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)

The objective of this study was to assess the oxidative stability and presence of antibiotic residues in tissues of broilers fed diets supplemented with alpha-tocopheryl acetate and treated with enrofloxacin. The activities of antioxidant enzymes and antibiotic concentrations in chicken breast, leg, and liver were determined. Iron-induced TBA-reactive substances (TBARS) and vitamin E were evaluated in muscles. The antioxidant effectiveness of vitamin E was reflected by TBARS values being lower in antioxidant-supplemented treatments than in the other dietary groups. On the other hand, antioxidant enzyme activities were not substantially affected by dietary treatments. The concentration of enrofloxacin in tissues was considerable, even after withdrawal 12 d before slaughter. Contrary to the findings in previous studies, enrofloxacin was not extensively metabolized to ciprofloxacin. Supplementation of the diet with 100 mg/kg of alpha-tocopheryl acetate did not have a significant effect on the level of antibiotic found in breast muscle samples. When comparing treatments without antibiotic withdrawal time, alpha-tocopheryl acetate supplementation led to a significant decrease in enrofloxacin level in leg and liver samples. These results showed that mutual interactions between different molecules could modify the drug residues in the tissue, which should be taken into account when considering the drug administration and the establishment of a correct withdrawal time.
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PMID:Influence of enrofloxacin administration and alpha-tocopheryl acetate supplemented diets on oxidative stability of broiler tissues. 1514 38

Oxidative stress has been increasingly postulated as a major contributor to endothelial dysfunction in preeclampsia (PE), although evidence supporting this hypothesis remains inconsistent. This study aimed to analyze in depth the potential role of oxidative stress as a mechanism underlying endothelial damage in PE and the pregnant woman's susceptibility to the disease. To this end, indicative markers of lipoperoxidation and protein oxidation and changes in antioxidant defense systems were measured in blood samples from 53 women with PE and 30 healthy pregnant controls. Results, analyzed in relation to disease severity, showed PE women, compared with women with normal pregnancy, to have: (1) significantly enhanced antioxidant enzyme SOD and GPx activities in erythrocytes; (2) similar plasma alpha-tocopherol levels and significantly increased alpha-tocopherol/lipids in both mild and severe PE; (3) significantly decreased plasma vitamin C and protein thiol levels; (4) similar erythrocyte glutathione content, total plasma antioxidant capacity, and whole plasma oxidizability values; (5) significantly elevated plasma total lipid hydroperoxides, the major initial reaction products of lipid peroxidation, in severe PE; (6) no intracellular or extracellular increases in any of the secondary end-products of lipid peroxidation, malondialdehyde or lipoperoxides; (7) similar oxidative damage to proteins quantified by plasma carbonyl levels, immunoblot analysis, and advanced oxidation protein products assessment; and (8) significantly elevated and severity-related soluble vascular cell adhesion molecule-1 serum levels reflecting endothelial dysfunction. No correlations were found among plasma levels of circulating adhesion molecules with regard to lipid and protein oxidation markers. Globally, these data reflect mild oxidative stress in blood of preeclamptic women, as oxidative processes seem to be counteracted by the physiologic activation of antioxidant enzymes and by the high plasma vitamin E levels that would prevent further oxidative damage. These results do not permit us to conclude that oxidative stress might be a pathogenetically relevant process causally contributing to the disease.
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PMID:A comprehensive study of oxidative stress and antioxidant status in preeclampsia and normal pregnancy. 1525 27

Endosulfan is widely used in insect control and it is absorbed by both humans and animals through ingestion, inhalation and percutaneously. The aim of this work was to study antioxidant enzyme system which include superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) and malondialdehyde (MDA), the end product of lipid peroxidation and ultrastructural changes that might occur in the heart tissue of adult male Wistar rats as a result of endosulfan intoxication. Vitamin E (200 mg/kg, twice a week), endosulfan (2 mg/kg, per day, once a day in corn oil) and vitamin E (200 mg/kg, twice a week)+endosulfan (2 mg/kg, per day, once a day in corn oil) combination were given to rats (n = 10/group) orally via gavage for 6 weeks. SOD, GPx, CAT activities and MDA level increased in the endosulfan-treated group heart tissue compared to control group (P < 0.01, P < 0.01, P < 0.05 and P < 0.01, respectively). SOD, GPx activities and MDA level decreased in the vitamin E + endosulfan-treated group compared to endosulfan-treated group (P < 0.05, P < 0.05 and P < 0.05, respectively). Decrease of CAT activity was not significant statistically in the vitamin E + endosulfan-treated group compared to endosulfan-treated group. CAT activity increased in the vitamin E + endosulfan treated group compared to control group (P < 0.05). Increase of SOD, GPx activities and MDA levels were not significant statistically in the vitamin E + endosulfan-treated group compared to control group. In electron microscopic investigations while cytoplasmic edema and swelling and vacuolization of mitochondria of myocardial cells in endosulfan-treated group was observing, only a weak swelling of mitochondria of myocardial cells in vitamin E + endosulfan-treated group was observed. We conclude that vitamin E significantly reduce endosulfan-induced cardiotoxicity in rats.
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PMID:Endosulfan-induced cardiotoxicity and free radical metabolism in rats: the protective effect of vitamin E. 1533 85

Defective intracellular antioxidant enzyme production (IAP) has been demonstrated in adults with diabetic nephropathy. To evaluate the effects on IAP of vitamin E administration in adolescents with type 1 diabetes and early signs of microangiopathy, 12 adolescents (aged 11-21 y; diabetes duration 10-18) were studied. Eight had retinopathy [background (four), preproliferative (three), or proliferative (one)], four had persistent microalbuminuria, and seven had both. Skin fibroblasts were obtained by biopsies and cultured in Dulbecco's modified Eagle's medium. CuZn superoxide dismutase (SOD), MnSOD, catalase (CAT), and glutathione-peroxidase (GPX) activity and mRNA expression were measured before and after 3 mo of synthetic vitamin E supplementation (600 mg twice daily); on both occasions, IAP was evaluated at different ex vivo glucose concentrations (5 and 22 mM). Ten adolescents with type 1 diabetes (aged 12-20 y) without angiopathy and eight healthy volunteers (aged 15-22 y) participated as control subjects. Vitamin E serum levels were measured throughout the study. In normal glucose concentrations, CuZnSOD, MnSOD, CAT, and GPX activity and mRNA expression were not different among the groups. In high glucose, CuZnSOD activity and mRNA increased similarly in all groups [angiopathics: 0.96 +/- 0.30 U/mg protein; 9.9 +/- 3.2 mRNA/glyceraldehyde-3-phosphate dehydrogenase). CAT and GPX activity and mRNA did not increase in high glucose only in adolescents with angiopathy (0.35 +/- 0.09; 4.2 +/- 0.1 and 0.52 +/- 0.14; 2.4 +/- 0.9, respectively). MnSOD did not change in any group. Vitamin E supplementation had no effect on any enzymatic activity and mRNA in both normal and hyperglycemic conditions. Adolescents with early signs of diabetic angiopathy have defective IAP and activity, which are not modified by vitamin E.
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PMID:Effects of vitamin E supplementation on intracellular antioxidant enzyme production in adolescents with type 1 diabetes and early microangiopathy. 1534 73

Prenatal exposure to excessive glucocorticoids may alter the developing fetus inducing metabolic and endocrine imbalance in various organs, including the kidney. This study aimed at evaluating whether prenatal exposure to high levels of glucocorticoids adversely affects renal cell survival and predisposes to renal cell death. Pregnant rats were injected with 0.1 mg/kg dexamethasone (DEX) i.p. from day 1 of gestation. Renal proximal tubular cells (PTCs) were prepared from 20-day-old offspring in the DEX (DEX cells) and control groups (CON cells). After 4 days' culture, cells were exposed to uropathogenic Escherichia coli ARD6 toxins at concentrations known to induce apoptotic cell death. We found that cell death rate was significantly higher in DEX than in CON cells. Cells exhibited morphological and biochemical features of apoptosis. Conversely, the activity of the antioxidant enzyme catalase was significantly increased in renal cortex homogenate from 20-day-old DEX rats. The antioxidant vitamin E did not prevent apoptosis. These results indicate that prenatal exposure to high levels of glucocorticoids induces alterations in renal PTCs rendering them more sensitive to E. coli toxins via nonoxidative stress. With the increasing use of multiple doses of glucocorticoids in preterm infants, the possibility that antenatal glucocorticoids may lead to renal adverse consequences is of clinical relevance.
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PMID:Prenatal exposure to high level of glucocorticoids increases the susceptibility of renal proximal tubular cells to apoptosis induced by uropathogenic Escherichia coli toxins. 1535 12

Docosahexaenoic acid (DHA, 22:6 n-3), a polyunsaturated fatty acid found in fish oil, exerts cytotoxic effects on cancer cells. Although DHA was toxic toward five human cancer cell lines (MCF-7, MDA-MB-231, SiHa, Raji, and DHL-4), the lines were not uniformly sensitive. DHL-4, a bcl-2 overexpressing lymphoid line, was the most sensitive (IC50, 5.2 micromol/L) and the cervical cancer cell line, SiHa, was the most resistant (IC50, >300 micromol/L). Lipid peroxidation has been cited by others as an important component of DHA toxicity, and we confirmed that vitamin E prevents the cytotoxic effects of DHA. Lipid peroxidation was greater following DHA treatment of the sensitive DHL-4 cells than in the resistant SiHa cells, as assessed by thiobarbituric acid reactive substance generation. DHL-4 cells treated with DHA for 20 hours showed a 3.5-fold increase in thiobarbituric acid reactive substances, whereas SiHa cells showed no increase. Reverse transcription-PCR analysis detected a down-regulation of the expression of the major antioxidant enzyme, superoxide dismutase (SOD) 1, in DHL-4 cells but not in SiHa cells after DHA treatment. Knockdown of SOD1 expression in SiHa cells with small interfering RNA significantly enhanced lipid peroxidation and cytotoxicity on exposure to DHA. These results show that DHL-4 cells are highly sensitive to the cytotoxic effect of DHA and that regulation of SOD1 expression may play an important role in determining the sensitivity of different tumor cells to the cytotoxic effects of DHA.
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PMID:Differential sensitivity of cancer cells to docosahexaenoic acid-induced cytotoxicity: the potential importance of down-regulation of superoxide dismutase 1 expression. 1536 5

This study was conducted to determine the antioxidant effects of a Polygonatum extract compared with the major antioxidant, vitamin E, in rabbits fed a high-cholesterol diet. Rabbits were given a high-cholesterol (0.5%, wt/wt) diet with vitamin E (0.03%, wt/wt) or a Polygonatum extract (0.05%, wt/wt) for 8 weeks. The body weight gain (g/week) was only significantly increased only in the high-cholesterol-fed control group, yet the relative liver weight was significantly lower in the Polygonatum group compared with the other groups. The supplementation of vitamin E and Polygonatum extract led to an increase in the hepatic catalase (CAT) activity without any change in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. Hepatic total glutathione content was significantly higher in the Polygonatum group than in the other groups. The level of hepatic mitochondrial H(2)O(2) was significantly lower in the two supplemented groups compared with the control group, whereas the level of cytosolic H(2)O(2) was only significantly lower in the Polygonatum group than in the control group. The level of plasma thiobarbituric acid-reactive substances (TBARS) was only significantly lower in the vitamin E group, whereas the level of hepatic TBARS was slightly lower in the Polygonatum group than in the other groups. In the case of the high-density lipoprotein-related antioxidant enzyme, vitamin E supplementation produced the highest plasma paraoxonase (PON) activity compared with the other groups, although there was no difference in the hepatic PON activity among the groups. Meanwhile, the plasma vitamin E concentration was significantly higher in the vitamin E and Polygonatum groups than in the control group; however, plasma vitamin A concentration did not differ significantly between the groups. As regards the mRNA expressions of hepatic antioxidant enzymes, the vitamin E and Polygonatum extract supplementation had no effect on the SOD, CAT, GSH-Px, and PON mRNA expression. Accordingly, these results indicate that the Polygonatum extract had a positive effect on the antioxidant defense system based on decreasing the content of hepatic TBARS and hydrogen peroxide, increasing the CAT activity and total glutathione level in the liver, and sparing the plasma vitamin E. Thus, further studies on the functional components in Polygonatum extract and their biological efficacies are needed.
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PMID:Polygonatum rhizoma affects antioxidant defense systems without changing mRNA expression in diet-induced hypercholesterolemic rabbits. 1538 32

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

Taking into account the possibility of interaction of immune and antioxidant systems, the aim of this study was to investigate the changes in the parameters of immune and antioxidant systems in patients with cervical cancer and to compare them with the corresponding data obtained from healthy women. Ninety-four women with cervical cancer at II and III stage comprised the patient group and 69 healthy women were taken as the control group. The investigation results showed that the cellular immunity functions of patients with cervical cancer were suppressed in comparison with the same of healthy women. Though with respect to age, in 35-49-year-old women group with cervical cancer, some immune system indices were suppressed (quantity of T-, B-lymphocytes, NK); however in order to maintain the immune homeostasis of the organism other immune system functions were compensatorily stimulated (neutrophils and its phagocytic activity, CD8(+), IgG and IgA concentration were higher). The activity of the antioxidant system in patients with cervical cancer was impaired: the concentration of lipid peroxidation products was increased, the level of the endogenous antioxidant vitamin E and the activity of the antioxidant enzyme superoxide dismutase were decreased in comparison with the control group.
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PMID:[Changes in the parameters of immune and antioxidant systems in patients with cervical cancer]. 1563 Mar 41

The aim of this work was to demonstrate the occurrence of oxidative stress during exhaustive exercise and to determine the antioxidant response. Eight voluntary male subjects participated in this study. The exercise was a cycling mountain stage (171 km) and the cyclists took a mean+/-S.E.M. time of 270+/-12 min to complete it. Blood samples were taken before the cycling stage, immediately after the stage, 3 h after finishing the stage and on the morning of the following day. We determined the activities of erythrocyte antioxidant enzymes, blood levels of oxidised glutathione, plasma levels of antioxidant vitamins and carotenoids, and the serum lipid and cholesterol profile. The mountain cycling stage induced significant increases in catalase and glutathione reductase activities. Significant decreases in glutathione peroxidase activity, both determined with hydrogen peroxide and with cumene hydroperoxide as substrates, were observed. Blood oxidised glutathione and serum uric acid rose after the stage. Plasma vitamin E increased after the stage but dropped to below basal values after 3 h of recovery. Triglycerides and VLDL-cholesterol increased significantly after the stage and remained high 3 h after the cycling stage. The mountain cycling stage induced oxidative stress, as was evidenced by the increases in blood GSSG and in serum urate concentrations and by the pattern of change of erythrocyte antioxidant enzyme activities. A specific utilisation of alpha-tocopherol against oxidative stress during recovery was evidenced.
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PMID:Antioxidant response to oxidative stress induced by exhaustive exercise. 1564


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