Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Selenium status was investigated in patients with chronic renal failure, with special regard to its relations to the dialysis treatments, dietary habits and clinical signs of atherosclerosis. 2. Serum selenium concentration and platelet glutathione peroxidase activity were measured in 45 patients with chronic renal failure subdivided into three groups according to the type of treatment: 15 non-dialysed, 15 on haemodialysis, 15 on continuous ambulatory peritoneal dialysis. A 7-day diet history was carried out in all patients. Seventeen of the patients with chronic renal failure had clinically overt cardiovascular disease. Forty-five age-matched healthy subjects were considered as controls. 3. Both serum selenium concentration and platelet glutathione peroxidase were significantly reduced in all patients with chronic renal failure compared with control subjects; a direct and significant correlation was found between the two parameters. No differences in selenium status were observed among the non-dialysed, haemodialysis and continuous ambulatory peritoneal dialysis groups. No correlation between total calorie or protein intakes and selenium indices were observed. The chronic renal failure patients with cardiovascular complications showed a further significant reduction in both serum selenium concentration and platelet glutathione peroxidase activity as compared with the patients without cardiovascular complications; these two groups were similar with respect to the other well-known cardiovascular risk factors (age, smoking, plasma lipids, hypertension, body mass index). 4. It is concluded that a low selenium concentration is present in chronic renal failure, which is independent of dialysis and is accompanied by biological repercussion in terms of reduced platelet glutathione peroxidase activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low platelet glutathione peroxidase activity and serum selenium concentration in patients with chronic renal failure: relations to dialysis treatments, diet and cardiovascular complications. 833 7

Thirty two pregnancies with pregnancy-induced hypertension (PIH) and twenty seven control normal pregnancies were analysed with regard to maternal and fetal blood enzymatic antioxidants. In PIH maternal erythrocyte, platelet and serum blood and in umbilical cord blood levels of lipid peroxides were higher than in normal pregnancy. Also the activities of platelet and erythrocyte superoxide dismutase and glutathione peroxidase were lower in PIH women. The concentration of lipid peroxides was higher, and the activity of glutathione peroxidase were lower in umbilical cord elements of women with PIH, than corresponding values of women with normal pregnancy. We suggest that disturbances in antioxidant enzymatic system are involved in the pathogenesis of maternal PIH, and it may also have effects on the function of antioxidant status of the fetus.
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PMID:[Decreased activity of oxidoreductases in erythrocytes and blood platelets from venous and umbilical blood of women with pregnancy-induced hypertension]. 864 79

Oxy-free radicals may be involved in the pathogenesis of accelerated atherosclerosis in hypertension. We evaluated the direct antioxidant potential of probucol in hypertensive arteries by studying the spatial immunohistochemical distribution of three primary antioxidant enzymes (AEs). Nineteen normocholesterolemic New Zealand White rabbits were divided into two groups: normotensive controls (NT; n = 6) and 13 animals rendered hypertensive by surgical coarctation of abdominal aorta. The hypertensive group was subdivided into hypertensive alone (HT; n = 8) and hypertensive treated with 1% probucol (PO) for 9 weeks (HT-P; n = 5). Blood pressure rose significantly in both hypertensive groups (P < .005). At autopsy, both hypertensive groups showed similarly significant increases in mean arterial intima-media thickness (IMT) whether or not they were treated with probucol. However, only HT rabbits revealed significant increases in the intima-media depth penetration of glutathione peroxidase, superoxide dismutase, and catalase AEs. By contrast, in HT-P animals probucol produced significant reductions of immunostaining of all three AEs compared to the HT group (P < .05). Additionally, specific macrophage immunostaining revealed that the arterial wall of HT rabbits had numerous (10 to 12 per high power field) subintimal and medial macrophages as compared to the HT-P animals (1 to 2 per high power field). The blood pressure level correlated significantly with IMT in all three groups, but with depth penetration of the three AEs only in the NT and HT groups. Probucol, therefore, appears to act in concert with the native arterial antioxidant enzymes as a potent free radical scavenger to reduce oxidative stress and thus attenuate the macrophage invasive response in hypertensive arteries.
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PMID:Probucol suppresses oxidant stress in hypertensive arteries. Immunohistochemical evidence. 878 83

1. To determine biochemically the incipient timing of cerebral stroke in stroke-prone spontaneously hypertensive rats (SHRSP) the relation between the glutathione peroxidase (GSH-Px) activity in erythrocytes and the extent of stroke lesion was investigated. 2. When the blood pressure of SHRSP was maintained over 250 mmHg, the GSH-Px activity was lowered and the body weight also decreased. In the SHRSP where the GSH-Px activity in erythrocytes dropped below 23 units/mL blood, the incidence of cerebral stroke was 98% (n = 88/90). 3. The haemoglobin and haematocrit level were unchanged even after the GSH-Px activity dropped to 23 units/mL blood. 4. Lowering of GSH-Px activity in erythrocytes observed during continued hypertension was found to be due to decreased GSH-Px protein, but not to an inactivation of enzymes, as evidenced from immunochemical titration. 5. Lowering of GSH-Px activity in erythrocytes was found to be closely related with the incidence of cerebral stroke in SHRSP. These findings suggest that tracing of the GSH-Px activity in erythrocytes in SHRSP may serve as an indicator for prediction and prognosis of stroke lesion.
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PMID:Relationship between erythrocytes glutathione peroxidase and incidence of stroke lesion in the stroke-prone spontaneously hypertensive rat. 907 38

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

Normal ageing is associated with different changes in the cardiovascular system that lead to an increase in pathological processes such as hypertension and heart failure. Therefore the importance of glutathione peroxidase and catalase for protection against peroxidation was studied in the rat heart. Each of the these enzymes was regulated by feeding rats a low selenium diet either unsupplemented or supplemented with 0.4 parts per million of selenium, with or without the catalase inhibitor, sodium fluoride, in their drinking water. After 2 months, selenium deficient rats had 87% reductions in mitochondrial and cytosolic glutathione peroxidase activities. These reductions were accompanied by increased peroxidation in heart homogenates and mitochondrial suspensions. Since increased mitochondrial peroxidation only occurred when both the cytosolic and mitochondrial glutathione peroxidase activities were involved, these selenoenzymes appear to work in tandem and reductions in both are a prerequisite for increased peroxidation in the heart. Peroxidation did not occur in sodium fluoride treated rats even though cytosolic catalase activity was inhibited by 70%. Moreover, inhibition of catalase activity did not exacerbate the level of peroxidation in selenium deficient rats depleted of glutathione peroxidase activity. Because increased peroxidation was only associated with reductions in glutathione peroxidase activity irrespective of catalase activity, the selenoenzyme appears to be more important for detoxification of hydrogen peroxide in the heart.
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PMID:Enzymatic defenses of the rat heart against lipid peroxidation. 922 21

The activities of glomerular intrinsic antioxidant enzymes (AOEs) were measured in a diabetic spontaneously hypertensive rat (SHR) model. The effects of antihypertensive drugs, i.e. captopril or triple therapy (hydralazine, reserpine, and hydrochlorothiazide), on glomerular intrinsic AOE activities in this model were evaluated. The effects of blood glucose control on the AOE activities were also determined. The aim of the present study was to determine whether activities of glomerular intrinsic AOEs might correlate with disease activity in diabetic SHR. This study showed a decrease of glomerular intrinsic AOE, i.e. Cu/Zn-SOD and Mn-SOD (SOD = superoxide dismutase), glutathione peroxidase, and catalase, activities in diabetic SHR. Glomerular Cu/Zn-SOD or Mn-SOD, glutathione peroxidase, and catalase activities in nondiabetic SHR were slightly lower than those in nondiabetic WKY rats. These activities in diabetic SHR were significantly improved after captopril or triple therapy or blood glucose control. The levels of urinary albumin excretion, creatinine clearance, and glomerular tuft areas in diabetic SHR were also improved after the therapy. It appears that hypertension and hyperglycemia may influence the glomerular intrinsic AOE activities, albuminuria, creatinine clearance, and glomerular tuft areas in diabetic SHR. Thus, it is indicated that control of blood pressure or blood glucose is a very important factor for preventing renal injuries in the diabetic SHR model.
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PMID:Effects of antihypertensive drugs or glycemic control on antioxidant enzyme activities in spontaneously hypertensive rats with diabetes. 922 34

This study was designed to investigate the alterations in thiobarbituric acid reactants (TBA-reactants) and enzymatic and nonenzymatic antioxidant levels induced by dexamethasone (Dex) in heart and kidney and to find out whether these alterations induced by Dex and its hypertensive effect had any role in the maintenance of hypertension in this model. Administration of dexamethasone induced severe loss of body weight, significant increase in heart and kidney weights and also marked electrocardiographic changes. The protein content in heart and kidney increased significantly during Dex administration and returned to near normalcy after withdrawal. Total activity of lactate dehydrogenase showed a significant increase in heart till day 8 of treatment, whereas in serum, it exhibited a significant decrease. The activity of CK in heart showed an increase till day 8 of treatment and approached normalcy thereafter. In serum, CK exhibited a decrease till day 8, remaining insignificant thereafter. CKMB in heart showed an insignificant increase initially, reaching normal levels on Dex withdrawal, whereas in serum, it showed a significant decrease throughout the experimental period. Mean arterial pressure (MAP) and heart rate increased significantly, while a significant elevation in the ST segment was noticed during administration as well as after withdrawal of Dex. The TBA-reactants levels were found to increase in heart and kidney during days 12 and 16 of administration with Dex and even after withdrawal of Dex, the levels were insignificantly elevated. The level of glutathione in heart and kidney increased from day 4 onwards and reached normalcy during the later stages of treatment and after withdrawal of Dex. The total sulfhydryl groups exhibited a significant increase in both heart and kidney throughout the experiment. The antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione S-transferase exhibited a significant decrease in heart during Dex administration whereas, in kidney, they exhibited a significant increase during treatment and after withdrawal of Dex. Thus, Dex induced rise in mean arterial pressure, significant alterations in electrocardiographic parameters and also marked alterations in enzymatic and nonenzymatic antioxidant levels and in the TBA-reactants level in heart and kidney.
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PMID:Dexamethasone induced alterations in enzymatic and nonenzymatic antioxidant status in heart and kidney of rats. 956 44

To study the mechanism of the fall of glutathione peroxidase (GSH-Px) activity in erythrocyte after cerebral strokes in stroke-prone spontaneously hypertensive rats (SHRSP), erythrocytes were fractionated into low density erythrocytes (LD-E) and high density erythrocytes (HD-E) by a density gradient centrifugal method using Percoll solution, and fluctuation of the distribution ratio and changes of GSH-Px activity in fractionated erythrocytes were investigated. The distribution ratio of LD-E and HD-E in erythrocytes of SHRSP was about 4:1 at 5 weeks of age (n = 6), and the distribution to HD-E increased along with aging. While the distribution ratio was changed, however, there was no change in the GSH-Px activity in both LD-E and HD-E of erythrocytes. In senile, 30-week-old SHRSP (n = 4) with advanced hypertension, the GSH-Px activity in the HD-E was lower, in proportion to the increase of the distribution rate against HD-E. On the other hand, in SHRSP (n = 5) having cerebral stroke, the distribution ratio of LD-E and HD-E was about 1:4. The GSH-Px activity was 31.4 +/- 2.9 units/10(10) erythrocytes in LD-E, which was hardly different from the value of SHRSP without stroke (35.7 +/- 3.3 units/10(10) erythrocytes). In HD-E, however, the activity was 18.2 +/- 2.2 units/10(10) erythrocytes, being lower than the activity of SHRSP without stroke. At the moment when the GSH-Px activity had dropped to 17 units/mg hemoglobin, and the control diet was changed to one based on fish or a hydralazine treatment given, the activity recovered, and an increase in body weight and the distribution rate of the LD-E over HD-E was increased. It is clear from these experiments that the fall of erythrocyte GSH-Px activity observed after cerebral stroke is due to a decrease of LD-E and increase of HD-E, which has lowered activity. However, nothing definite is known on the relationship between the fall of GSH-Px activity in erythrocytes and disorder in cerebral tissue. It appears that the fall of the GSH-Px activity causes at least functional and structural changes in erythrocytes, which interfere with the delivery of oxygen to peripheral tissues, triggering oxidation stress in cerebral tissues.
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PMID:Cell age distribution of erythrocytes at the incidence of cerebral stroke in stroke-prone spontaneously hypertensive rats, and their glutathione peroxidase activity. 957 77

Plasma and lipoprotein lipid composition and endogenous hepatic antioxidant status were investigated in hypertensive, 14-week-old spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats fed a standard commercial rat chow. Total plasma calcium and magnesium concentrations were similar between both rat strains; however, systolic blood pressure in SHR was greater than in WKY at 13 weeks of age (197 +/- 12 vs. 132 +/- 14 mmHg; p < or = 0.05), confirming hypertension in SHR. Total plasma cholesterol and triacylglycerol concentrations were lower (p < or = 0.05) in SHR compared with WKY. A lower (p < 0.05) HDL cholesterol level in SHR plasma resulted in a higher LDL to HDL cholesterol ratio compared with WKY counterparts. No significant differences in the relative proportion of HDL apolipoprotein A-I fraction were observed between SHR and WKY. Both SHR VLDL and HDL triacylglycerol fractions were lower (p < 0.05) in SHR than WKY. Analysis of liver antioxidant enzyme activities showed no differences in rat liver superoxide dismutase (SOD), but lower (p < 0.05) liver glutathione peroxidase (GSH-Px) activity in SHR. However, liver glutathione (GSH) levels were similar in SHR and WKY counterparts. A possible compensatory effect to the oxidative status of SHR was suggested by the significant (p < 0.05) increase in both liver catalase (CAT) and glutathione reductase (GSSG-Red) activities. Despite these results, in vitro oxidative challenge studies with H2O2 demonstrated a greater susceptibility of liver to GSH depletion in the SHR, although no parallel change in thiobarbituric acid reactive substances (TBARS) production was observed. The comparatively lower plasma cholesterol observed in hypertensive SHR paralleled specific differences in liver catalase and glutathione redox antioxidant enzyme activities.
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PMID:Plasma and lipoprotein lipid composition and hepatic antioxidant status in spontaneously hypertensive (SHR) and normotensive (WKY) rats. 963 61


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