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)

Relative cell survival and activity of the free radical scavenging enzymes superoxide dismutase, catalase, and glutathione peroxidase were measured in cloned normal (MEA) and SV40-transformed (SVMEA) mouse embryo cells exposed at 44 degrees C for 0-3 h. At 37 degrees C, all three enzymes were 2-5 times higher in MEA than in SVMEA. Hyperthermia did not significantly alter enzyme levels in either cell line but selectively reduced transformed cell survival to less than 5% while relative survival of normal cells remained above 75%. The latter, however, could be reduced to 25% when normal cells were pretreated with 3 mM diethyldithiocarbamate, an inhibitor of copper- and zinc-containing superoxide dismutase. Similar treatment rendered SVMEA extremely thermosensitive. On the other hand, sublethal heat treatment (15 min at 45 degrees C) of cultured cells resulted in a relative thermal resistance upon subsequent exposure to 45 degrees C for 1-4 h. This induced thermotolerance was associated with a rise in antioxidant enzyme levels and both became significant only 4-6 h after the initial heat treatment. Induced enzyme and thermotolerance levels in transformed cells remained, nonetheless, far below those of normal cells. The data show that inherent (in MEA) as well as induced (in SVMEA) thermotolerance is associated with high antioxidant enzyme levels while the reverse is true in the case of inherent (in SVMEA) and induced (in MEA) thermosensitivity. These findings suggest that increased production of oxygen free radicals may be involved in hyperthermic cell injury, which then becomes a function of basal or inducible levels of antioxidant enzymes. Induction of the latter by hyperthermia is apparently inefficient in transformed cells making them more vulnerable. Enzyme induction seems also to require a lag period of 4-6 h suggesting the possible involvement of an intermediate inducer(s) at molecular level. The so-called heat shock proteins may be candidates for such a role.
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PMID:Antioxidant enzymes and survival of normal and simian virus 40-transformed mouse embryo cells after hyperthermia. 303 17

Preexposure of rats to sublethal levels of hyperoxia or ozone reduces morbidity and mortality when the animals are subsequently exposed to lethal levels of either oxidant stress. Lung homogenates and isolated type II pneumocytes from rats exposed to these oxidant stresses demonstrate enhanced antioxidant enzyme activities. Antioxidant enzymes, superoxide dismutase, catalase, and glutathione peroxidase are responsible for the detoxification of partially reduced oxygen species, superoxide and hydrogen peroxide, to less reactive states. Potential pulmonary cellular loci of partially reduced oxygen include mitochondrial NADH dehydrogenase, endoplasmic reticulum-derived NADPH cytochrome c reductase, and cytosolic xanthine oxido reductase. Thus partially reduced oxygen species are hypothesized to mediate hyperoxia and ozone-induced pulmonary damage. This damage may be attenuated by enhanced intracellular antioxidant enzyme activities. Pharmacologic augmentation of pulmonary antioxidant enzymes may be accomplished via intratracheal or intravascular delivery of liposomes containing antioxidant enzymes. Rats pretreated with liposomes containing both superoxide dismutase and catalase, when subsequently exposed to lethal levels of hyperoxia, demonstrate enhanced survival compared with control animals or with animals treated with control liposomes or native antioxidant enzymes. Finally, knowledge obtained from in vitro investigations optimizing liposomal delivery to specific pulmonary cell types may further aid in reducing in vivo pulmonary damage to hyperoxia and ozone.
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PMID:Pulmonary metabolism of reactive oxygen species. 306 93

In this study enzyme glutathione peroxidase was localized in ocular tissue of Lewis rats using the peroxidase antiperoxidase immunohistochemical technique. Antisera to glutathione peroxidase was raised in a rabbit. Immunoreactive glutathione peroxidase was found to be distributed predominantly in the corneal epithelium and endothelium, choroid, inner segment of photoreceptors and retinal pigmented epithelium. Its presence in these sites suggests an adaptation to oxidative stress where this antioxidant enzyme along with other antioxidant systems serves to prevent damage.
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PMID:Immunohistochemical localization of glutathione peroxidase in ocular tissue. 306 81

Serum levels of the trace metals copper, zinc, and selenium were measured in premature infants. White blood cell glutathione peroxidase and superoxide dismutase levels were measured in conjunction with the trace metals. Three groups of infants were evaluated: group I was relatively healthy, group II were infants with stage 2 bronchopulmonary dysplasia (BPD) or less, group III were infants with stage 3 BPD or worse. Zinc and selenium levels declined in all groups during conventional parenteral nutrition (TPN) regimens, while copper remained stable. Copper did decline in groups I and II coincident with an acceleration in growth rate. An expected rise in antioxidant enzyme levels in infants with pulmonary oxygen toxicity was not seen. This study suggests that supplemental selenium as well as an increased zinc intake over current recommendations for premature infants receiving TPN may be indicated.
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PMID:Relationship of antioxidant enzymes to trace metals in premature infants. 310 37

Oxygen free radicals have the potential to mediate cell injury. Defenses against such radicals include the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX). The purposes of this study were (1) to develop an in vitro model using human cells in which to investigate a potential pharmacologic agent as an inducer of these antioxidant enzymes; (2) to investigate the phenylurea derivative N-[2-(2-oxo-1-imidazolindinyl)ethyl]-N-phenylurea (EDU) in this model with paraquat (PQ) serving as the positive control; and (3) to determine if induction of the antioxidant enzymes by EDU occurs in vivo. Human gingival fibroblasts (Gin-1) were used as the target cell in vitro; PQ and EDU, an inducer of SOD and CAT activities in plants, were evaluated as antioxidant enzyme inducers. Total SOD activity in Gin-1 cells increased 2-fold (p less than 0.05) in the presence of 1.0 mM PQ for 18-48 hr compared with untreated controls. Gin-1 cells incubated with 0.25-2.0 mM PQ for 24 hr had significantly increased total SOD (1.5 to 2.0-fold; p less than 0.05). CAT activity increased with 1.0 and 2.0 mM PQ (p less than 0.05). In the presence of PQ, GSH-PX activity decreased (p less than 0.05) in a concentration-dependent manner, indicating inactivation of this enzyme. No toxicity, indicated by lactate dehydrogenase released into the incubation medium, was noted at PQ concentrations below 5.0 mM. In the presence of 0.125-2.0 mM EDU, total SOD activity in Gin-1 cells significantly increased (1.5 to 2.0-fold; p less than 0.05). CAT activity significantly increased in a dose-dependent manner (p less than 0.05), while GSH-PX activity remained constant following exposure to 0.125-2.0 mM EDU. Intraperitoneal administration of EDU to rats twice a day for 2 days at 100 mg/kg induced SOD activity in heart, liver, and lung compared to controls (p less than 0.05). CAT activity increased in the liver 56% and in the lung 36% (p less than 0.05). GSH-PX activity remained constant. Our findings indicate that Gin-1 cells are a useful model in which to study inducers of antioxidant enzymes in vitro and that the phenylurea compound EDU induces SOD and CAT activities both in vitro and in vivo.
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PMID:Induction of antioxidant enzyme activities by a phenylurea derivative, EDU. 318 24

Buthionine sulfoximine (BSO), an inhibitor of de novo synthesis of glutathione (GSH), was used to deplete rats of GSH and determine the effect of treatment on antioxidant enzyme responses, lung injury, and the susceptibility to concurrent sublethal or lethal hyperoxia. In a preliminary experiment, total lung nonprotein sulfhydryl (NPSH) and GSH levels were measured at various times after single doses of BSO. The lowest concentrations were observed at 12 to 18 h. These experiments were used to establish a repeated dosing protocol for more prolonged GSH depletion. The lungs of rats treated with BSO for 4 days demonstrated markedly decreased GSH and NPSH levels (10 to 40% of control values) and glutathione peroxidase activity (45 to 60% of control values). Superoxide dismutase activities were elevated, glutathione reductase activity was slightly elevated, and catalase activity was unchanged. These changes were dose-responsive. The lungs of treated rats were grossly and microscopically normal. BSO treatment of additional rats did not increase susceptibility to lethal hyperoxia (greater than 98% oxygen). Combined treatment of rats with both BSO and sublethal hyperoxia (80% oxygen) for 4 days did not alter the biochemical responses demonstrated by rats treated solely with BSO. The marked increase in catalase activity obtained after hyperoxia alone was not observed in rats treated with both hyperoxia and BSO. The lungs of saline- and BSO-treated rats exposed to sublethal hyperoxia demonstrated a patchy distribution of slight perivascular and peribronchiolar edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pulmonary effects of buthionine sulfoximine treatment and glutathione depletion in rats. 320 1

Analyses were made of the phsopholipid fatty acids and the antioxidant enzymes in the carp (Cyprinus carpio morpha) at three different oxygen concentrations, corresponding to hyperoxia, hypoxia and anoxia. Variations of the oxygen concentration were found to influence the quantities of phsopholipid fatty acids, as well as the antioxidant enzyme activities. In hyperoxia and hypoxia the amount of polyunsaturated fatty acids in carp liver was higher than in anoxia, but in other tissues there was no significant differences. As to the antioxidant enzyme system, the glutathione peroxidase activity and the lipid peroxidation value increased significantly with decrease of the oxygen concentration, while the total superoxide dismutase activity decreased on lowering of the oxygen level.
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PMID:Effects of various oxygen concentrations on antioxidant enzymes and the quantity of tissue phospholipid fatty acids in the carp. 325 9

The growth of mycobacteria on perfluorodecalin-modified media was shown to be accompanied by distinct alterations in the activity of the antioxidant enzyme system in M. bovis BCG and M. lufu. In M. bovis BCG the levels of glutathione transferase and glutathione peroxidase-hydrogen peroxidase activity are decreased by 45.47% and 100.88%, respectively. In M. lufu, on the contrary, the level of superoxide dismutase is increased by 42.23%, with no changes observed in the levels of glutathione transferase and glutathione peroxidases. The data obtained suggest physiological heterogeneity of mycobacteria and, thus, open prospects for the differential approaches to the problem of increasing the efficacy of in vitro cultivation of various mycobacterial species, including M. leprae.
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PMID:[Functional characteristics of the antioxidative system in mycobacteria grown on perfluorodecalin-modified media]. 328 44

We investigated the possible involvement of reactive oxygen radical-related processes in chronic (12-wk) diabetes induced in rats by streptozocin (STZ). Diabetes was associated with significantly increased activities of catalase (CAT), glutathione reductase (GSSG-RD), and CuZn-superoxide dismutase (SOD) in the pancreas and of CAT and GSSG-RD in the heart. On the other hand, the liver of diabetic rats showed a generalized decrease in CAT, glutathione peroxidase (GSH-PX), and SOD as well as in the levels of reduced glutathione (GSH). Diabetic kidney also showed decreases in CAT and SOD, but the activities of GSH-PX were increased. Insulin treatment (9-12 U/kg body wt) that was started after 8 wk of diabetes and continued for 4 wk reversed all of the foregoing alterations in tissue antioxidant status. Our results suggest the presence of increased oxidative stress in uncontrolled diabetes as manifested by the marked alterations in tissue antioxidant enzyme activities, the magnitude of which increased with the degree of emaciation. The complex patterns of changes observed in the various tissues examined are believed to be the result of compensatory increases in enzyme activities (usually involving enzymes whose activity in control tissues is low) and direct inhibitory effects, possibly resulting from an increased tissue-oxidant activity. Our findings support the view that tissue antioxidant status may be an important factor in the etiology of diabetes and its complications.
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PMID:Alterations in free radical tissue-defense mechanisms in streptozocin-induced diabetes in rat. Effects of insulin treatment. 330 71

The effect of increased intracellular oxygen activation on cellular antioxidant defenses in CHO and HeLa cells was studied. In both cell types, hyperoxic exposure (up to 4 days, 600-700 mm Hg O2) and in CHO cells menadione (up to 3 days, 15 microM) failed to affect the enzymatic antioxidant defenses Mn-containing superoxide dismutase (Mn-SOD), CuZn-SOD, catalase and glutathione peroxidase. The markedly increased antioxidant enzyme activities observed in a recently obtained oxygen-tolerant CHO variant persisted under normoxia. These data suggest that the synthesis of antioxidant enzymes is constitutive. Glutathione levels of HeLa cells did not respond to hyperoxia whereas in CHO cells hyperoxia and menadione exposure resulted in a 2- and 7-fold increase in glutathione contents, respectively. However, considering the large variations in glutathione contents observed under normal culture conditions, it is uncertain whether this increase is to be considered as a true adaptive response.
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PMID:Effect of normobaric hyperoxia on antioxidant defenses of HeLa and CHO cells. 334 21


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