UNIPROT:P30044 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

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

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.
...
PMID:Effects of monensin on selenium status and related factors in genetically hypo- and hyperselenemic growing swine. 146 9

An in vitro model of alveolar epithelial oxidant injury was developed based on exposure to hyperoxia of cultured guinea pig type II pneumocytes using a biphasic cell culture system in aerobiosis. The present study investigates the roles of intracellular antioxidant enzymes and of glutathione in providing protection against hyperoxia. A 2-day type II cell culture in normoxia was associated with a significant decrease in protein, catalase, and Cu-Zn SOD cell content, whereas ATP cell content, Mn-SOD, and glutathione peroxidase (GPx) activities did not change and glutathione cell content significantly increased. Exposure of type II cells to hyperoxia did not induce significant changes in cell content in protein, SOD, catalase, GPx, or glutathione cell content when compared to control cells (exposed to normoxia). With ATP cell content expressed as a cell injury index (CII), type II cell injury was found to increase with increasing O2 concentrations. Indeed, a 2-day 50% O2 and 95% O2 exposure resulted in a CII of -7.5 +/- 6.2% and 17.9 +/- 5.9%, respectively, LDH release by type II cells was not significantly increased after hypoxic exposure. Cell injury effects of hyperoxia did not correlate with the endogenous antioxidant enzyme activities (SOD, Mn-SOD, catalase). In marked contrast, there was a significant correlation between the CII and total glutathione content of type II cells (p < .01). This correlation was largely due to the close relationship between CII and reduced glutathione. Hyperoxic induced cell injury (as demonstrated by CII > 0) was clearly associated with significantly lower intracellular glutathione level when compared to experiments without hyperoxia induced cell injury (CII < 0). In addition, in the presence of buthionine sulfoximine (BSO), the ability of type II cells to synthetize new glutathione was severely impaired, whereas ATP cell content and cell antioxidant enzyme activities did not change. As a consequence, the reduction of intracellular glutathione significantly increased the susceptibility of cells to hyperoxia injury (p < .05). The results strongly support the hypothesis that the regulation of glutathione levels is an important mechanism in protecting hyperoxia-induced type II cell injury.
...
PMID:In vitro effects of hyperoxia on alveolar type II pneumocytes: inhibition of glutathione synthesis increases hyperoxic cell injury. 146 13

1. A discontinuous gradient in the region of 45-65% "Percoll" has been utilized for the separation of trout erythrocytes. Three different fractions were obtained. 2. We have evaluated antioxidant enzyme activities and membrane fluidity. The results indicated that catalase and glutathione peroxidase activities increased with the density of the fraction while the membrane fluidity was unchanged. 3. The observed results show a marked difference between nucleated (fish) and unnucleated (human) separated erythrocytes.
...
PMID:Biochemical characterization of density-separated trout erythrocytes. 148 81

Because hypertrophied rat hearts display an increase in antioxidant enzyme activities and because hypoxia-reoxygenation injury is known to involve free radicals, we tested the hypothesis that the hypertrophied heart may be more resistant to this type of injury. Hypertrophied rat hearts after 10 weeks of chronic pressure overload showed elevated superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) activities and a decrease in lipid peroxidation as indicated by malondialdehyde (MDA) content. Glucose-free hypoxia for 15 min resulted in a complete failure of developed tension and about 200% increase in resting tension in both hypertrophied and sham control groups (p < 0.05). Upon reoxygenation for up to 30 min, hypertrophied hearts recovered developed tension to 60% and resting tension was higher by only 80% of prehypoxic values. In contrast, sham hearts showed only a 25% recovery of developed tension, whereas resting tension remained 130% higher than prehypoxic control values. During hypoxia, the SOD activity was significantly reduced in both sham and hypertrophied groups, whereas GSHPx was reduced only in the sham group. Upon reoxygenation there was no further change in these enzyme activities. Both the SOD and GSHPx activities in the hypertrophied group remained significantly higher than the corresponding reoxygenated sham hearts. During hypoxia, there was no apparent change in MDA content in either the sham or hypertrophied hearts. However, reoxygenation resulted in a significant increase in MDA content in both sham and hypertrophied hearts, but the MDA content was significantly less in the hypertrophied group (p < 0.05). It is suggested that maintenance of an adequate endogenous antioxidant reserve during hypoxia may be important in recovery upon reoxygenation.
...
PMID:Antioxidant changes in heart hypertrophy: significance during hypoxia-reoxygenation injury. 149 Feb 52

Prenatal dexamethasone (DEX) treatment is known to accelerate the maturation of both the surfactant system and the fetal lung antioxidant enzyme (AOE) system (Frank L, Lewis P, Sosenko IRS: Pediatrics 75:569-574, 1985). Because of this stimulatory effect of prenatal DEX on the normal late gestational development of the AOE system, we questioned whether this treatment might have a salutary effect on the ability of the newborn rat to tolerate early and prolonged exposure to hyperoxia, inasmuch as the AOE are the primary lung defensive system against high O2 challenge. In nine experiments with term newborn rats in greater than 95% O2, the composite percentage of survival was significantly greater in the prenatal DEX pups at all time periods in hyperoxia from 7 d [control pups, 67 of 94 (71%); prenatal DEX, 96 of 99 (97%)] to 14 d [controls, 10 of 32 (31%); prenatal DEX, 18 of 33 (55%)] (p less than 0.01). In addition to survival per se, the prenatal DEX pups showed significantly decreased lung wet weight/dry weight ratios, pathologic evidence of pulmonary edema, and lung conjugated dienes versus the O2 control newborn group. Of the many comparative parameters examined, the major difference found between the two groups was in the pulmonary AOE responses to hyperoxia. By 2 d in hyperoxia, the prenatal DEX rat pups showed significantly elevated superoxide dismutase, catalase, and glutathione peroxidase activities compared to air control pups, and at 4 and 7 d in O2 the AOE levels were consistently greater in the DEX group than the AOE responses in the control O2 pups.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Prenatal dexamethasone treatment improves survival of newborn rats during prolonged high O2 exposure. 150 13

This study reports on the effect of streptozotocin (STZ) induced diabetes on water soluble-SH and -SS, as well as on hepatic glutathione peroxidase (GSH-Px), catalase and superoxide dismutase (SOD) activity and on malondialdehyde (MDA) content. In addition, we determined serum concentrations of glucose, cholesterol, triglycerides and thyroxine, and thyroid weight. To elucidate the possible impact of exogenous iodine on impaired free radical tissue defense mechanisms STZ-diabetic rats were exposed to iodine brine providing for a daily iodide uptake of about 300 micrograms/kg body weight. STZ-exposure caused a decline in thyroid weight (p less than 0.01) and in total serum thyroxine (p less than 0.001), as well as a fall in hepatic catalase (CAT) activity (p less than 0.01) versus control group. Impairment of catalase activity was related to serum glucose level (r = -0.569, p less than 0.01), while hepatic MDA was positively related to serum glucose (r = + 0.5, p less than 0.01). No protective effects of iodine brine were seen with regard to impairment by STZ of antioxidant enzyme status. We conclude that impairment by STZ of antioxidant enzymes may contribute to STZ-dependent experimental diabetes.
...
PMID:Alterations of antioxidant tissue defense enzymes and related metabolic parameters in streptozotocin-diabetic rats--effects of iodine treatment. 150 40

Bacterial endotoxin has been shown to protect rats from lethal hyperoxia. The structure of endotoxin contains diphosphoryl lipid A (DPL) as the lipid backbone stripped of protein and polysaccharides. DPL is the component of the endotoxin molecule that has been demonstrated (in previous studies) to be responsible for the immunologic, mitogenic, pyrogenic, and lethal properties of endotoxin. Monophosphoryl lipid A (MPL) is a nonpyrogenic, nontoxic modification of the DPL molecule that retains its immunostimulatory and mitogenic properties. We hypothesized that DPL may be the actual active component of endotoxin that protects rats from lethal hyperoxia. We also hypothesized that the protection from hyperoxia that is afforded by the DPL component may be related to endogenous release of tumor necrosis factor alpha which should allow MPL to also be protective. To test these hypotheses, we performed a series of experiments in which rats were treated with endotoxin, DPL, MPL or vehicle and exposed to room air or hyperoxia. We found that DPL and endotoxin both protected rats from lethal hyperoxia, but MPL alone was not protective. Even though MPL was not protective, DPL and MPL both increased endogenous release of tumor necrosis factor alpha early after injection (peak DPL level, 3619 +/- 1500 pg/ml, peak MPL level, 4038 +/- 500 pg/ml). Protection in both the endotoxin- and DPL-treated animals was associated with increases in lung antioxidant enzyme activities. We concluded that DPL protect rats from hyperoxia but that MPL is not protective in spite of its immunostimulatory and mitogenic effects.
...
PMID:Diphosphoryl lipid A protects rats from lethal hyperoxia. 151 89

To understand better the effect of oxidant injury on vascular endothelial cells, human saphenous vein endothelial cells were cultured at atmospheric (pO2 of 150 mmHg) or low (pO2 of 40 mmHg) oxygen tensions. The cellular rates of growth, antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase), phospholipid fatty acids and cellular susceptibility to extracellularly generated oxidants (hypoxanthine-xanthine oxidase) were measured. The antioxidant enzyme activities were regulated by oxygen tension and significantly differed by day 14. The cells cultured at the low oxygen tension had significantly (P less than 0.01) lower antioxidant activities than the cells cultured at the high oxygen tension. The cells cultured at an oxygen tension of 150 mmHg were more resistant to shrinkage and lipid peroxidation from the oxidants than the cells cultured at a pO2 of 40 mmHg by day 14. Since arterial and venous endothelial cells are perfused with blood at a pO2 of 100 and 40 mmHg, respectively, the postcapillary venous endothelial cells should have lower antioxidant enzyme activities than the precapillary arterial endothelial cells.
...
PMID:Cultured vascular endothelial cell susceptibility to extracellularly generated oxidant injury. 151 77

Limited data exist concerning exercise training-induced alterations in skeletal muscle oxidative and antioxidant enzyme activity in senescent animals. Therefore, the purpose of this study was twofold: 1) to examine the exercise training-induced changes in oxidative and antioxidant enzyme activity in skeletal muscle of old rats; and 2) to critically analyze the relationship between oxidative and antioxidant enzyme activities in skeletal muscle in both trained and untrained senescent rats. Female Fischer-344 rats (approximately 24-mo-old) were divided into 1) exercised trained (ET; n = 10) and 2) sedentary (S; n = 6) groups. The ET rats performed a 10-week training program of treadmill exercise (approximately 60 min, 5 days/wk). Training significantly (p less than 0.05) improved VO2max (delta 22.8%) in the ET rats above their age-matched controls. Further, the ET group had significantly elevated (p less than 0.05) activities of succinate dehydrogenase (SDH) in the soleus and red gastrocnemius (RG) muscles as well as greater (p less than 0.05) 3-hydroxyacyl-CoA dehydrogenase (HADH) activity in the RG when compared to the S group. However, training did not alter (p greater than 0.05) HADH activity within the white gastrocnemius (WG) or soleus muscles. Activity of the antioxidant enzyme, glutathione peroxidase (GPX) was higher (p less than 0.05) in the soleus and RG in ET rats when compared to the S rats; in contrast, training did not alter (p less than 0.05) GPX activity in the WG. Finally, the correlation coefficients between SDH and GPX activities (combined ET and S groups) for the RG, WG, and soleus muscles were r = .73, .17 and .36, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Exercise training-induced alterations in skeletal muscle oxidative and antioxidant enzyme activity in senescent rats. 152 60

Rats fed low copper show a high incidence of dimethylhydrazine (DMH)-induced colon tumors compared with rats fed very high Cu. The difference could be due to Cu deficiency in the low group or to Cu toxicity in the high group. In the present study, rats fed low Cu (0.2 ppm) showed greater DMH-stimulated colon tumorigenesis than rats fed adequate Cu (8 ppm). Differences were seen in the number of rats developing tumors (5 of 11 vs 1 of 10), total tumors (7 vs 2), and average tumor mass (1.02 g vs 0.29 g). Low Cu intake did not cause any general DMH toxicity as assessed by body weight gain. To prevent Cu deficiency-induced mortality, low Cu feeding was begun in postweanling rats (weight, about 80 g) housed in groups of five to six, rather than individually. This limited the effects of low Cu feeding to only a moderate Cu deficiency based on several parameters, including three Cu antioxidant enzyme activities. Group-housed rats fed marginal Cu levels (2.5 ppm) showed normal Cu status, and DMH produced only one tumor in 10 rats. In conclusion, high DMH-induced colon tumorigenesis can be found in rats with low activities of Cu antioxidant enzymes.
...
PMID:Effects of low copper intake on dimethylhydrazine-induced colon cancer in rats. 152 14

<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>