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)

Thioredoxin reductase (E.C.1.6.4.5.) has been purified to about 95% homogeneity from the Novikoff ascites rat tumor. The enzyme contained two subunits of approximately 58,000 daltons, with one FAD per subunit. The amino acid analysis is reported. An immunoadsorbent was prepared and used for affinity chromatography in order to improve the yield of the enzyme.
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PMID:Purification of thioredoxin reductase from the Novikoff rat tumor. 19 34

Small dosages of endotoxin (100--500 micrograms/kg) provide significant protection against the acute manifestations of pulmonary O2 toxicity and lethality. Ninety-seven percent of endotoxin-treated adult rats survived a 72-h exposure to greater than or equal to 95% O2 with mimimal lung changes, compared to 32% of control animals (P less than 0.01). Exposure to greater than or equal to 95% O2 for 7 days resulted in a 20% survival rate in untreated control rats vs. 98% survival in endotoxin-treated rats (P LESS THan 0.01). Histological evaluation of lung from survivors revealed substantially less collagen and reticular fiber deposition in the endotoxin-treated animal lungs. Endotoxin treatment was associated with increased activity of the protectant antioxidant enzyme systems of the lung in an apparent dose-response manner. Endotoxin's protective activity against O2 toxicity does not appear to depend on an initial toxic insult to the lung like with alpha-naphthylthiourea, oleic acid, or alloxan treatment. The data support a protective role for endotoxin against the acute and the more chronic manifestations of O2-induced pulmonary injury.
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PMID:Endotoxin protection against oxygen-induced acute and chronic lung injury. 53 52

Adult rats show evidence of severe lung damage after 72h of continuous exposure to hyperoxia (96-98% O2). Treatment of adult rats with a solution of Plasmanate, inadvertently contaminated with endotoxin-producing organisms, or with purified endotoxin itself markedly altered the lung toxicity associated with hyperoxic exposure (survival in treated animals = 110/113 [97%] versus survival in untreated animals = 56/172 [33%]). After 72h of hyperoxic exposure, the endotoxin-treated rats demonstrated significant increases in lung superoxide dismutase, catalase, and glutathione peroxidase activity, a protectant enzyme response not seen in untreated adult rats. The basis for endotoxin's protective effect from hyperoxic lung damage is believed to be related to the stimulated increase in activity of the pulmonary antioxidant enzyme defense system. Some previously known actions of endotoxin are speculated to also serve a protective function by opposing some of the usual detrimental effects of high concentrations of O2 on the lung.
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PMID:The role of endotoxin in protection of adult rats from oxygen-induced lung toxicity. 62 Dec 74

Neonatal and adult animals of five species were exposed to 95+% O2. Survival time and changes in lung antioxidant enzyme activity (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP)) in response to hyperoxia were determined. Adult animals succumbed to O2 lung toxicity in 3--5 days. Neonatal rats, mice and rabbits showed minimal lung changes after 7 days of hyperoxic exposure and these same neonatal animals showed rapid and significant increases in lung antioxidant enzyme activities. In contrast, neonatal guinea pigs and hamsters had no lung antioxidant enzyme response to hyperoxia and these neonates died in 95+% O2 as readily as their respective parent animals. Results from an in vitro hyperoxic exposure system suggest that the lack of enzymic response of the guinea pig (and hamster) neonates to O2 challenge is due to an inherent pulmonary biochemical unresponsiveness rather than to a deficiency of a necessary "serum factor." The results of this species and age study support the important role of the lung antioxidant enzyme defense system in protection of the lung from O2-induced injury.
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PMID:Oxygen toxicity in neonatal and adult animals of various species. 73 May 65

Polyclonal antisera to manganese and copper-zinc superoxide dismutases, catalase, glutathione peroxidase (GPx), and isozymes of glutathione S-transferase (liver and placental isolates, GST-L and GST-P, respectively) were used to localize these enzymes in normal rat lung by immunostaining. Light-microscopic results, using an immunoperoxidase technique, were expanded on by electron-microscopic immunogold localization. The findings were consistent with previous biochemical work. However, both GPx and GST-P were predominantly localized to extracellular connective tissue of the lung. These findings demonstrate the basal antioxidant enzyme phenotypes for parenchymal lung tissue at light- and electron-microscopic levels. Significant components of enzymatic defense to oxidant stress are heterogeneously distributed throughout rat lung tissue including both epithelial cell surfaces and the extracellular matrix.
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PMID:Immunolocalization of antioxidant enzymes and isozymes of glutathione S-transferase in normal rat lung. 128 3

The activity of the antioxidant enzymes catalase (CAT), peroxidases (POD), and superoxide dismutases (SOD) in whole blood and different blood fractions was analyzed in 20 normal human beings and correlated with the chromosomal sensitivity of lymphocytes to bleomycin (BLM) (measured as frequency of dicentric chromosomes per BLM dose). Our results demonstrate that both the physiologic activities of the enzymes and the chromosomal sensitivity to BLM exhibit an ample and significant interindividual variability. An inverse and linear correlation between chromosomal sensitivity to BLM and the concentration of 1) CAT and POD in plasma and 2) SOD in whole blood, erythrocytes, and plasma was found. On the other hand, the chromosomal sensitivity to BLM showed a direct correlation with the concentration of SOD and POD in mononuclear leukocytes. It is suggested that a determination of antioxidant enzyme (AOE) activities in a given cell population may serve to predict the chromosomal sensitivity to BLM.
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PMID:Chromosomal sensitivity of human lymphocytes to bleomycin. Influence of antioxidant enzyme activities in whole blood and different blood fractions. 128 12

Dose intensity is emerging as a crucial determinant of success in cytotoxic cancer therapy; however, myelosuppression presents as one of the major complications encountered with increased dose intensity. Therefore, investigators are looking at the use of cytokine administration in combination with cytotoxic therapy to overcome this problem. Interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha) have been shown to be beneficial in protecting the hematopoietic system from radiation and chemotherapy. In this report, we give an overview of studies using IL-1 and TNF-alpha as protective agents and discuss possible mechanisms involved in their protective action. Mice pretreated with IL-1 and/or TNF-alpha were shown to be protected from the lethal effects of radiation and it has been suggested that the mechanism for this protection may be through the production of the antioxidant enzyme manganese superoxide dismutase. Similarly, aldehyde dehydrogenase, an enzyme important in the metabolic pathway of cyclophosphamide compounds, has been implicated as being important in the protection of hematopoietic cells from 4-hydroperoxycyclophosphamide. While IL-1 and TNF-alpha stimulate both of these enzymes, other mechanisms are probably also operative for other forms of chemotherapy, i.e. IL-1 and TNF-alpha were shown to protect hematopoietic progenitors from phenylketophosphamide, a cyclophosphamide derivative that is not metabolized by the enzyme aldehyde dehydrogenase. Furthermore, malignant as well as normal cells may possess receptors for these cytokines; therefore, IL-1 and TNF-alpha will have to be selective in their protection. They must be capable of protecting normal hematopoietic cells while rendering malignant cells susceptible to the toxic actions of the chemotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The therapeutic potential of interleukin-1 and tumor necrosis factor on hematopoietic stem cells. 129 Sep 56

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 purpose of the studies was to determine the effect of Ambroxol on the activity of antioxidant enzymes and on the glutathione level as well as the intensity of the peroxidative processes in the lung tissue, alveolar macrophages and plasma in dogs after unilateral pulmonectomy. On the 2nd and 6th day after the surgery the activity of antioxidant enzymes and the glutathione level were studied in the remaining lung. The levels of the lipid peroxidation products were determined in the analogous system. In both examined groups the increase in the antioxidant enzyme activity and the lipid peroxidation product levels was observed in the remaining lung after the surgery. In Ambroxol-treated animals the statistically significant increase in the antioxidant enzyme activity was noted while the intensity of peroxidative processes was found to be lower. This fact may suggest that Ambroxol stimulates the resistance of the lung tissue to the free radical activity and inhibits the lung peroxidative processes in dogs after pulmonectomy.
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PMID:The influence of Ambroxol on peroxidative processes in lung and plasma in dogs after pulmonectomy. 130 8

Copper-zinc-superoxide dismutase (CuZn-SOD), a cytosolic antioxidant enzyme that is specific for scavenging superoxide radicals, is involved in neuroprotective mechanisms in brain injury following trauma and cerebral ischemia. Liposome-entrapped CuZn-SOD exhibit beneficial effects in vivo on cold-induced vasogenic edema and on blood-brain barrier disruption. The increased levels of edema and infarction following a focal cerebral ischemia also are decreased by the pretreatment of liposome-entrapped CuZn-SOD. The protective role of SOD on brain injury was further extended and confirmed in studies using transgenic mice overexpressing human CuZn-SOD. Our studies so far suggest that increased cerebral levels of SOD, either by means of external pharmacological application or by genetic manipulations, ameliorate brain edema and infarction induced by trauma and focal cerebral ischemia.
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PMID:Antioxidant-dependent amelioration of brain injury: role of CuZn-superoxide dismutase. 131 99


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