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)

Antioxidant enzymes (CAT, catalase; GPx, selenium nondependent glutathione peroxidase; GST, glutathione-S-transferase; GR, glutathione reductase; DHAR, dehydroascorbate reductase) were determined in the mitochondria of diapausing and non-diapausing larvae and pupae of both diapausing and non-diapausing larvae of the European corn borer (Ostrinia nubilalis, Hubn., Lepidoptera: Pyralidae). CAT, GST, and DHAR activity in mitochondria of diapausing larvae were reduced compared to non-diapausing larvae. Pupae of diapaused-larvae possessed lower GST, but higher DHAR activities compared to pupae of non-diapaused individuals. Comparison between larvae and pupae revealed lower GPx activity in the mitochondria of pupae. CAT activity in the mitochondria of pupae was higher compared to diapausing larvae, but lower than in non-diapausing ones. Correlation and canonical discriminant analyses revealed different antioxidant enzyme compositions for a particular stage and developmental pattern. Our results show that antioxidant enzymes have a similar role in the regulation of energetics in mitochondria as that in diapause and metamorphosis.
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PMID:Antioxidant defense in mitochondria during diapause and postdiapause development of European corn borer (Ostrinia nubilalis, Hubn.). 1729 23

The objective of this study was to investigate the role of the Pap1 transcription factor in response to long-term Cd(2+) stress. The Schizosaccharomyces pombe wild-type strain and the Deltapap1 mutant, treated with 0.5 mM CdSO(4), were used in antioxidant enzyme and gene expression experiments. The Deltapap1 mutant proved to be sensitive to Cd(2+) in the spot test assay, suggesting that the Pap1 transcription factor plays an important role in the response to Cd(2+) stress. The Cd(2+) uptake was the same in both strains. Determination of the superoxide level in the wild-type strain proved that superoxide was generated, suggesting that long-term Cd(2+) treatment could trigger oxidative stress. Furthermore, the Deltapap1 mutant displayed higher amounts of superoxide. These results were supported by the significantly lower amount of peroxide generated in the reaction catalyzed by superoxide dismutase (SOD). The Deltapap1 mutant had a significantly lower glutathione S-transferase specific activity than that of the wild-type strain during long-term Cd(2+) stress, caused by the lower GSH and sulfide assimilation. We have demonstrated that GST III activity was not induced by Cd(2+) stress in the Deltapap1 mutant. The overall low GST activity was not sufficient for the cell to eliminate Cd(2+) caused damage and could result in a Cd(2+)-sensitive phenotype of the Deltapap1 mutant. The RT-PCR and Northern blot experiments proved that gst2 was not induced either by short-term or by long-term Cd(2+) treatment. The SPCC965.06 (a putative K(+) ion channel subunit) gene expression increased, while the hmt1 (an ABC-type vacuolar transporter protein) expression decreased in both strains. No detectable alteration in the mRNA levels of, gpx1, hmt2, sod1, sod, and trx1 was observed. SOD enzyme analyses revealed that the absence of Pap1 protein could result in a lower SODs activity and affect the sulfate assimilation. This is the first report on the fact that the Pap1 transcription factor could play an important role in the cellular post-transcriptional/post-translational enzyme activity induction processes of SODs that occur in response to Cd(2+).
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PMID:Gene expressions and enzyme analyses in the Schizosaccharomyces pombe Deltapap1 transcription factor mutant exposed to Cd(2+). 1730 22

The development of diabetic complications has usually been attributed to the nonenzymic glycation of tissue proteins. Only recently, however, have researchers examined the possible role on free radicals in the pathogenesis of diabetes. In the present study, glutathione (GSH) and major antioxidant enzyme levels in plasma of patients with type II diabetes mellitus were assessed both before and after 3 months of N-acetylcysteine (NAC) therapy. Thirty-two diabetic patients were examined as well as fifteen healthy controls. Before treatment with NAC, glutathione peroxidase (GPx), catalase (CAT), and (GSH) levels of diabetic patients and control subjects showed no significant differences, whereas glutathione S-transferase (GST) levels were higher in type II diabetic patients. Following 3 months of Following NAC supplementation, GSH, GST, and CAT levels were found to be similar to the levels before treatment. On the other hand, GPx activity was significantly lower compared with the values before treatment. According to this finding, NAC treatment could have a positive effect on GPx values in type II diabetic patients showing abnormally high values.
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PMID:The role of N-acetylcysteine treatment on anti-oxidative status in patients with type II diabetes mellitus. 1733 80

Individuals affected by liver steatosis seldom have symptoms of liver injury, but may be particularly vulnerable to oxidative insults. In this study, we evaluated liver redox alterations produced by acute ethanol administration to rats that were fed a high-fat diet (HFD). Adult male Wistar rats were fed HFD or standard diet (controls) for 1 month; a group of animals from each condition were gavaged with 35% (vol/vol) ethanol every 12h for the last 3 days of the experiment. Total lipid content determined in liver showed lipid accumulation after HFD or HFD combined with ethanol. HFD alone induced a significant rise of seric alanine aminotransferase levels and a marked reduction of antioxidant enzyme activities (catalase, superoxide dismutase, glutathione transferase). Ethanol alone caused a significant rise of seric cholesterol levels and enhanced mitochondrial H2O2 production, but without apparent oxidative stress as evaluated by thiobarbituric acid-reactive substances (TBARS) assay. The combination of HFD and acute ethanol caused an increase of TBARS, indicating lipid peroxidation, most likely as a consequence of a decrease in antioxidant defenses induced by HFD and of an increase in reactive oxygen species production induced by ethanol. Principal component analysis, based on all the measured parameters, that is, serum liver function tests, antioxidant enzyme activities, mitochondrial H2O2 release, and TBARS, indicated that HFD and ethanol act as two independent factors. In conclusion, our results show that HFD or acute ethanol alone produce, at the most, mild liver injury, whereas their combination triggers oxidative stress, possibly inducing a progression toward liver disease. Hence, our data indicate that a diet too rich in fat is a serious risk factor for the occurrence of liver injury deriving from acute ethanol consumption.
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PMID:Combined effects of high-fat diet and ethanol induce oxidative stress in rat liver. 1741 98

Our aim was to study the protective effect of quercitin on liver cirrhosis induced by carbon tetrachloride (CCl(4)) in rats and its relationship with liver morphology. Thirty male Wistar rats weighing 200-250 g were randomly divided into three groups: control, CCl(4), and CCl(4)+ quercetin. Rats in the experimental groups were given CCl(4) (0.5 ml/kg i.p.), diluted 1:6 in vegetable oil (5 mmol/kg body wt), at 10:00 p.m. every 4 days for 17 weeks. Quercetin (500 microl/kg i.p.; 150 micromol/kg body wt) or vehicle was administered at 6:00 p.m. for the last 3 weeks of the study. Control group rats were given only olive oil for the same period. At the end of the 17 weeks, all rats were sacrificed. Blood samples were taken for determination of serum indicators (ALT, AST, total bilirubin, conjugated bilirubin, factor V) and the livers were dissected out and divided into two parts: one was homogenized and the supernatant was used for measurement of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities, as well as lipid peroxidation. The other part was used for the histopathological study. CCl(4) caused a marked rise in serum levels of ALT, AST, total bilirubin, and conjugated bilirubin, as well as a decrease in factor V (P<0.05). Lipid peroxidation levels were significantly increased, whereas GSH, SOD, catalase, GPx, and GST levels were decreased in the liver of CCl(4)-treated rats. Quercetin (50 mg/kg/day) successfully attenuated these effects of CCl(4). We conclude that quercetin has beneficial effects on liver fibrosis in rats by enhancing antioxidant enzyme activity and decreasing the pro-oxidant effect.
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PMID:Quercetin prevents oxidative stress in cirrhotic rats. 1743 69

Stannous chloride (SnCl2) is a reducing chemical agent used in several man-made products. SnCl2 can generate reactive oxygen species (ROS). Therefore, the present study has been carried out to investigate the antioxidant action of l-ascorbic acid (AA) in minimizing SnCl2 toxicity on lipid peroxidation, antioxidant enzyme, and biochemical parameters in male New Zealand white rabbits. Animals were assigned to one of four treatment groups: 0mg AA and 0mg SnCl2/kg BW (control); 40 mg AA/kg BW; 20mg SnCl2/kg BW; 20mg SnCl2 plus 40 mg AA/kg BW. Rabbits were orally administered the respective doses every other day for 12 weeks. Results obtained showed that SnCl2 significantly (P<0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma, while the activities of glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT), and the level of sulfhydryl groups (SH-group) were decreased (P<0.05) in blood plasma. Aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP) and lactate dehydrogenase (LDH) activities were decreased (P<0.05). Stannous chloride significantly (P<0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL), glucose, urea and total bilirubin. On the other hand, the level of plasma high-density lipoprotein (HDL), total protein (TP), albumin (A) and globulin (G) were significantly (P<0.05) decreased. Ascorbic acid alone significantly decreased the levels of TBARS, lipids and urea, and increased the activities of GST, SOD and CAT, and the levels of SH-group and proteins. While the rest of the tested parameters were not affected. Also, the presence of AA with SnCl2 alleviated its harmful effects on most of the tested parameters. Therefore, the present results revealed that treatment with AA could minimize the toxic effects of stannous chloride.
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PMID:Study of the protective effect of ascorbic acid against the toxicity of stannous chloride on oxidative damage, antioxidant enzymes and biochemical parameters in rabbits. 1743 20

We examined the antioxidant effects of polyphenol/anthocyanin-rich potato (Solanum tuberosum cv. Shadow-Queen) flakes in male rats fed a high-cholesterol diet. The rats were served either a high-cholesterol (0.5% cholesterol plus 0.125% sodium cholate) diet, or a high-cholesterol diet containing a mixture of 243 g alpha-maize starch/kg supplemented with one of the following (per kg diet): 300 g medium purple potato (Shadow-Queen), 300 g white potato (Solanum tuberosum cv. Toyoshiro) or 300 g dark purple sweet potato (Ipomoea batatas cv. Ayamurasaki) flakes for 28 d. We analysed thiobarbituric acid reactive substance (TBARS) levels in the serum and liver, and antioxidant enzyme activities in the liver. At this dosage, TBARS levels in the serum and liver of the Shadow-Queen and Ayamurasaki groups were significantly lower than those in the control and Toyoshiro groups. The serum urate levels in all the flake groups were significantly lower than that in the control group. The hepatic glutathione levels in the Shadow-Queen and Ayamurasaki groups were significantly higher than in the control and Toyoshiro groups. The activities of hepatic glutathione reductase and glutathione S-transferase in the Shadow-Queen and Ayamurasaki groups were significantly greater than those in the control group. These results show that modulation of antioxidant enzymes and oxidative status in the serum and liver by the purple potato flake diet (Shadow-Queen) containing polyphenols/anthocyanins may play an important role in the protection against adverse effects related to oxidative damage in rats fed a high-cholesterol diet.
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PMID:Effects of anthocyanin-rich purple potato flakes on antioxidant status in F344 rats fed a cholesterol-rich diet. 1755 1

In rat liver, in addition to their intrinsic transferase activity, alpha-class GSTs have Se-independent glutathione peroxidase activity toward fatty acid hydroperoxides, cumene hydroperoxide and phospholipids hydroperoxides but not toward H(2)O(2.) We have previously shown that hepatic GST activity by these isoenzymes is significantly increased 24h after cadmium or manganese administration (Casalino et al., 2004). Here it is reported that Se-independent glutathione peroxidase activity by alpha-class GSTs is also stimulated in the liver of intoxicated rats. The stimulation is associated with a higher level of alpha-class GST proteins, whose induction is blocked by actinomycin D co-administration. The observed Se-independent glutathione peroxidase activity is due to alpha-class GST isoenzymes, as indicated by the studies with diethyldithiocarbamate which, at any concentration, equally inhibits both GST and Se-independent glutathione peroxidase and is an uncompetitive inhibitor of both enzymes. As for liver Se-GSPx, it is not at all affected under these toxic conditions. For comparison, we have evaluated the status of another important antioxidant enzyme, NAD(P)H:quinone reductase, 24h after cadmium or manganese administration. NQO1 too results strongly stimulated in the liver of the intoxicated rats. In these animals, a higher expression of Nrf2 protein is observed, actively translocated from the cytoplasm to the nucleus. The results with the transcription inhibitor, actinomycin D, and the effects on Nrf2 protein are the first clear indication that acute manganese intoxication, similarly to that of cadmium and other heavy metals, increases both the hepatic level of Nrf2 and its transfer from the cytoplasm to the nucleus where it actively regulates the induction of phase II enzymes.
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PMID:The Nrf2 transcription factor contributes to the induction of alpha-class GST isoenzymes in liver of acute cadmium or manganese intoxicated rats: comparison with the toxic effect on NAD(P)H:quinone reductase. 1757 73

Oxidative stress has been suggested to be an important molecular mechanism of toxic effects of lead in the kidney. Thioredoxin reductase-1 is a selenoprotein involved in many cellular redox processes. This study evaluated the effect of acute and chronic exposure intraperitoneally to lead acetate on thioredoxin reductase-1 activity and on other oxidative stress parameters in the rat kidney, as well as on indicators of renal function commonly used to assess lead poisoning. Acute exposure to 25 mg/kg lead acetate increased superoxide dismutase and thioredoxin reductase-1 activity (after 6, 24 and 48 hr), while exposure to 50 mg/kg lead acetate increased catalase activity (after 48 hr) and inhibited delta-aminolevulinate dehydratase activity (after 6, 24 and 48 hr) in the kidney (P < 0.05). Chronic exposure (30 days) to 5 mg/kg lead acetate inhibited delta-aminolevulinate dehydratase and increased glutathione S-transferase, non-protein thiol groups, catalase, thioredoxin reductase-1 and uric acid plasma levels, while exposure to 25 mg/kg lead acetate reduced body weight and delta-aminolevulinate dehydratase, but increased glutathione S-transferase, non-protein thiol groups and uric acid plasma levels (P < 0.05). No changes were observed in thiobarbituric acid reactive substances, glutathione peroxidase, creatinine or inorganic phosphate levels after either acute or chronic exposure. Our results suggest that thioredoxin reductase-1 may be an early indicator of acute exposure to low lead doses.
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PMID:Effect of lead acetate on cytosolic thioredoxin reductase activity and oxidative stress parameters in rat kidneys. 1765 9

The aim of this investigation was to evaluate toxicity effects of pesticides in aquatic invertebrates using in situ bioassays with the local species, Daphnia magna. Investigations were carried out in the Delta del Ebro (northeast Spain) during the main growing season of rice (May-August). Measures of energy consumption (i.e., algal grazing) and of specific biochemical responses (biomarkers) were conducted in individuals transplanted at four stations, including a clean site upstream of the affected area and the three main channels that collect and drain the water from the rice fields into the sea. Seventeen pesticides were analyzed in water by on-line solid-phase extraction-liquid chromatography-tandem mass spectrometry. The results obtained indicated high levels of pesticides in water, with peak values of 487 microg/L for bentazone, 8 microg/L for methyl-4-chlorophenoxyacetic acid, 5 microg/L for propanil, 0.8 microg/L for molinate, and 0.7 microg/L for fenitrothion. Measured biological responses denoted severe effects on grazing rates; a strong inhibition of cholinesterases and carboxylesterases, which are specific biomarkers of organophosphorous and carbamate pesticides; and altered patterns of the antioxidant enzyme catalase and the phase II metabolizing enzyme glutathione S-transferase. Correlation analysis with pesticide residue levels converted to toxic units relative to its acute 48-h median lethal concentration of D. magna indicated significant and negative coefficients between the dominant pesticide residues and the observed biological response, thus denoting a clear cause-and-effect relationship. The results emphasize the importance of considering specific (biomarkers) as well as more generalized and ecologically related (grazing) in situ responses to identify and evaluate biological effects of environmental contaminants in the field.
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PMID:Combined use of biomarkers and in situ bioassays in Daphnia magna to monitor environmental hazards of pesticides in the field. 1771 26


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