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)

After a 13-day space mission, in the rats flown on Cosmos-1887 biosatellite the parameters of lipid peroxidation and antioxidant defense system--the contents of diene conjugates, malonic dialdehyde, Schiff bases, tocopherol, total antioxidant activity (in blood plasma only), antioxidant enzyme activity (in tissues only)--superoxide dismutase, catalase, glutathio peroxidase, glutathio reductase have been measured in the blood plasma, myocardium, skeletal muscles and liver. The liver level of diene conjugates, Schiff bases and tocopherol decreased, and an activity of superoxide dismutase and catalase increased. In the skeletal muscles there was an elevation of diene conjugate contents followed by the decreases in malonic dialdehyde and superoxide dismutase activity. In rat myocardium, superoxide dismutase activity and tocopherol levels increased significantly. In the blood plasma the levels of tocopherol, malonic dialdehyde and total antioxidant activity were elevated. It is concluded that the observed changes in lipid peroxidation developed probably in response to an effect of the last dynamic stage of space flight and during re-adapting to the Earth environments.
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PMID:[Lipid peroxidation and the system of antioxidant protection in rats following a 13-day space flight on the Kosmos-1887 biosatellite]. 129 45

The effect of experimental cryptorchidism on the level of oxidative stress and antioxidant functions in rat testis was studied. Adult male Sprague-Dawley rats were rendered unilaterally cryptorchid (by suturing one testis to the abdominal wall) and killed 1, 3, or 7 days after the operation. As an indicator of oxidative stress, lipid peroxidation was measured by the diene conjugation method in testis homogenates. The activities of the antioxidant enzymes were determined either in the 10,000 x g supernatant fraction (glutathione [GSH] peroxidase, GSH transferase, hexose monophosphate shunt) or in crude testis homogenates (superoxide dismutase, catalase). An expected reduction (48%) in weight of the abdominal testes was evident by postoperative Day 7. The catalytic activities per testis of superoxide dismutase (Cu/Zn form) and catalase were found to decrease in cryptorchidism. The effect was seen on the first postoperative day and was most profound on Day 7 after surgery. The principal antioxidant enzyme, superoxide dismutase, was most sensitive to cryptorchidism, the activity in the abdominal testes being 74% or 85% (per gram of tissue or per whole testis, respectively; p less than 0.01). After impairment of the reactive oxygen detoxifying capacity, lipid peroxidation was increased in the abdominal testis by 46% (p less than 0.01) on postoperative Day 7. Slight concomitant increases were detected in the activities of GSH-peroxidase (p less than 0.01), GSH-transferase (p less than 0.001), and the hexose monophosphate shunt (p less than 0.001). This effect was seen only when calculated per gram of tissue, not per whole testis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired detoxification of reactive oxygen and consequent oxidative stress in experimentally cryptorchid rat testis. 135 92

1. The effect of the increasing concentrations of CuSO4 and HgCl2 (0.01-0.3 mmol/l) on erythrocyte haemolysis and the activities of peroxide metabolism enzymes: superoxide dismutase, catalase, peroxidase and glutathione peroxidase was investigated in human erythrocytes and the nucleated red blood cells of marine fish (Dicentrarchus labrax). 2. The results show that both heavy metal ions had only little effect on haemolysis and antioxidant enzyme activities in human erythrocytes; in contrast the effect of heavy metals on fish erythrocytes was statistically significant when compared to control values. 3. Copper was found to have more pronounced effect than mercury on the erythrocytes of Dicentrarchus labrax; otherwise there were no significant differences between the toxic effects of both ions on human erythrocytes. 4. We suggest that the mechanism of copper-induced haemolysis may be different from that of mercuric ion in the erythrocytes of Dicentrarchus labrax.
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PMID:The comparison of the effects of heavy metal ions on the antioxidant enzyme activities in human and fish Dicentrarchus labrax erythrocytes. 135 29

Antioxidant enzyme activities of cultured human foreskin fibroblasts, keratinocytes, and melanocytes from healthy black and Caucasian donors were measured and compared. Fibroblasts had more (p less than 0.05) peroxidase, catalase, glutathione peroxidase, and superoxide dismutase activity than keratinocytes. Keratinocytes had more (p less than 0.05) peroxidase, catalase, glutathione peroxidase, and superoxide dismutase activity than melanocytes. No differences in antioxidant enzyme activities were observed between the cells of any type taken from black or Caucasian people. Antioxidant enzyme activities may affect resistance to damage by oxidants induced by ultraviolet radiation and inflammation.
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PMID:Disparate antioxidant enzyme activities in cultured human cutaneous fibroblasts, keratinocytes, and melanocytes. 187 41

Nitrogen dioxide (NO2), a major oxidant constituent of vehicle emissions, is toxic to lung cells including endothelial cells. Since NO2 is a reactive free radical, one of the postulated mechanisms of NO2-induced pulmonary injury involves the peroxidation of membrane lipids. Therefore, this study evaluated the dose- and time-dependent effects of nitrogen dioxide exposure by measuring the biochemical and biophysical parameters, as well as the metabolic function, in porcine pulmonary artery and aortic endothelial cells in monolayer cultures. To evaluate the biochemical changes, the antioxidant enzyme GSH-reductase (GSH-red), GSH-peroxidase (GSH-per), and glucose-6-phosphate dehydrogenase (G6PDH) activities, as well as the lipid peroxide formation, glutathione (GSH) content, and lactate dehydrogenase (LDH) release were measured. Biophysical changes were measured by monitoring lipid fluidity in both the hydrophobic and hydrophilic regions of the plasma membrane. The uptake of 5-hydroxytryptamine (5-HT) was measured as a metabolic function of endothelial cells. Confluent porcine pulmonary artery and aortic endothelial cells were exposed to 3 or 5 ppm NO2 or air (control) for 3-24 hours. After 3-, 6-, or 12-hour exposures to 3 or 5 ppm NO2, the GSH-red and G6PDH activities, as well as the lipid peroxide formation and LDH release, were not different from those of controls in both pulmonary artery and aortic endothelial cells. Exposure of the cells to 3 or 5 ppm NO2 for 24 hours resulted in significant increases in GSH-red (p less than 0.05) and G6PDH (p less than 0.001) activities in both cell types. Exposure to 5 ppm NO2 for 24 hours significantly (p less than 0.05) increased lipid peroxide formation and increased (p less than 0.01) LDH release in both the pulmonary artery and aortic endothelial cells. GSH-per activity and GSH content in NO2-exposed pulmonary artery and aortic endothelial cells were not different from those of controls, irrespective of NO2 concentration and exposure time. Fluorescence spectroscopy was used to measure the membrane lipid fluidity. Membrane fluidity in the hydrophobic region was measured by 1,6-diphenyl-1, 3, 5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic interior of the lipid bilayer.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemical and metabolic response to nitrogen dioxide-induced endothelial injury. 247 62

Rats were pretreated with various inducers of cytochrome P-450 before being exposed to pure normobaric oxygen (O2) in order to determine whether the inducers interfere with toxicity. The pulmonary and liver inducers beta-naphthoflavone (beta NF) and 3-methylcholanthrene (3MC) increased the survival rate and decreased the amount of pleural and lung fluid accumulation in adult rats exposed to oxygen. Phenobarbital (PB), which is essentially active in the hepatic microsomal cytochrome P-450, was less effective in counteracting oxygen toxicity. After 7 days of exposure to oxygen, none of the untreated rats survived, whereas 40, 73, and 90% survival was observed in rats treated with PB, 3MC, and beta NF, respectively. After 60 h of O2 exposure, significantly less pleural and lung fluid accumulation was observed in beta NF- and 3MC-treated rats than in untreated or PB-treated rats (p less than 0.001). Both beta NF and 3MC prevented the increase of lung peroxidation (assessed by measuring of malondialdehyde) and that of hydrogen peroxide production by lung microsomes induced by O2 exposure. These protective effects are associated with a large increase in the components of the pulmonary cytochrome P-450 system and its peroxidase activity and with an increased response to hyperoxia by lung antioxidant enzyme activities. In contrast, in control rats, the activities of the antioxidant enzymes were not increased, and both the quantity and the peroxidase activity of cytochrome P-450 were significantly decreased by O2 exposure. We conclude that in the rat, pretreatment by inducers of pulmonary cytochrome P-450 results in marked protection against O2 toxicity and an increase of antioxidant enzyme response to hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection of rat from oxygen toxicity by inducers of cytochrome P-450 system. 283 Aug 13

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

Nitrogen dioxide (NO2), an environmental oxidant pollutant, is toxic to lung cells. We evaluated the changes in antioxidant enzyme activities in porcine pulmonary artery (PA) and aortic (AO) endothelial cells in monolayer cultures. Confluent PA or AO endothelial cells were exposed to 3 or 5 ppm NO2 or air (control) for 3-24 h and assayed for GSH-reductase (GSH-red), GSH-peroxidase (GSH-per), and glucose-6-phosphate dehydrogenase (G6PDH) activities as well as for intracellular GSH content. After 3, 6, or 12 h exposure to 3 or 5 ppm, GSH-red and G6PDH activities were not different from those of controls in both PA and AO endothelial cells. Exposure to 3 or 5 ppm NO2 for 24 h resulted in significant increases in GSH-red (P less than 0.05) and G6PDH (P less than 0.001) activities in both cell types. GSH-per activity and GSH content in NO2-exposed PA and AO endothelial cells were not different from those of controls, irrespective of NO2 concentration and exposure time. These results indicate that enzyme activities of G6PDH and GSH-red are increased in PA and AO endothelial cells exposed to NO2, and this response is comparable, in part, to that in the lungs from animals exposed to NO2.
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PMID:Effect of NO2 exposure on antioxidant defense of endothelial cells. 377 82

Current evidence suggests that bleomycin toxicity may be attributable to its DNA degradative activity possibly via generation of free radicals and O2 metabolites as mediators. Since lipopolysaccharide (LPS) has been known to provide protection against O2 toxicity, which is correlated with increased activity of O2 metabolite-detoxifying enzymes, the effect of this agent on bleomycin-induced pulmonary fibrosis was examined. Endotracheal bleomycin administration caused increased lung collagen synthesis. A single intraperitoneal injection of LPS (500 micrograms/kg) at day zero significantly decreased these increases. Total bleomycin-induced lung collagen increase was also significantly reduced. LPS alone had no significant effect on total lung catalase activity. Glutathiione peroxidase activity, however, was significantly decreased by 15.8% compared to untreated animals at 2 days after LPS treatment and remained unchanged at other time points. In addition, superoxide dismutase activity was significantly elevated by 30% above untreated animals only at 14 days after LPS administration and remained unchanged at other time points. Endotracheal bleomycin administration alone caused significant reductions in catalase activity at 2 days and 2 weeks after treatment, whereas glutathione peroxidase activity increased above control untreated animals at 2 and 4 weeks, respectively. Superoxide dismutase activity was unaffected by bleomycin treatment. Pretreatment with LPS before bleomycin prevented these reductions or caused increases in the activities of these enzymes at 2 days. Glutathione peroxidase was increased and was significantly greater than those animals treated with bleomycin alone. Catalase also was higher in the LPS plus bleomycin group (by 22.2%, p less than 0.05) than the bleomycin group alone. Compared to the effects on lung collagen synthesis and content, LPS treatment resulted in much less dramatic changes in total lung antioxidant enzyme activities. This discrepancy between the intensity of LPS effects on lung O2 metabolite-detoxifying enzymes and that on pulmonary fibrosis implies that the LPS-ameliorating effect on pulmonary fibrosis could not be totally explained by increased ability to detoxify O2 metabolites. Rather, the data would favor the possibility that LPS inhibits bleomycin-induced pulmonary fibrosis either by its known immunosuppressive effects or some other unknown mechanism. The former would be in agreement with previous data which suggest that an intact immune response is necessary for complete expression of the fibrogenic response to bleomycin.
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PMID:Inhibition of bleomycin-induced pulmonary fibrosis by lipopolysaccharide. 620 76

The dose and duration limiting toxic effects of cisplatin are ototoxicity and nephrotoxicity. While several studies have attempted to shed some light on the causes of nephrotoxicity, the reasons for ototoxicity induced by cisplatin are poorly understood. Therefore, this investigation was undertaken to delineate the potential mechanisms underlying cisplatin ototoxicity. The role of glutathione (GSH), oxidized glutathione (GSSG) and malondialdehyde levels, and antioxidant enzyme activities [superoxide dismutase, catalase, GSH peroxidase, and GSH reductase] were examined in cochlear toxicity following an acute dose of cisplatin. Male Wistar rats were treated with various doses of cisplatin. Pretreatment auditory brain stem evoked responses (ABR) were performed and then post-treatment ABRs and endocochlear potentials were also performed after three days. Acute cochlear toxicity (ototoxicity) was evidenced as elevated hearing thresholds and prolonged wave I latencies in response to various stimuli (clicks and tone bursts at 2, 8, 16 and 32 kHz) on ABRs. The endocochlear potentials were reduced (50% control) in cisplatin-treated rats as compared to control animals. The rats were sacrificed and cochleae isolated. The GSH, GSSG and malondialdehyde levels, and antioxidant enzyme activities were determined. Cisplatin ototoxicity correlated with a decrease in cochlear GSH [0.45 +/- 0.012 nmol/mg] after cisplatin administration compared to 0.95-012 nmol/mg in control cochleae (P < 0.05). Superoxide dismutase, catalase activities and malondialdehyde levels were significantly increased in the cochleae of cisplatin injected rats. Cochlear GSH-peroxidase and GSH reductase activity significantly decreased after cisplatin administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of cisplatin ototoxicity: antioxidant system. 747 81


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