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)

We have previously demonstrated that induction of the heat-shock response in rats results in improved recovery of isolated Langendorff-perfused rat hearts subjected to low-flow ischemia followed by reperfusion (Currie et al., 1988). The mechanisms underlying this protective effect of heat-shock are uncertain although the protection was associated with enhanced content of the antioxidant enzyme catalase but not superoxide dismutase or glutathione peroxidase (Currie et al., 1988). Various investigators have suggested the importance of improved energy metabolism in determining recovery following ischemia (Pasque and Wechsler, 1984; Haas et al., 1984; Devous and Lewandowski, 1987). We therefore examined, using a working rat heart model subjected to 10 or 15 min zero flow ischemia whether changes in energy metabolites could account for the protective effect of the heat-shock response. Hearts perfused 24 h after induction of heat-shock failed to demonstrate significant improvement of recovery following 10 min ischemia, however recovery was significantly enhanced in hearts reperfused after 15 min ischemia. Ischemia produced a depression in both ATP and creatine phosphate (CP) content whereas a moderate elevation in ADP and AMP and a marked increase in tissue lactate were evident. These changes were unaffected by prior heat-shock treatment. For both durations of ischemia tissue metabolites were determined during early (5 min) and late (30 min) reperfusion. Although partial recovery in high energy phosphates and a return of ADP, AMP and lactate to near-normal levels were evident, no differences in energy products were observed between hearts from normal or heat-shocked animals, in spite of significantly enhanced recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved post-ischemic ventricular recovery in the absence of changes in energy metabolism in working rat hearts following heat-shock. 223 33

The ethanol-preferring (EP) rats have a higher level of lipid peroxidation in the brain and blood serum than the water-preferring rats. At the same time it was found that EP rats have a decreased antioxidant enzyme activity in the brain tissue (catalase and superoxide dismutase) and blood serum (ceruloplasmin and superoxide dismutase). This antioxidant status can lead to a greater sensitivity of the EP rat brain to ethanol toxicity. The increased catalase activity in blood of EP rats reflects the elevated metabolic tolerance of this group of animals to ethanol.
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PMID:[The characteristics of the enzyme status of the antioxidant protection and the level of lipid peroxidation in the brain tissue and blood of rats with differing preferences for ethanol]. 225 54

Endothelial cells are primary targets for injury by reactive oxygen species. Endothelial catalase, copper-zinc superoxide dismutase (CuZnSOD), and manganous superoxide dismutase (MnSOD) provide potential antioxidant enzymatic defenses against oxidant-induced cellular damage. Previous studies in vivo and in vitro have demonstrated that in certain cell types exposure to oxidants may increase the expression of one or more of these antioxidant enzymes, thus providing greater intracellular potential to withstand oxidant-induced cell stress. To test whether endothelial antioxidant enzyme expression is influenced by similar oxidant-induced stresses in vitro, we have exposed endothelial cells to tumor necrosis factor-alpha (TNF-alpha) and have measured levels of catalase, CuZnSOD and MnSOD mRNA, and protein. Our results demonstrate a selective increase of MnSOD mRNA, with coordinate increases of both MnSOD protein and enzyme activity in endothelial cells treated for 24/h with TNF-alpha. In contrast, levels of catalase and CuZnSOD mRNA and protein remained unchanged in these cells after TNF-alpha treatment. These observations were made in microvessel endothelial cells derived from murine and bovine sources. Our results indicate that TNF-alpha can act specifically to increase enzymatic antioxidant potential in endothelial cells by induction of a particular antioxidant enzyme encoding mRNA species. These data demonstrate the capacity of endothelial cells to mount an antioxidant defense in response to exposure to an inducer of oxidative damage.
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PMID:Expression of bovine and mouse endothelial cell antioxidant enzymes following TNF-alpha exposure. 225

Tracheal insufflation of tumor necrosis factor (TNF) enhances pulmonary antioxidant enzyme activities and protects rats against oxygen toxicity (J. Appl. Physiol. 68: 1211-1219, 1990). We now report that tracheal insufflation of TNF selectively induced pulmonary Mn-superoxide dismutase (SOD) mRNA in normoxia- and hyperoxia-exposed rats, leading to increased amounts of Mn-SOD specific protein and enzyme activity. Tracheal insufflation of TNF had no effect on the levels of pulmonary Cu,Zn-SOD mRNA or specific protein. Hyperoxia alone also selectively induced pulmonary Mn-SOD mRNA. However, the hyperoxia-induced increase in Mn-SOD mRNA was not associated with an increase in Mn-SOD specific protein or enzyme activity. The results suggest that the increased pulmonary Mn-SOD in TNF-insufflated rats may contribute to the TNF-induced protection against oxygen toxicity.
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PMID:Molecular basis for tumor necrosis factor-induced increase in pulmonary superoxide dismutase activities. 226 Jun 78

The changes in lipid peroxides (LP) content and antioxidant enzyme activities were investigated on airway surface during the aggravating process of bronchitis induced by SO2 exposure in rats. LP content in broncho-alveolar lavage fluid (BALF) has gradually increased from 3 weeks after starting of SO2 exposure. Whereas, the activities of antioxidant enzymes, superoxide dismutase and glutathione peroxidase, increased at 1 week and then gradually reduced from 3 weeks. The ratio of LP to each antioxidant enzyme activity in BALF of the exposed rats was higher than that of normal rats. Morphological changes of the lung, a decrease of PaO2 and an increase of PaCO2 of blood depended on the increase of LP on airway surface. These findings indicate that LP may be involved in the development of bronchitis.
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PMID:[Changes in lipid peroxides content and antioxidant enzyme activities on airway surface in SO2-induced bronchitic rats]. 227 53

Treatment with endotoxin protects rats against lung injury during hyperoxia (greater than 98% oxygen at 1 atmosphere absolute for 60 h). This study demonstrates that serum from endotoxin-treated donor rats also protects recipients from oxygen toxicity. Rats treated with serum from saline-treated donors were not protected, and protection was not explained by residual endotoxin in protective sera. Unlike endotoxin-protected rats (where lung antioxidant enzyme activity is elevated after hyperoxia), postexposure superoxide dismutase (SOD) and catalase (CAT) activities in the lungs of serum-protected rats were not affected. Levels of tumor necrosis factor (TNF) and interleukin 1 (IL-1) in protective sera were increased. This study demonstrates that increases in lung SOD and CAT activity are not required for endotoxin protection from hyperoxia and suggests that TNF and IL-1 may participate in the mechanism of endotoxin protection.
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PMID:Endotoxin protection of rats from pulmonary oxygen toxicity: possible cytokine involvement. 231 67

Preexposure of male Lewis rats to Cd aerosols (1.6 mg Cd/m3, 3 hr/day, 5 days/week, for 4 weeks) has been found to produce a marked degree of tolerance to hyperoxia (greater than 96% O2). Cd-pretreated animals were still alive after 8 days of continuous exposure to oxygen. In contrast, hyperoxia was fatal to all air-preexposed animals within 54-62 hr. Lungs of Cd-pretreated animals were characterized by hyperplasia and/or hypertrophy of the type II alveolar cell compartment which may have enabled them to more rapidly repair oxidant damage resulting from hyperoxia. Cd pretreatment augmented enzymatic antioxidant enzyme activities, including total lung Se-dependent glutathione peroxidase, catalase, glutathione reductase, and Mn-superoxide dismutase, and caused elevations in pulmonary nonprotein thiols and metallothionein (MT). MT, a thiol-rich, low-molecular-weight protein, was 400-fold higher in Cd-pretreated animals and bound more than 80% of the total Cd in the lung. We have hypothesized that MT serves as an expendable yet renewable cellular target for free radical damage during oxygen exposure. A systemic acute-phase response, characterized by alterations in plasma Zn and Cu concentrations and increased ceruloplasmin oxidase activity, was initiated in Cd-pretreated animals by the fourth day of hyperoxia. This response was accompanied by improvement in pulmonary status and extensive pulmonary repair.
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PMID:Cross-tolerance to hyperoxia following cadmium aerosol pretreatment. 233 May 88

Maximal activities of antioxidant enzymes involved in oxygen free radical metabolism in skeletal muscle and liver were investigated in 4-, 26-, and 31-mo-old male Wistar-Furth rat at rest and after a single bout of treadmill exercise. In skeletal muscle, cytosolic (Cu-Zn) and mitochondrial (Mn) superoxide dismutase (SOD) specific activities were significantly higher in the aged rats and at 31 mo reached 135 and 218%, respectively, of those at 4 mo. Resting catalase activity was doubled at 31 mo compared with that at 4 mo. Glutathione peroxidase (GPX) activity increased twofold in muscle cytosol and by 47% in mitochondria of aged rats. Glutathione S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G-6-PDH) activities in muscle were also significantly elevated. Hepatic antioxidant enzymes were altered differentially with aging. Cytosolic SOD and GST activities were decreased, whereas mitochondrial GPX, GR, and G-6-PDH activities were increased. Lipid peroxidation was greater in skeletal muscle homogenate and mitochondria but lower in liver homogenate in the aged rats. An acute exercise bout had little effect on muscle or liver antioxidant enzymes regardless of the animal's age. It is concluded that aging is accompanied with an elevation of antioxidant enzyme activities and lipid peroxidation in skeletal muscle probably due to the increased oxygen free radical production and reaction.
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PMID:Alteration of antioxidant enzymes with aging in rat skeletal muscle and liver. 233 Oct 35

Cultured pneumocytes, prepared from fetal rat lung, are growth inhibited and have increased lactate dehydrogenase release and prostaglandin synthesis in response to 50 and 95% O2 exposure. The uptake of cationic liposomes by these fetal cells is more rapid and extensive than is the case with cultured adult pneumocytes. Protection of fetal pneumocytes against the cytotoxic effects of 50 or 95% O2 by liposome-entrapped antioxidant enzymes requires a liposome phospholipid concentration of only 1 nmol/cm2, compared with 45 nmol/cm2 for adult cells, which is a cytotoxic phospholipid concentration for the fetal cells. Despite this capacity of low concentrations of liposomes containing superoxide dismutase and catalase to increase endogenous antioxidant enzyme content, and to protect against cell death, such treatment does not attenuate O2-mediated alterations of cell growth or prostaglandin release. Inhibition of pneumocyte DNA synthesis, by elevated O2 concentrations, cannot be attributed to an autocrine effect of enhanced prostaglandin synthesis, because the addition of 50 microM ibuprofen to inhibit prostaglandin synthesis does not prevent O2-mediated effects on DNA synthesis.
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PMID:Liposome-mediated augmentation of antioxidant defenses in fetal rat pneumocytes. 233 78

Tracheal insufflation of tumor necrosis factor (TNF; 5 micrograms or 1.2 x 10(5) U) markedly enhanced the survival of adult rats exposed to 100% O2: 12 of 17 rats (71%) survived for greater than 11 days, whereas 30 of 30 control (Hanks' balanced salt solution) insufflated rats (100%) died within 3 days of O2 exposure. Insufflation of gamma-interferon (5 micrograms) or intraperitoneal injection of up to 40 micrograms TNF did not afford any protection. At 55 h after O2 exposure, TNF-insufflated rats showed less pulmonary edema, as determined by the extravascular lung water content-to-bloodless lung dry weigh ratio and less alveolar capillary leak as determined by the protein content in the bronchoalveolar lavage fluid, than control insufflated rats similarly exposed. This protection against O2 toxicity by TNF insufflation was associated with increased lung superoxide dismutase, catalase, and glutathione peroxidase activities. The enhancement of lung antioxidant enzyme activities was noted at 55 h of O2 exposure, when control animals began to die of O2 toxicity. This temporal relationship suggests that TNF-induced increase in antioxidant enzyme activities contributes, at least in part, to the observed protection.
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PMID:Tracheal insufflation of tumor necrosis factor protects rats against oxygen toxicity. 234 45


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