidant enzymatic status in essential hypertension. 1087 91

Catalase is an important antioxidant enzyme that detoxifies H2O2 into oxygen and water and thus limits the deleterious effects of reactive oxygen species (ROS). Because chronic exposure to excess ROS may contribute to vascular damage, we investigated whether genetic variation in catalase was associated with susceptibility to essential hypertension (EHYT) in 324 individuals (at least 50 years old) who were randomly sampled from an isolated population living in Xiangchang, China. They were screened for genetic variation in the promoter of catalase by direct sequencing. In total, four single nucleotide polymorphisms (SNPs) were identified. The association between the SNPs and EHYT was investigated by a linear regression model under phenotypic selection; in our analyses, we used both SBP>150 mmHg and SBP>160 mmHg as thresholds. A SNP 844 bp upstream of the start codon (SNP-844) demonstrated strong evidence of association with EHYT (SBP>150 mmHg: F=5.09, P=0.008; SBP>160 mmHg: F=7.13, P=0.002). This is the first study to implicate genetic variation in catalase in susceptibility to EHYT and suggests that polymorphisms in promoter regions may be particularly relevant to the study of complex diseases.
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PMID:A polymorphism in the promoter region of catalase is associated with blood pressure levels. 1147 40

Despite evidence that essential hypertension (EH) is a state of increased oxidative stress, the data on oxidative protein modifications is lacking. Besides, the role of extracellular antioxidant enzymes in EH has not been systematically studied. Study was performed in 45 subjects with EH and 25 normotensive controls. Patients were divided into three groups according to the 2003 ESH/ESC guidelines (grade 1-3). Plasma protein reactive carbonyl derivatives (RCD) and SH-groups (as byproducts of oxidative protein damage) as well as antioxidant enzyme activities superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase were studied spectrophotometrically and correlated with blood pressure (BP). RCD levels were increased in EH patients compared to controls and correlated significantly with both systolic blood pressure (SBP) (r = 0.495, P<0.01) and diastolic blood pressure (DBP) (r = 0.534, P<0.01). Plasma SH-groups content was significantly lower in all patients with EH, with no correlation with BP. SOD and catalase activity in patients with grade 1 EH were similar to that of controls. Patients with grade 2 and 3 of EH had lower SOD and catalase activity. However, significant correlation with SBP and DBP was observed for catalase only (r = -0.331; P<0.05 and r = -0.365; P<0.05, respectively). EH patients exhibited higher plasma GPX activity compared to those in controls, and it correlated with SBP (r = 0.328; P<0.05). The results presented show that increased oxidative protein damage is present in all grades of EH. In mild hypertension extracellular antioxidant enzyme activities are not decreased, suggesting they are probably not critical in early EH, but could be important in moderate to severe EH.
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PMID:Byproducts of oxidative protein damage and antioxidant enzyme activities in plasma of patients with different degrees of essential hypertension. 1634 Oct 53

Dysfunction of D2-like receptors has been reported in essential hypertension. Disruption of D2R in mice (D2-/-) results in high blood pressure, and several D2R polymorphisms are associated with decreased D2R expression. Because D2R agonists have antioxidant activity, we hypothesized that increased blood pressure in D2-/- is related to increased oxidative stress. D2-/- mice had increased urinary excretion of 8-isoprostane, a parameter of oxidative stress; increased activity of reduced nicotinamide-adenine dinucleotide phosphate oxidase in renal cortex; increased expression of the reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits Nox1, Nox2, and Nox4; and decreased expression of the antioxidant enzyme heme-oxygenase-2 in the kidneys, suggesting that regulation of reactive oxygen species (ROS) production by D2R involves both pro-oxidant and antioxidant systems. Apocynin, a reduced nicotinamide-adenine dinucleotide phosphate oxidase inhibitor, or hemin, an inducer of heme oxigenase-1, normalized the blood pressure in D2-/- mice. Because D2Rs in the adrenal gland are implicated in aldosterone regulation, we evaluated whether alterations in aldosterone secretion contribute to ROS production in this model. Urinary aldosterone was increased in D2-/- mice and its response to a high-sodium diet was impaired. Spirolactone normalized the blood pressure in D2-/- mice and the renal expression of Nox1 and Nox4, indicating that the increased blood pressure and ROS production are, in part, mediated by impaired aldosterone regulation. However, spironolactone did not normalize the excretion of 8-isoprostane and had no effect on expression of Nox2 or heme-oxygenase-2. Our results show that the D2R is involved in the regulation of ROS production and that, by direct and indirect mechanisms, altered D2R function may result in ROS-dependent hypertension.
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PMID:Reactive oxygen species-dependent hypertension in dopamine D2 receptor-deficient mice. 1719 Aug 75

Biliverdin reductase A (BLVRA) is a powerful intracellular antioxidant enzyme and an antagonist to insulin-mediated glucose uptake by the cells. Increased oxidative stress and insulin-resistance (IR) are associated with increased risk for hypertension. Therefore, we hypothesized that BLVRA might be attributable to the variation of susceptibility to essential hypertension, and investigated single nucleotide polymorphism (SNP) rs699512 (Thr3Ala), the only common non-synonymous SNP within BLVRA, in population-based samples of 999 Kazak herdsmen from the villages in Xinjiang, China. The minor allele of SNP rs699512 reduced the risk of essential hypertension (age- and gender-adjusted odds ratio 0.76; 95% confidence interval 0.61-0.94; p = 0.010). Single nucleotide polymorphism rs699512 showed association with both systolic and diastolic blood pressures: the minor allele homozygous carriers had lowest systolic and diastolic blood pressures (139.6 mmHg, 89.6mmHg), followed by heterozygous carriers (145.3 mmHg, 92.3 mmHg), and then major allele homozygous carriers (150.3 mmHg, 95.1 mmHg) (p = 0.005 and 0.009, respectively). These findings provide the first genetic evidence for the role of BLVRA on the susceptibility to human essential hypertension and blood pressure.
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PMID:Association of a BLVRA common polymorphism with essential hypertension and blood pressure in Kazaks. 2172 74