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)

Endotoxin treatment in normal rats has a marked protective effect against O2 toxicity (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47: 577-581, 1979 and 51: 577-583, 1981), and endotoxin's protective action is associated with stimulation of the lung's enzymatic antioxidant defense system (superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase). Vitamin E-deficient animals are especially sensitive to hyperoxidant stresses, including pulmonary O2 toxicity. In these studies we tested whether endotoxin could reverse the increased susceptibility of vitamin E-deficient rats to hyperoxic challenge. We found that untreated vitamin E-deficient rats do succumb more readily to O2 toxicity [0/11 alive at 72 h in greater than 95% O2, lethal time for 50% of the animals (LT50) = 50 h] than rats fed a regular diet (4/14 alive, LT50 = 69 h). In contrast, 15 of 16 vitamin E-deficient rats treated with endotoxin survived the same O2 exposures (P less than 0.001) and showed significantly reduced pulmonary edema compared with the other groups. The endotoxin-treated vitamin E-deficient group was also the only one to demonstrate significant elevations of all the antioxidant enzymes during O2 exposure, suggesting that the antioxidant enzyme defenses of the lung have a more primary and important role in prevention of O2-induced lung injury than the lipid-associated antioxidant, vitamin E.
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PMID:Endotoxin treatment protects vitamin E-deficient rats from pulmonary O2 toxicity. 638 80

The effects of oxygen inhalation for 48 h on the antioxidant capacity of lungs, livers, and brains in normal and vitamin E-deficient rats at various ages were examined. The activity levels of catalase, glutathione peroxidase, and superoxide dismutase, and the level of vitamin E in tissue homogenates were assayed as the indices of antioxidant capacity. Oxygen inhalation mostly decreased antioxidant enzyme activity in lungs. In particular, the catalase activity was much decreased. The glutathione peroxidase activity tended to be decreased. The superoxide dismutase activity was decreased in 32-month-old rats. Vitamin E deficiency did not augment oxidative damage due to oxygen inhalation. There appears to be no age effect on the oxygen-induced decrease in the antioxidant enzyme activities of lungs, except the superoxide dismutase activity in very old rats. Oxygen inhalation had some effects on the antioxidant capacity of livers and brains. For example, oxygen inhalation decreased the vitamin E concentration of livers in 32-month-old, normal rats. These results suggest that the antioxidant capacity of lungs is directly damaged by oxygen inhalation and that the antioxidant capacity of livers and brains is indirectly affected through lung damage. Antioxidant capacity may be maintained without large variation during young and middle ages, but its redundancy for emergency use may be diminished in old age.
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PMID:Effects of oxygen inhalation on the antioxidant capacity of lungs, livers, and brains in normal and vitamin E-deficient rats at various ages. 761 20

Several studies have described the determination of selenium in protein extracts from tissues of marine or terrestrial animals, but have not identified the different chemical forms of selenium that are present. Selenium may be present as seleno-amino acids. Selenocysteine, for example, is a normal component of glutathione peroxidase, an antioxidant enzyme which may behave like other antioxidants, such as vitamin E, protecting tissues against methylmercury toxicity. The present study illustrates a method for the characterization of seleno-amino acids, such as selenocysteine and selenomethionine, in proteins extracted from the liver of marine mammals. The mechanism of detoxification of methylmercury, which involves seleno-compounds, is identified. The analytical determination was carried out using high-performance anion-exchange chromatography coupled with integrated pulsed amperometric detection (HPAEC-IPAD). This method allows the direct determination of underivatized amino acids, eliminating the procedure of pre- or postcolumn derivatization. The chromatographic separation was carried out on an anion-exchange column using a quaternary gradient elution. In order to optimize this method, interferences of amino acids and the influence of pH and ionic strength on the separation and electrochemical detection were studied. The IPAD response for the direct detection of amino acids is optimum at pH > 11. The detection limit (S/N = 3) for selenocysteine was found to be 450 micrograms/l. The application of this method for the identification of seleno-amino acids in protein hydrolysates is also shown.
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PMID:Direct determination of seleno-amino acids in biological tissues by anion-exchange separation and electrochemical detection. 764 Jul 74

The goal of this study was to determine to what extent aging affects the antioxidant defense system of the rat adrenal and to evaluate the impact of any change in this system on the recognized age-related decline in steroidogenic capacity of adrenocortical cells. The studies were conducted on young (2-5 mo) and aging (12-27 mo) Sprague-Dawley rats and involved procedures measuring steroidogenesis; oxidative damage to tissue; non enzymatic antioxidants such as vitamin C, E, and glutathione; and tissue antioxidant enzyme (Mn and CuZn superoxide dismutases, catalase, and glutathione peroxidase) activity and expression (mRNA, protein mass, and location). Some measurements were made also on rats maintained on vitamin E-deficient diets. The data show that adrenals from young animals are especially well protected against oxidative events; i.e., these adrenals show the least endogenous lipid peroxidation and the highest level of resistance to prooxidant-induced damage (of various tissues measured) and show exceedingly high levels of tissue antioxidants. Aging, on the other hand, results in oxidative changes in adrenal tissue that are generally linked in time to a reduction in efficiency of the normally protective antioxidant defense system and to the decline in corticosterone production. We speculate that these events are causally related, i.e., that the age-related reduction in oxidative mechanisms in adrenal tissues leads to oxidative damage of membrane or cytosolic factors important to cholesterol transport, and, as a consequence of this damage, cholesterol cannot reach appropriate mitochondrial cholesterol side chain cleavage sites, and corticosterone production fails.
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PMID:Alteration of the adrenal antioxidant defense system during aging in rats. 765 14

The debilitating consequences of age-related brain deterioration are widespread and extremely costly in terms of quality of life and longevity. One of the potential major causes of age-related destruction of neuronal tissue is toxic free radicals that are a natural result of aerobic metabolism. The brain is particularly susceptible to free radical attack because it generates more of these toxicants per gram of tissue than does any other organ. The major defense mechanisms the brain uses to combat reducing equivalents is via their enzymatic metabolism. The vitamin antioxidants, vitamin E (alpha-tocopherol in particular) and vitamin C (ascorbate), also aid in protecting the brain from oxidative stress by directly scavenging toxic radicals. A newly discovered, potentially highly important antioxidant in the brain is the indole melatonin. The pineal hormone melatonin is rapidly taken up by the brain. In vitro melatonin is more effective than glutathione in scavenging the highly toxic hydroxyl radical and also more efficient than vitamin E in neutralizing the peroxyl radical. Furthermore, it stimulates the main antioxidant enzyme of the brain, glutathione peroxidase. In vivo melatonin is a potent antioxidant and it lacks prooxidant actions.
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PMID:Oxidative processes and antioxidative defense mechanisms in the aging brain. 773 61

Human fibroblasts (HFW) were 10-fold more susceptible than Chinese hamster ovary (CHO-K1) cells to sodium arsenite. Comparison of cellular antioxidant enzyme activities showed that CHO-K1 cells contained 3- and 8-fold more glutathione-peroxidase and catalase activities, respectively, than HFW cells. Since vitamin E, methylamine, and benzyl alcohol could prevent, in part, the arsenite-induced killing of HFW cells, we suggest that arsenite can induce oxidative damage in HFW cells. We have also established arsenic-resistant cells, SA7 and CL3R, from CHO cells and from a human lung adenocarcinoma cell line (CL3), respectively. The arsenic resistance of SA7 cells was attributed mainly to elevation of glutathione S-transferase pi levels, and that of CL3R cells was possibly due to an increase in heme oxygenase activity. Since induction of heme oxygenase is a general response to oxidative stress, we suspect that the differential toxicity of arsenic to human and animal cells could be due to arsenic's more efficient induction of oxidative damage in human cells.
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PMID:Differential cytotoxic effects of arsenic on human and animal cells. 784 80

The effects of endurance training on tissue antioxidant and oxidative enzyme activities were determined in heart, liver, and five skeletal muscles of female rats. Rats were fed either normal (+E) or vitamin E free (-E) diets for 16 wk. For the final 8 wk, subgroups of +E and -E diet animals were trained by treadmill running at 40 m.min-1, 15% grade for 60 min.d-1. No significant differences in training abilities were observed between diet groups. Endurance training significantly increased citrate synthase (CS) activity in all skeletal muscles for both the +E and -E diet animals with no significant difference in degree of response between diet groups. Neither vitamin E deprivation, training, or their combination generally affected the activities of the antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), or glutathione peroxidase (GPX) in skeletal muscles, heart, or liver of the animals. These results suggest that despite an anticipated increase in free radical induced tissue "oxidative stress" brought about by a combination of vitamin E deprivation and endurance training, antioxidant enzyme adaptations were not evident and the response of citrate synthase to training was not impaired in female rats.
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PMID:Antioxidant and oxidative enzyme adaptations to vitamin E deprivation and training. 818

Feeding diets depleted of vitamin E and Se to cattle can induce a disease known as nutritional degenerative myopathy. It is believed that an increased peroxidative challenge in muscle is involved in the pathogenesis of this disease. A number of species can up-regulate the activity of some antioxidant enzymes, including glutathione reductase (EC 1.6.4.2), glutathione transferase (EC 2.5.1.18), glucose-6-phosphate dehydrogenase (EC 1.1.1.49), catalase (EC 1.11.1.6), and superoxide dismutase (EC 1.15.1.1), in an attempt to mitigate the effects of a peroxidative challenge. A 2 x 2 factorial study was set up to examine possible changes in the activities of these antioxidant enzymes in muscles of ruminant calves fed on diets low in either vitamin E or Se. Four groups of four calves each were fed on a basal diet of NaOH-treated barley which was supplemented with alpha-tocopherol or Se or both for a total of 50 weeks. Calves fed on diets depleted of vitamin E, but not those fed on diets low in Se, developed subclinical myopathy, as judged by increases in the activity of plasma creatinine kinase (EC 2.7.3.2), and had increased muscle concentrations of two indices of lipid peroxidation, namely thiobarbituric acid-reactive substances, with and without ascorbate activation. Feeding diets depleted of vitamin E and diets low in Se both increased muscle activities of glucose-6-phosphate dehydrogenase in heart, biceps and supraspinatus. This change may have occurred in an attempt to maintain intracellular pools of reduced glutathione. No other changes in antioxidant enzyme activity were observed.
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PMID:Antioxidant enzyme activity in the muscles of calves depleted of vitamin E or selenium or both. 826 Apr 86

Ultraviolet B radiation (UVB) induces oxidative damage in DNA, resulting in the formation of the adduct 8-hydroxydeoxyguanosine. Previous studies from this laboratory have demonstrated a decrease in antioxidant enzyme defenses after UVB radiation in Skh: HR-1 hairless mice, implicating antioxidant status in protection against oxidative damage. The present study was undertaken to examine mechanisms of UVB damage to DNA and modulation by vitamin C, selenite, or Trolox, a water-soluble vitamin E analog. BALB/c MK-2 mouse keratinocytes were exposed to a dose range of UVB from 4 to 750 mJ/cm2. DNA damage in the form of 80 HdG was measured using high-pressure liquid chromatography coupled with electrochemical and UV absorbance detection. Preincubation of the cells for 2 days with 0.4 or 0.8 microgram/ml ascorbic acid, 10 or 20 micrograms/ml Trolox, and 5 or 12.5 microM selenite resulted in a significant decrease in the number of 8-hydroxydeoxyguanosine adducts per 10(5) deoxyguanines induced by 500 mJ/cm2 UVB. The results indicate a potential role for antioxidant nutrients in protection against UVB damage to skin cells.
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PMID:Antioxidant nutrients protect against UVB-induced oxidative damage to DNA of mouse keratinocytes in culture. 861 44

We investigated the effects of chronic volume overload in the absence or presence of vitamin E supplements on the cardiac function and contractility, cardiac malondialdehyde (MDA)--a lipid peroxidation product--cardiac antioxidant enzyme activity and antioxidant reserve in canine model. The dogs were divided into three groups of seven dogs each: group I, control; group II, mitral regurgitation (MR) of 4 months duration; and group III, MR of 4 months duration receiving vitamin E (40 U/kg/daily) orally. MR was created by detaching two or more chordae tendinae to raise left atrial pressure to 2.5 to three times normal. MR produced a decrease in the index of myocardial contractility with little change in myocardial function. Decrease in myocardial (left and right ventricles) contractility was associated with an increase in cardiac MDA, and a decrease in cardiac antioxidant reserve and antioxidant enzyme activity. Prevention of volume overload-induced decrease in myocardial contractility by vitamin E was associated with a decrease in cardiac MDA and an increase in cardiac antioxidant reserve and glutathione peroxidase activity towards control levels. Superoxide dismutase and catalase activity remained depressed in vitamin E-treated group. The results indicate that chronic volume overload decreases the contractility of both right and left ventricles and is associated with oxidative stress in both ventricles. These results support the hypothesis that oxygen free radicals are involved in the chronic volume overload-induced cardiac depression.
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PMID:Oxidative stress as a mechanism of cardiac failure in chronic volume overload in canine model. 872 69


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