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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antioxidant enzyme activities, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and total glutathione concentration were determined in guinea pig lung and liver over the final period of gestation (days 50-68) and at several ages post-partum. Pulmonary antioxidant capacity increased markedly over the final days of gestation, individual changes ranging from 29% (glutathione) to 198% (GSH-Px). Liver antioxidant capacity was always 4-fold to 10-fold greater than that of the lung and exhibited very similar developmental profiles to those observed in the lung. From day 60 gestation to term (68 days), activity of the liver antioxidants increased, ranging from 246% (CAT) to 610% (glutathione). A number of antioxidants in both lung and liver exhibited either immediate pre- or post-birth decreases in activity. These falls could not be attributed to the way in which the results were expressed: i.e. they were similar, expressed per unit DNA, per unit protein, or per g wet wt. Following birth, liver antioxidant capacity increased such that the highest enzyme activities or glutathione concentration were recorded at 66 days post-partum. In lung, only Mn-SOD and glutathione exhibited higher levels at 66 days postpartum than at birth. In combination, these results of pulmonary and hepatic antioxidant enzyme activity indicate that the lung is not unique in acquiring increased antioxidant protection in the final period of gestation. They also suggest that a tissue's antioxidant requirement is dictated more by metabolic rate (hence free radical production) than incident partial pressure of oxygen.
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PMID:Developmental expression of antioxidant enzymes in guinea pig lung and liver. 235 Oct 72

Tissues from adult Syrian hamsters were studied with immunoperoxidase techniques using polyclonal antibodies to three antioxidant enzymes (copper, zinc and manganese forms of superoxide dismutase, and catalase). Tissues from labile organs, in which cell renewal is prominent (uterus, intestine, and transitional epithelium of the urinary tract), showed strong antioxidant enzyme immunostaining in differentiated cells but not in stem cells. In stable organs, in which cell renewal occurs at a high rate only in response to injury (kidney and adrenal), each cell type showed a specific pattern of antioxidant enzyme immunostaining. In permanent organs (brain and heart), antioxidant enzymes were regionally specific markers. Axons of the cerebellum showed more intense antioxidant enzyme staining than those of the cerebral cortex; in the heart, atria stained more intensely than ventricles. Germ cells of the testis resembled cell renewal systems in their antioxidant enzyme-immunostaining pattern: spermatogonia were negative, whereas spermatozoa were strongly positive. The tubules of the kidney showed no antioxidant enzyme immunostaining until after birth. Our results suggest that there is a prominent role for antioxidant enzymes in cell differentiation during development and cell renewal.
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PMID:Immunohistochemical localization of antioxidant enzymes in adult Syrian hamster tissues and during kidney development. 237 42

The purposes of this study were to determine whether exercise training induces increases in skeletal muscle antioxidant enzymes and to further characterize the relationship between oxidative capacity and antioxidant enzyme levels in skeletal muscle. Male Sprague-Dawley rats were exercise trained (ET) on a treadmill 2 h/day at 32 m/min (8% incline) 5 days/wk or were cage confined (sedentary control, S) for 12 wk. In both S and ET rats, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities were directly correlated with the percentages of oxidative fibers in the six skeletal muscle samples studied. Muscles of ET rats had increased oxidative capacity and increased GPX activity compared with the same muscles of S rats. However, SOD activities were not different between ET and S rats, but CAT activities were lower in skeletal muscles of ET rats than in S rats. Exposure to 60 min of ischemia and 60 min of reperfusion (I/R) resulted in decreased GPX and increased CAT activities but had little or no effect on SOD activities in muscles from both S and ET rats. The I/R-induced increase in CAT activity was greater in muscles of ET than in muscles of S rats. Xanthine oxidase (XO), xanthine dehydrogenase (XD), and XO + XD activities after I/R were not related to muscle oxidative capacity and were similar in muscles of ET and S rats. It is concluded that although antioxidant enzyme activities are related to skeletal muscle oxidative capacity, the effects of exercise training on antioxidant enzymes in skeletal muscle cannot be predicted by measured changes in oxidative capacity.
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PMID:Skeletal muscle oxidative capacity, antioxidant enzymes, and exercise training. 238 14

Instillation of intratracheal surfactant is known to limit the morbidity and mortality of patients and animals with oxidant-induced lung injury. In this study we quantified the antioxidant properties of natural lung surfactant (NLS), consisting of 90% lipid and 10% protein, and of calf lung surfactant extract (CLSE) consisting of 99% lipid and 1% protein. NLS, but not CLSE, contained significant amounts of superoxide dismutase (SOD) and catalase activities (7 U SOD/mumol phospholipid (PL) and 1 U catalase/mumol PL). More than 90% of the SOD activity was abolished by 1 mM KCN, suggesting that this was the CuZn form of the enzyme. In addition, NLS significantly reduced extracellular H2O2 without losing its ability to reach minimum surface tensions below 1 dyn/cm upon dynamic compression. The NLS scavenging of H2O2 could not be accounted for by albumin. The presence of catalase and SOD activities in NLS was also verified by activity stains of proteins separated by native polyacrylamide gel electrophoresis. Intratracheal instillation of 7 ml of NLS (308 mumol PL) into rabbits significantly increased SOD content in type II cells isolated 12 h later. It is concluded that, in addition to promoting alveolar stability, instillation of pulmonary surfactant may offer significant protection to the alveolar epithelium by scavenging extracellularly generated partially reduced oxygen species and by enhancing intracellular antioxidant enzyme content.
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PMID:Characterization of antioxidant activities of pulmonary surfactant mixtures. 239 61

Longitudinal studies were carried out over 55 weeks in vitamin E deficient and control rats. It was shown that neurological tissues (brain, cord and nerve) retained a greater percentage of vitamin E (alpha-tocopherol) than other tissues (serum, liver and adipose tissue), and that there was no evidence for compensation by other antioxidant enzyme systems (superoxide dismutase and glutathione peroxidase). An increased uptake of alpha-[3H]tocopherol (150% of controls) was observed in peripheral nerve of deficient animals from 11 weeks, whereas similar increases were not found in brain and cord until 36 weeks. These results were correlated with tests of neurological function which included electrophysiological studies and measurement of axonal transport. Recordings of somatosensory evoked potentials showed a significant delay (P less than 0.001) of central conduction velocity after 40 weeks of deficiency, whereas peripheral conduction was unchanged. After 40 weeks of deficiency, abnormal electromyographic activity of the hind limbs was obtained which was suggestive of chronic partial denervation. By 52 weeks there were significant reductions of both fast anterograde (P less than 0.02) and retrograde (P less than 0.05) transport of acetylcholinesterase in the deficient rats.
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PMID:Longitudinal studies of the neurobiology of vitamin E and other antioxidant systems, and neurological function in the vitamin E deficient rat. 246 31

1. A number of dietary sugars are known to mediate the effects of copper deficiency. The effects of lactose (compared with sucrose) and a dietary Cu deficiency on hepatic and cardiac antioxidant enzyme activities and tissue mineral element status were investigated in the rat. 2. Groups (n 6) of male weanling Wistar rats were provided ad lib. with deionized water and diets containing sucrose (580 g/kg) or sucrose and lactose (387 g/kg and 193 g/kg respectively) with either control (12.0 mg/kg) or deficient (1.5 mg/kg) quantities of Cu for 77 d. 3. Animals consuming the low-Cu diets exhibited significantly decreased tissue Cu levels (P less than 0.01), hepatic and cardiac cytochrome c oxidase (EC 1.9.3.1, CCO) activities (P less than 0.01 and P less than 0.001 respectively) and hepatic Cu-zinc superoxide dismutase (EC 1.15.1.1, CuZnSOD) activity (P less than 0.05). The low-Cu diets also significantly decreased cardiac manganese superoxide dismutase (EC 1.15.1.1, MnSOD), catalase (EC 1.11.1.6) and glutathione peroxidase (EC 1.11.1.9, GSH-Px) activities (P less than 0.01, P less than 0.05 and P less than 0.001 respectively). 4. Hepatic Mn was significantly increased in both lactose-fed (P less than 0.001) and Cu-deficient (P less than 0.01) animals. These increases were unrelated to hepatic MnSOD activity. Cardiac Zn was significantly (P less than 0.01) increased in Cu-deficient animals. 5. Lactose feeding resulted in significantly increased cardiac CCO activity (P less than 0.001) but significantly decreased hepatic CuZnSOD (P less than 0.05), catalase (P less than 0.01) and GSH-Px (P less than 0.001) activities. 6. The activities of lactose dehydrogenase (EC 1.1.1.27, LDH) and glucose-6-phosphate dehydrogenase (EC 1.1.1.49, G6PDH) were found to be significantly (P less than 0.05 and P less than 0.01 respectively) increased in Cu-deficient animals and G6PDH activity was significantly (P less than 0.01) decreased as a result of lactose consumption. 7. The observed changes in antioxidant enzyme activities associated with both Cu deficieny and lactose consumption may have important implications for the development of free radical mediated cell damage. However, no significant differences in either hepatic or cardiac levels of thiobarbituric acid reactive substances, a measure of lipid peroxidation, were found.
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PMID:Effects of copper deficiency on hepatic and cardiac antioxidant enzyme activities in lactose- and sucrose-fed rats. 253 51

Asbestos resembles the phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA), in its ability to elicit release of superoxide (O2-.) from rodent alveolar macrophages (AM) in vitro. In addition, superoxide dismutase (SOD), the antioxidant enzyme scavenging O2-, is increased in cultures of tracheobronchial epithelial cells and lung fibroblasts after exposure to either crocidolite or chrysotile asbestos. Our objectives here were to determine: (1) the chemical and physical properties of asbestos important in the generation of O2- from rat AM; and (2) the effects of O2- in comparison with asbestos on biosyntheses of collagen and non-collagen protein in rat lung fibroblasts in vitro. We were also interested in whether increased production of SOD occurred in the lungs of rats after inhalation of crocidolite asbestos. To determine whether O2- was elicited in response to a variety of asbestiform fibres, AM lavaged from Fischer 344 rat lungs were exposed in vitro to equivalent non-toxic amounts of crocidolite asbestos, erionite, Code 100 fibreglass, sepiolite, and their non-fibrous analogues, riebeckite, mordenite and glass particles. In addition, sized preparations of long (greater than 10 microns) and short (less than 2 microns) asbestos were introduced at identical concentrations to determine whether length of fibres is critical in O2- release. The amount of O2- released from AM in response to dusts was then determined by measuring SOD-inhibitable reduction of cytochrome C. All asbestiform fibres caused a significant (p less than 0.05) increase in generation of O2- from epithelial cells, whereas non-fibrous particles were less active at comparable concentrations. Experiments with long (greater than 10 microns) versus short (less than 2 microns) chrysotile showed that long fibres caused a more striking, dosage-dependent release of O2-. To determine whether O2- plays a role in the causation of fibrotic lung disease, rat lung fibroblasts were exposed to a biochemical generation system (xanthine-xanthine oxidase) for O2- before quantitation of cell-associated collagen and non-collagen protein at 24, 48 and 72 h thereafter. At the latter time periods, significant increases in total collagen per ng DNA were observed. In comparison with controls, the generation system for O2- also caused an initial decrease in synthesis of non-collagen protein followed by increases in synthesis of non-collagen protein at 48 and 72 h.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mechanisms of fibre-induced superoxide release from alveolar macrophages and induction of superoxide dismutase in the lungs of rats inhaling crocidolite. 254 20

Variations in superoxide dismutase, catalase and glutathione peroxidase activity were studied in fibroblasts cultured in the presence of hydralazine, a drug known to be an inducer of the so-called collagen-like syndrome. The results demonstrated that both superoxide dismutase and catalase undergo a marked decrease in their activity, whereas glutathione peroxidase manifests a significant increase in its activity after treatment with hydralazine as compared to control cell cultures. Also the lipid peroxide concentration as expressed by the malondialdehyde amount was estimated in the above cultures. The altered antioxidant enzyme activity and the presence of byproducts of free radical damage support the possibility that the action of hydralazine leading to the pathogenesis of collagen disease-like syndrome involves an abnormal free-radical metabolism.
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PMID:Activities of antioxidant enzymes in fibroblasts cultured in vitro in the presence of hydralazine. 261 21

Pretreatment with the combination of tumor necrosis factor/cachectin (TNF/C) and interleukin 1 (IL-1) increased glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), glutathione peroxidase (GPX), catalase (CAT), and superoxide dismutase (SOD) activities in lungs of rats continuously exposed to hyperoxia for 72 h, a time when all untreated rats had already died. Pretreatment with TNF/C and IL-1 also increased, albeit slightly, lung G6PDH and GR activities of rats exposed to hyperoxia for 4 or 16 h. By comparison, no differences occurred in lung antioxidant enzyme activities of TNF/C and IL-1- or saline-pretreated rats exposed to hyperoxia for 36 or 52 h; the latter is a time just before untreated rats began to succumb during exposure to hyperoxia. The results raise the possibility that TNF/C and IL-1 treatment can increase lung antioxidant enzyme activities and that increased lung antioxidant enzymes may contribute to the increased survival of TNF/C and IL-1-pretreated rats in hyperoxia for greater than 72 h.
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PMID:Cytokines increase rat lung antioxidant enzymes during exposure to hyperoxia. 265 81

Recent data available in literature on mechanisms for regulation of the activity of superoxide dismutase (an antioxidant enzyme) and its interrelation to other enzymes and antioxidants are generalized. The role of superoxide dismutase in the ontogenesis and under different pathologies accompanied by the formation of free radicals is considered.
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PMID:[The biological role of superoxide dismutase]. 265 28


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