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)

Offspring of experimentally induced diabetic animals demonstrate delays in functional, biochemical, and morphological aspects of lung maturation, dealing mainly with the surfactant system. To investigate whether the development of the lung antioxidant enzyme system would be similarly delayed, and thus compromise their tolerance to high O2 exposure, we did the following: 1) produced the diabetic state in rats with streptozotocin injection 24 h after the onset of pregnancy; 2) examined fetal animals from streptozotocin and control rats at gestational days 19, 20, and 21, and newborn animals at day 22 for whole lung disaturated phosphatidylcholine and total phospholipid and for the three antioxidant enzymes: superoxide dismutase, catalase, glutathione peroxidase; and 3) exposed newborn offspring from streptozotocin-treated and control rats to greater than 95% O2 for several days and their survival, changes in antioxidant enzymes and disaturated phosphatidylcholine and light microscopic findings in response to hyperoxic challenge were compared. Streptozotocin offspring demonstrated essentially no developmental differences in whole lung disaturated phosphatidylcholine, total phospholipid, or antioxidant enzymes activity at the 4 gestational days studied. However, newborns of streptozotocin mothers had consistently superior tolerance to hyperoxic exposure, consisting of increased survival [23/34 (68%) versus 8/26 (31%) in controls, after O2-exposure for 13 days, p less than 0.001], microscopic evidence of reduced inhibition of alveolarization (p less than 0.05), and a trend toward greater antioxidant enzymes response. Thus, in this animal model of experimental diabetes, neither the development of the antioxidant enzymes system nor the development of the surfactant system (as assessed by whole lung disaturated phosphatidylcholine and total phospholipid) appear delayed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lung development in the streptozotocin rat fetus: antioxidant enzymes and survival in high oxygen. 375 56

The surfactant system and the antioxidant enzyme system of the fetal lung have chronologically similar developmental patterns and both can be accelerated by the administration of exogenous glucocorticoids. To test whether the antioxidant enzyme system, like the surfactant system, is regulated, at least in part, by endogenous glucocorticoids, we injected pregnant rats for 3 days prior to delivery with metyrapone, an adrenal 11-beta hydroxylase inhibitor which crosses the placenta and blocks endogenous glucocorticoid synthesis, or saline. Metyrapone offspring had significantly decreased lung tissue disaturated phosphatidylcholine/total phospholipids (p less than 0.05) compared to controls at days 21 and 22 of gestation. Activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase were similarly significantly reduced (p less than 0.01) in the lungs of metyrapone offspring at both gestational days studied. One day premature metyrapone pups demonstrated poorer survival than control pups from 25 min after delivery (44% survival versus 83%, p less than 0.05) to 90 min (6% survival versus 78%, p less than 0.01). These findings of delayed maturation of the surfactant and antioxidant enzyme systems following adrenal glucocorticoid blockade suggest that both systems are regulated, at least in part, by an endogenous glucocorticoid mechanism.
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PMID:Metyrapone delays surfactant and antioxidant enzyme maturation in developing rat lung. 375 36

We examined the chronology of development of both fetal lung antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) and disaturated phosphatidylcholine ("surfactant") during late gestation in four laboratory animal species: rat, rabbit, hamster, and guinea pig. An essentially similar pattern of prenatal biochemical maturation was found in all four species. The developmental changes were characterized by (1) rapid elevations in fetal lung antioxidant enzyme levels during the final 10% to 15% of gestation, and (2) an essentially parallel rapid rise in lung surfactant content during the final 10% to 15% of gestation. The increase in the lung activity of the individual antioxidant enzymes prior to birth averaged approximately 150% to 200%. Our findings suggest that late gestational changes in the principal pulmonary antioxidant defense system (like the changes in the surfactant system) represents a normal "preparation for birth," required to assure successful functioning of the neonatal lung in the relatively oxygen-rich ex utero environment.
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PMID:Prenatal development of lung antioxidant enzymes in four species. 379 68

It has recently been determined that fetal lung antioxidant enzyme activity markedly increases late in gestation. A test was made of whether this normal late-in-gestation change in O2-protective enzymes would be responsive to the maturing effect of hormonal (glucocorticoid) treatment. Pregnant rats received 0.2 mg/kg of dexamethasone (or saline) at 48 and 24 hours prior to delivery of their fetuses on gestational days 19, 20, 21, and 22 (newborn). Lung disaturated phosphatidylcholine showed an expected response to prenatal dexamethasone exposure with significant elevations of surfactant lipid at gestational days 20 and 21. A similar effect of prenatal dexamethasone treatment on the lung antioxidant defensive system was found. Superoxide dismutase, catalase, and glutathione peroxidase--enzymes protective against hyperoxia-induced lung injury--showed an accelerated pattern of maturation with significant increases in the dexamethasone-treated fetal lungs compared with control fetal lung enzyme levels at gestational days 20 and 21. The results suggest that prenatal dexamethasone treatment may have dual benefits when used in impending premature deliveries--that is, it may stimulate maturation of both the surfactant system and also the antioxidant enzyme system, and this maturation can help protect the premature newborn's lungs from the toxic complications of hyperoxic therapy that may be required because of immaturity.
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PMID:Dexamethasone stimulation of fetal rat lung antioxidant enzyme activity in parallel with surfactant stimulation. 384 97

Total glutathione levels and the activity of enzymes associated with antioxidant protection in neonatal lung are increased in response to hyperoxia. Glutathione levels in developing rat lung decreased from 24 nmol/mg protein on day 19 of gestation to approximately 12 nmol/mg protein at birth. The initial decrease in glutathione may be due to emergence of other antioxidant systems. Newborn rats placed in 100% oxygen showed a rapid and sustained increase in total glutathione levels which was primarily due to an increase in reduced glutathione. Explants obtained from 16-wk gestation human fetal lung or from 17- to 18-day fetal rat lung also showed increased total and reduced glutathione when cultured in 95% oxygen, 5% CO2 as compared with explants cultured in room air. Type II cells isolated from neonatal rats maintained in oxygen for 6 days also showed glutathione levels twice those found in cells isolated from animals in room air. The activity of antioxidant enzymes (glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase) was increased in lungs of newborn rats exposed to 100% oxygen either at birth or 2 days of age. Antioxidant enzyme activity of lung explants cultured in 95% oxygen, 5% CO2 was also higher than in explants maintained in room air. These results suggest that the increases in glutathione and of antioxidant enzymes in vivo and in vitro are a direct effect of oxygen exposure in lung and that the increase of both glutathione and antioxidant enzyme activity is intrinsic to the lung cell itself. It is likely that increases in glutathione in lung represent an important protective mechanism against oxidant injury.
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PMID:The responses of glutathione and antioxidant enzymes to hyperoxia in developing lung. 403 84

The purpose of this study was to correlate the exercise-induced changes of oxidant stress enzymes with possible modification of the response to the putative oxidant stressor doxorubicin. Enzymatic and histological changes were studied in mice placed on a 21-wk swim training program (1 h/day, 5 days/wk) with and without anthracycline administration. Doxorubicin (4 mg/kg) was administered intravenously through a tail vein on 10 separate days over a 7-wk period (twice weekly during weeks 10, 11, 14, 15, and 16). Blood, liver, and heart levels of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GP) were measured following the 9th and 21st wk. Myocardial histomorphological observations were made by light microscopy after 21 wk. Following 9 wk of training swim-trained animals had significantly elevated levels of CAT, SOD, and GP in blood, as well as elevated GP in liver. After 21 wk, trained animals, regardless of drug status, had elevated blood CAT and SOD activity and increased liver CAT and GP. Training also produced increases in blood GP, liver SOD, and heart CAT; however, in conjunction with doxorubicin these changes were not seen. The degree of cardiotoxicity was significantly greater in the sedentary drug-treated animals than in the swim-trained drug-treated animals. The results suggest a correlation between antioxidant enzyme levels in blood and liver and the degree of damage caused by an anthracycline drug. It was concluded that exercise ameliorates severe toxic damage caused by doxorubicin administration, possibly by increasing enzymes that combat free radical damage.
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PMID:Effect of exercise training on antioxidant enzymes and cardiotoxicity of doxorubicin. 405 7

This study was designed to investigate the effect of the natural bioflavonoid compound cianidanol on the blood lipid peroxide status of patients with chronic hepatitis. Nine patients had chronic active liver disease--seven of them hepatitis B virus-positive--and five had chronic alcoholic hepatitis. Besides some biochemical liver function tests (serum bilirubin, aminotransferases and gamma-glutamyl transferase), the changes in the serum level of malondialdehyde (a thiobarbituric acid reactive substance) as one of the end-products of lipid peroxidation, as well as the quantity/or activity of enzymes controlling peroxidation (superoxide dismutase (SOD), glutathione peroxidase and catalase) were measured. In addition, the serum level of the natural antioxidant vitamin E was followed-up. Cianidanol treatment (at a dose of 3.0 g/day for one month and of 1.5 g/day for two months) resulted in a slight improvement in aminotransferases and a significant fall (normalization) of high serum malondialdehyde level. After a marked transient increase, serum SOD content decreased while glutathione peroxidase and catalase activities as well as the vitamin E blood level increased during the treatment. Results suggest that (cianidanol in vivo inhibits lipid peroxidation and influences antioxidant enzyme systems and vitamin E in the blood of patients with chronic hepatitis.
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PMID:Effects of cianidanol on the blood lipid peroxide status in patients with chronic hepatitis. 409 18

Neonatal, adult, and fetal rat lungs of 18, 20, and 22 d gestation from four to six litters were examined for cytochrome oxidase, glucose-6-phosphate dehydrogenase, catalase, glutathione peroxidase, copper-zinc and manganese superoxide dismutase activities. All results were corrected for the contribution of enzymes in blood that contaminate homogenates. Because lung protein/DNA ratios and body water change significantly with gestational age, enzyme activities were expressed as U/mg DNA. All activities were low in d 18 lung and increased with advancing gestational age. Only catalase and copper-zinc superoxide dismutase increased activity in response to air breathing, suggesting that maturation of the antioxidant enzyme system is virtually complete before delivery. Activities of glucose-6-phosphate dehydrogenase, catalase, glutathione peroxidase, and manganese superoxide dismutase were higher in neonatal than in adult lung.
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PMID:Pulmonary antioxidant enzyme maturation in the fetal and neonatal rat. I. Developmental profiles. 608 81

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

Endotoxin treatment of adult rats before hyperoxic exposure significantly increases their survival rate in >95% O(2) (J. Clin. Invest.61: 269, 1978). In this study, we wished to determine: (a) whether endotoxin would protect against O(2) toxicity if it were administered after the animals were already in >95% O(2) for 12-48 h; and (b) the relationship between the endogenous antioxidant enzymes of the lung and the protective effect of endotoxin treatment. Our results showed that adult rats given a single 500 mug/kg dose of endotoxin up to 36 h after the onset of O(2) exposure had significantly increased survival rates and decreased lung fluid accumulation compared to untreated animals in O(2) (P < 0.05). (Survival, 16/49 [untreated rats]; 18/20 [endotoxin at 12 h after the start of O(2) exposure]; 25/26 [endotoxin-24 h]; 15/20 [endotoxin-36 h].)Endotoxin-treated animals in O(2) showed increases in pulmonary superoxide dismutase, catalase, and glutathione peroxidase activities before the usual time of onset of measurable pulmonary edema in untreated animals in O(2). When diethyldithiocarbamate was used to block the superoxide dismutase enzyme rise in the endotoxin-treated rats in O(2), the protective action of endotoxin against pulmonary O(2) toxicity was nullified. In endotoxin-treated, O(2)-exposed mice, there were no lung antioxidant enzyme increases, and no protective effect from O(2) toxicity was achieved. We conclude that, in the rat, a single dose of endotoxin given even 36 h after the onset of hyperoxic exposure results in marked protection against O(2)-induced lung damage; and the increased lung antioxidant enzyme activity in the endotoxin-treated rats appears to be an essential component of this protective action.
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PMID:Potection from oxygen toxicity with endotoxin. Role of the endogenous antioxidant enzymes of the lung. 624 6


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