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)

The influence of intratracheally instilled bleomycin (10 mg x kg-1) on antioxidant enzyme activity as well as on lipid peroxidation product levels after 7 and 14 days from drug administration in rat lungs was investigated. The 200-400% increase in superoxide dismutase, glutathione peroxidase, glutathione reductase, catalase and glucose-6-phosphate dehydrogenase activities were observed, as compared to control group. The levels of malondialdehyde, conjugated dienes and lipid hydroperoxides in lung tissue of bleomycin-treated rats were also higher than those in control group. These phenomena are the signs of adaptative mechanisms induction in lungs, protecting the tissue from dangerous effect of bleomycin-generated free radicals.
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PMID:[The influence of intratracheal bleomycin instillation on peroxidative processes in rat lung tissue]. 172 38

Air-breathing organisms experience an elevated concentration of oxygen mainly under two conditions. One occurs at birth when the O2 tension in the lung increases from approximately 25 torr present in utero to approximately 100 torr. The lungs, in particular, are also exposed to hyperoxia when oxygen is administered for therapeutic reasons. Under hyperoxic conditions, increased lung antioxidant enzyme activity is important for survival. The molecular basis for the increase in antioxidant enzyme gene expression under these circumstances is not well understood; in hyperoxia-exposed neonatal rats the elevation of lung catalase activity is not due to an increased rate of transcription but is associated with an increased concentration of catalase mRNA due to enhanced stability of the mRNA (Clerch, L.B., Iqbal, J., and Massaro, D. (1991) Am. J. Physiol. 260, L428-L433). We now show that neonatal rat lung protein forms specific complexes with catalase mRNA; this binding is redox-sensitive since when oxidizing agents are added binding is abolished but is restored by reducing agents. Our data also indicate lungs from hyperoxia-exposed rats have a larger proportion of catalase RNA-binding protein in oxidized form than lungs from air-breathing rats. This redox-sensitive binding of protein to catalase mRNA may be important in the control of catalase gene expression.
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PMID:Oxidation-reduction-sensitive binding of lung protein to rat catalase mRNA. 173 43

Intralipid, derived from soybean oil and containing a high percentage of n-6 family polyunsaturated fatty acids (PUFA) and also linolenic acid, an n-3 family PUFA, is commonly the first fat source provided to very low birth weight premature infants. Following up on our previous reports that newborn rats born to dams fed high-PUFA diets demonstrate superior tolerance to hyperoxia, we examined whether the high-PUFA fat source Intralipid might also protect against oxygen toxicity. Adult female rats were fed either regular Rat Chow or fat-free diet containing 20%-Intralipid as the fat source for 3 wk before and then throughout pregnancy and lactation. One- and 5-d-old offspring of Intralipid diet-fed dams demonstrated significant increases in lung lipid n-6 family PUFA plus elevated linolenic acid compared with regular diet-fed offspring. These characteristic fatty acid patterns, apparent in total lung lipids, were even more pronounced in the triglyceride fraction compared with the phospholipid fraction. Associated with these fatty acid changes were significantly improved hyperoxic survival rates (89 out of 95 = 94% survival after 7 d of greater than 95% O2 exposure) in Intralipid offspring (versus 89 out of 106 = 84%, p less than 0.05 in regular diet offspring) and evidence of superior clinical/pathologic status. No differences in pulmonary antioxidant enzyme or surfactant system development, response of antioxidant enzymes to hyperoxic exposure, or lung prostaglandin E2, 6-keto PGF1-alpha or leukotrienes C4-F4 were present. These findings continue to support the hypothesis that increasing lung PUFA content may provide increased O2 free radical scavenging capacity, thus protecting against hyperoxic lung damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intralipid increases lung polyunsaturated fatty acids and protects newborn rats from oxygen toxicity. 175 94

Mice of the C57BL/6 (B6) strain show a much lower proportion of marrow erythroid progenitor cells (BFU-E) in DNA synthesis in vivo than mice of the congeneic B6S strain. However, when assayed in vitro marrow cells from both strains show high proportions of BFU-E in S-phase. BFU-E from normal B6 mice have been previously shown to be specifically inhibited from entering S-phase in vitro by the antioxidant enzyme superoxide dismutase (SOD), however, in this study we have found that BFU-E taken from the marrow of B6S mice or B6 mice which have been subjected to bleeding are insensitive to SOD inhibition in vitro. Comparisons of results from in vivo and in vitro cycling assays done with cells from both strains indicate that a large proportion of marrow BFU-E in normal B6 mice are halted in the pre-S portion of the cell cycle in vivo, and these halted cells are prevented from going into S-phase in vitro by SOD. The insensitivity to SOD inhibition shown by BFU-E from B6S and bled B6 mice can be attributed to the absence of accumulation of SOD-susceptible cells in pre-S phase in these mice in vivo, and there is evidence to suggest that the difference in BFU-E cycling seen in vivo may be due to interactions between SOD and factors which stimulate cycling of BFU-E.
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PMID:Superoxide dismutase halts cycling of murine erythroid progenitor cells prior to S phase in vitro and possibly in vivo. 175 46

The antioxidant enzyme activities, the lipid peroxidation level, the parameters of glutathione metabolism, and the proportion of haemoglobin oxidation products were determined during the symptom-free period of childhood bronchial asthma. A decreased catalase activity and a significantly reduced glutathione instability were demonstrated as compared to the controls. The results indicate that antioxidant protection of the haemoglobin molecule in asthmatic children is considerably decreased.
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PMID:Examination of the role of oxygen free radicals in bronchial asthma in childhood. 175 97

The antioxidant enzyme superoxide dismutase (SOD) was previously shown to inhibit both the proliferation of murine erythroid DA-1 cells growing in the presence of Interleukin-3 (IL-3) and the DNA synthesis of marrow erythroid progenitor cells (BFU-E) in vitro. We show here that the inhibition of marrow cell DNA synthesis by SOD is specific for BFU-E and erythroid precursors (CFU-E), with other myeloid progenitors (CFU-GM) and stem cells (CFU-S) being unaffected, and IL-3 blocks the inhibitory effects of SOD on BFU-E in a dose-dependent manner. Extending earlier observations on the effects of SOD on cell proliferation, it was found that SOD was capable of inhibiting DA-1 cell proliferation supported by either IL-3 or erythropoietin (epo), but had no effect on IL-3 dependent FDCP-1 cells, nor on epo-dependent HCD-57 cells. Of several murine erythroleukemia cell lines tested, only those transformed with Friend SFFVa virus were inhibited by SOD, while those transformed with Friend SFFVp or MuLV virus were not affected. These results show that the effects of SOD are not antagonistic to particular growth factors but rather the inhibition is specific for erythroid cells, and cells of the proper stage can be inhibited even if they have been transformed to factor independence.
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PMID:Superoxide dismutase specifically inhibits erythroid cell DNA synthesis and proliferation. 176 66

One of the more fascinating aspects of in vivo research on pulmonary O2 toxicity is the striking difference in the response of the neonatal versus the adult animal to hyperoxia. In general, neonatal animals are much more resistant to the characteristic O2-induced lung pathology seen in adult animals in hyperoxia. Neonatal animals are also able to rapidly mount a protective lung biochemical response to high O2 exposure [increased pulmonary antioxidant enzyme (AOE) activities], an adaptive response which adult animals have lost the ability to manifest in greater than 95% O2. This review focuses on the disparate AOE responses of the neonatal versus adult animal in hyperoxia. It also explores other possible explanations for the striking O2 tolerance of young versus adult animals, including comparative O2 free radical production rates, inflammatory cell responses, lung lipid composition, repair capabilities, etc. Discussion also centers on a less well studied toxic complication associated with hyperoxic exposure in the neonatal animal, i.e., the marked inhibitory effect of O2 exposure on normal lung growth and development of an alveolarized lung with an expanded respiratory exchange surface area. Finally, effective experimental means of protecting adult (and neonatal) animals from pulmonary O2 toxicity are reviewed. A closing section considers the enlightening new information that molecular biology has revealed about the regulation of AOE gene expression during normal development and under conditions of hyperoxidant challenge.
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PMID:Developmental aspects of experimental pulmonary oxygen toxicity. 176 7

A concentration-response and C x T study were undertaken to determine the effect of phosgene (COCl2) inhalation on pulmonary antioxidant processes as determined by changes in endogenous glutathione (GSH) and antioxidant-associated enzymes (GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase, and superoxide dismutase). Rats were exposed to 0.0, 0.1, 0.25, 0.5, and 1.0 ppm phosgene for 4 hr and 0.25 ppm phosgene for 8 hr. The endpoints were assayed at 0, 1, 2, 3 and 7 days after exposure cessation. The lowest effective concentration was 0.1 ppm phosgene (increases in measured variables from 8 to 35% above control values). At all concentrations, major effects were observed 1 to 2 days after exposure (12 to 159% above control), peaking at 2 to 3 days postexposure (11 to 253% above control), and in some cases were still evident 7 days (10 to 65% above control) after exposure. The C x T study using the same dose (120 ppm-min), but different times and concentration (0.25 ppm for 8 hr and 0.5 ppm for 4 hr), showed a concentration dependence. The peak antioxidant enzyme changes observed for the higher concentration (0.5 ppm) were at least double those observed for the lower concentration (0.25 ppm). These enzyme changes were similar to those reported for the oxidants O3 and NO2. Although the suspected mechanism of initial damage between phosgene and these oxidants is different (acylation vs oxidation) the biological result is similar (i.e., damage, repair, and influx of cells), thus eliciting similar biochemical changes in response to pulmonary injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of inhaled phosgene on rat lung antioxidant systems. 177 56

Periodontitis induction causes a drastic elevation of free-radical lipid peroxidation, of ceruloplasmin level, and a reduction of antioxidant enzyme activities. Blood analysis shows hypercoagulation, appearance of paracoagulation products, reduced fibrinolysis, enhanced proaggregation activity of the periodontium, elevated levels of circulating immune complexes; this may by regarded as adaptation failure manifesting by these reactions. Morphologic examinations show foci of destructive changes. Administration of periodontal cytomedin reduced the level of free-radical oxidation, enhanced the activity of antioxidant enzymes, normalized antiaggregation activity of the periodontium and hemostasis and fibrinolysis parameters, and reduced the level of circulating immune complexes. The inflammatory reaction disappears completely, that is seen from reduced ceruloplasmin level and clinically. Morphologic study shows disappearance of foci of destruction. Thus, cytomedin of periodontal tissues may be regarded as an effective agent for the therapy of experimental periodontitis.
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PMID:[The mechanism of the therapeutic effect of periodontal cytomedin on the course of experimental periodontitis]. 178 Sep 21

To investigate the role of chronic oxidative stress in MPTP neurotoxicity, C57BL mice were maintained 6-8 weeks on diets deficient in nutrients essential to cellular antioxidant defenses, selenium (Se) and alpha-tocopherol (vit E), and the effects on tissue antioxidant status and MPTP toxicity were evaluated relative to controls on supplemented diets. Activities of the major antioxidant enzymes, glutathione peroxidase (GPx), catalase, and superoxide dismutase, and levels of malondialdehyde as a marker for oxidative stress, were measured in brain, lung, liver and blood. Caudate depletion of dopamine and its metabolites served as a measure of MPTP neurotoxicity. For mice on the Se deficient diet, levels of the selenoenzyme GPx decreased from 50% in brain to 90% in blood. No compensatory changes in the activities of the other antioxidant enzymes were observed and addition of vit E to the diet did not alter antioxidant enzyme activities or malondialdehyde levels. In animals not treated with MPTP, the Se deficient diet significantly increased malondialdehyde only in liver. No protective effect of the antioxidant supplements against caudate depletion of dopamine and its metabolites were observed. However, malondialdehyde levels were increased in the brains of MPTP treated mice on the low Se diets, suggesting the possibility of secondary oxidative damage to tissues accompanying the destruction of substantia nigra neurons by MPTP.
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PMID:Effects of low selenium diets on antioxidant status and MPTP toxicity in mice. 178 23


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