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)

This paper reports a method for extracting the antioxidant enzyme superoxide dismutase (SOD) from the needles of red spruce (Picea rubens Sarg.), loblolly pine (Pinus taeda L.), and scotch pine (Pinus sylvestris L.) with high efficiency and free from interfering compounds. The extraction employs phosphate buffer with polyvinylpolypyrrolidone and Triton X-100 followed by dialysis overnight. The isozymes of SOD in each species were separated electrophoretically and tested for their sensitivity to KCN and H(2)O(2). An isozyme resistant to these inhibitors was found in the spruce but not the pine needles. The isozymes from the spruce needles were examined for individual responses to aging and H(2)O(2) inhibition. Four of the five CuZn isozymes in spruce were found to have increased significantly but equally by October of their first year and two of those four isozymes were found to be more sensitive to H(2)O(2). The response of the SOD isozymes in loblolly pine seedlings to O(3) was also examined and the isozymes were found to be induced equally. Because the SOD activity in the young pine needles was too low to electrophorese, the SOD activity from the pines in the O(3) experiment had to be partially purified using CHCl(3) and ethanol, then concentrated.
 ...
PMID:Assay and Electrophoresis of Superoxide Dismutase from Red Spruce (Picea rubens Sarg.), Loblolly Pine (Pinus taeda L.), and Scotch Pine (Pinus sylvestris L.) : A Method for Biomonitoring. 1666 37

The study aim was to investigate the interaction of physical conditioning and chronic ethanol ingestion on blood pressure (BP), heart rate (HR), nitric oxide (NO) and oxidants/antioxidants balance in the plasma of rats. Male Fisher rats were divided into four groups of seven animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks; (2) ethanol (4 g kg(-1), orally) daily for 12 weeks; (3) exercise training on treadmill plus sucrose daily for 12 weeks and (4) exercise training on treadmill followed by ethanol (4 g kg(-1), orally) daily for 12 weeks. The body weight, BP and HR were recorded every week. The animals were sacrificed under ether anesthesia after 12 weeks, blood collected in heparinzed vials, plasma isolated and analyzed. The results show that exercise training significantly lowered the weight gain 6-12 weeks in ethanol treated rats compared to ethanol alone or control rats. The mean arterial BP was significantly elevated 6-12 weeks after ethanol ingestion without significant alterations in HR. Exercise training lowered the BP close to the normal control values in ethanol fed rats. Ethanol significantly decreased the plasma NO levels, reduced to oxidized glutathione ratio (GSH/GSSG) and antioxidant enzymes-superoxide dismutase (CuZn-SOD, and Mn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities while plasma NADPH oxidase activity and malondialdehyde (MDA) levels were significantly elevated compared to control. Exercise training significantly restored the depletion of plasma NO levels, GSH/GSSG ratio, and antioxidant enzyme activities and normalized the MDA levels and NADPH oxidase activity in the plasma of ethanol treated rats. The study concluded that physical conditioning attenuates the chronic ethanol-induced hypertension by augmenting the NO bioavailability and reducing the oxidative stress response in the plasma of rats.
 ...
PMID:Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model. 1671 71

The antioxidant enzyme catalase by reacting with H(2)O(2), forms the compound known as compound I (catalase-H(2)O(2)). This compound is able to oxidise ethanol to acetaldehyde in the CNS. It has been demonstrated that 3-nitropropionic acid (3-NPA) induces the activity of the brain catalase-H(2)O(2) system. In this study, we tested the effect of 3-NPA on both the brain catalase-H(2)O(2) system and on the acute locomotor effect of ethanol. To find the optimal interval for the 3-NPA-ethanol interaction mice were treated with 3-NPA 0, 45, 90 and 135min before an ethanol injection (2.4mg/kg). In a second study, 3-NPA (0, 15, 30 or 45mg/kg) was administered SC to animals 90min before saline or several doses of ethanol (1.6 or 2.4g/kg), and the open-field behaviour was registered. The specificity of the effect of 3-NPA (45mg/kg) was evaluated on caffeine (10mg/kg IP) and cocaine (4mg/kg)-induced locomotion. The prevention of 3-NPA effects on both ethanol-induced locomotion and brain catalase activity by L-carnitine, a potent antioxidant, was also studied. Nitropropionic acid boosted ethanol-induced locomotion and brain catalase activity after 90min. The effect of 3-NPA was prevented by l-carnitine administration. These results indicate that 3-NPA enhanced ethanol-induced locomotion by increasing the activity of the brain catalase system.
 ...
PMID:Acute administration of 3-nitropropionic acid, a reactive oxygen species generator, boosts ethanol-induced locomotor stimulation. New support for the role of brain catalase in the behavioural effects of ethanol. 1693 17

Yeast cytochrome c peroxidase (CCP) efficiently catalyzes the reduction of H(2)O(2) to H(2)O by ferrocytochrome c in vitro. The physiological function of CCP, a heme peroxidase that is targeted to the mitochondrial intermembrane space of Saccharomyces cerevisiae, is not known. CCP1-null-mutant cells in the W303-1B genetic background (ccp1Delta) grew as well as wild-type cells with glucose, ethanol, glycerol or lactate as carbon sources but with a shorter initial doubling time. Monitoring growth over 10 days demonstrated that CCP1 does not enhance mitochondrial function in unstressed cells. No role for CCP1 was apparent in cells exposed to heat stress under aerobic or anaerobic conditions. However, the detoxification function of CCP protected respiring mitochondria when cells were challenged with H(2)O(2). Transformation of ccp1Delta with ccp1(W191F), which encodes the CCP(W191F) mutant enzyme lacking CCP activity, significantly increased the sensitivity to H(2)O(2) of exponential-phase fermenting cells. In contrast, stationary-phase (7-day) ccp1Delta-ccp1(W191F) exhibited wild-type tolerance to H(2)O(2), which exceeded that of ccp1Delta. Challenge with H(2)O(2) caused increased CCP, superoxide dismutase and catalase antioxidant enzyme activities (but not glutathione reductase activity) in exponentially growing cells and decreased antioxidant activities in stationary-phase cells. Although unstressed stationary-phase ccp1Delta exhibited the highest catalase and glutathione reductase activities, a greater loss of these antioxidant activities was observed on H(2)O(2) exposure in ccp1Delta than in ccp1Delta-ccp1(W191F) and wild-type cells. The phenotypic differences reported here between the ccp1Delta and ccp1Delta-ccp1(W191F) strains lacking CCP activity provide strong evidence that CCP has separate antioxidant and signaling functions in yeast.
 ...
PMID:Phenotypic analysis of the ccp1Delta and ccp1Delta-ccp1W191F mutant strains of Saccharomyces cerevisiae indicates that cytochrome c peroxidase functions in oxidative-stress signaling. 1701 26

Steamed roots of Rehmannia glutinosa (R. glutinosa) have been traditionally used in Oriental medicine for the treatment of auditory diseases such as tinnitus and hearing loss. To investigate whether the ethanol extract of steamed roots of R. glutinosa (SRG) increases activity of antioxidant enzymes and the level of glutathione (GSH), we measured activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione reductase (GR) and GSH level in HEI-OC1 cells after treatment with 5-50 microg/ml of SRG. The SOD and CAT activities were significantly increased in the presence of SRG compared to the control group. Maximal activities of SOD and CAT were observed in these cells exposed to 10 microg/ml of SRG. The GPX activity also increased dramatically in response to the treatment with SRG in a dose-dependent manner. The GR activity was only increased in the presence of 50 microg/ml of SRG compared to the control group. The level of GSH gradually increased in the presence of 5-50 microg/ml of SRG. In the cytotoxicity test, 5-50 microg/ml of SRG did not show any significant cytotoxicity. These results suggest that the traditional use of R. glutinosa for the treatment of auditory diseases may be explained, in part, by activation of intracellular antioxidant enzyme systems. Further studies are necessary to clarify the active constituents of SRG responsible for such biomolecular activities.
 ...
PMID:Rehmannia glutinosa activates intracellular antioxidant enzyme systems in mouse auditory cells. 1716 96

1. The in vivo effects of the non-steroid anti-inflammatory drug (NSAID) amtolmetin guacyl (AMG) on lipid peroxidation (LP) and on antioxidant enzyme and non-enzyme defence systems were investigated in models of stomach and colon damages, induced by other NSAIDs, by ethanol or by 2,4,6-trinitrobenzenesulfonic acid (TNBS). 2. Indomethacin increased LP, glutathione peroxidase (GSH-PX) and glucose-6-phosphate dehydrogenase (Glu-6-P-DH) activities and decreased glutathione levels in gastric mucosa. Pretreatment with AMG normalized some of the parameters affected by indomethacin. 3. Treatment of rats with ethanol for 0.5 h led to a decrease in glutathione levels as well as activities of glutathione reductase and Glu-6-P-DH in gastric mucosa. AMG, administered 0.5 h before ethanol, limited the adverse actions of ethanol. 4. Amtolmetin guacyl failed to abolish the TNBS-induced changes in the followed-up parameters in colon mucosa and liver, but additional alterations (as with tolmetin) were not observed. 5. The beneficial profile of AMG in the various experimental models of free radical-induced damage investigated in this study suggests the possibility that this drug might possess antioxidant activity.
 ...
PMID:In vivo effects of amtolmetin guacyl on lipid peroxidation and antioxidant defence systems in different models of gastrointestinal injury. 1719 77

The purpose of this study was to evaluate the antioxidant activity and hepatoprotective effect of ethanol extracts of Actinidia rubricaulis (AR) on chronic liver injury induced by carbon tetrachloride (CCl(4)) in rats. CCl(4) (20%, 0.5 ml/rat) was given twice a week for 8 weeks, and animals received AR throughout the entire experimental period. AR reduced the elevated levels of serum glutamate-oxalate-transaminase (sGOT) and glutamate-pyruvate-transaminase (sGPT) caused by CCl(4) at weeks 1, 3, 6, and 8. The biochemical data were consistent with those of the histological observations. The AR extract recovered the CCl(4)-induced liver injury and showed antioxidant effect in assays of antioxidant enzyme activity, such as SOD, GSH-Px and GSH-Rd. Based on these results, we suggest that the hepatoprotective effect of the AR is related to its antioxidant activity.
 ...
PMID:Actinidia rubricaulis attenuates hepatic fibrosis induced by carbon tetrachloride in rats. 1726 53

Low ethanol intake is known to have a beneficial effect on cardiovascular disease. In cardiovascular disease, insulin resistance leads to altered glucose and lipid metabolism resulting in an increased production of aldehydes, including methylglyoxal. Aldehydes react non-enzymatically with sulfhydryl and amino groups of proteins forming advanced glycation end products (AGEs), altering protein structure and function. These alterations cause endothelial dysfunction with increased cytosolic free calcium, peripheral vascular resistance, and blood pressure. AGEs produce atherogenic effects including oxidative stress, platelet adhesion, inflammation, smooth muscle cell proliferation and modification of lipoproteins. Low ethanol intake attenuates hypertension and atherosclerosis but the mechanism of this effect is not clear. Ethanol at low concentrations is metabolized by low Km alcohol dehydrogenase and aldehyde dehydrogenase, both reactions resulting in the production of reduced nicotinamide adenine dinucleotide (NADH). This creates a reductive environment, decreasing oxidative stress and secondary production of aldehydes through lipid peroxidation. NADH may also increase the tissue levels of the antioxidants cysteine and glutathione, which bind aldehydes and stimulate methylglyoxal catabolism. Low ethanol improves insulin resistance, increases high-density lipoprotein and stimulates activity of the antioxidant enzyme, paraoxonase. In conclusion, we suggest that chronic low ethanol intake confers its beneficial effect mainly through its ability to increase antioxidant capacity and lower AGEs.
 ...
PMID:Beneficial effect of low ethanol intake on the cardiovascular system: possible biochemical mechanisms. 1732 32

N-Acetyltransferase Mpr1 of Saccharomyces cerevisiae can reduce intracellular oxidation levels and protect yeast cells under oxidative stress, including H(2)O(2), heat-shock, or freeze-thaw treatment. Unlike many antioxidant enzyme genes induced in response to oxidative stress, the MPR1 gene seems to be constitutively expressed in yeast cells. Based on a recent report that ethanol toxicity is correlated with the production of reactive oxygen species (ROS), we examined here the role of Mpr1 under ethanol stress conditions. The null mutant of the MPR1 and MPR2 genes showed hypersensitivity to ethanol stress, and the expression of the MPR1 gene conferred stress tolerance. We also found that yeast cells exhibited increased ROS levels during exposure to ethanol stress, and that Mpr1 protects yeast cells from ethanol stress by reducing intracellular ROS levels. When the MPR1 gene was overexpressed in antioxidant enzyme-deficient mutants, increased resistance to H(2)O(2) or heat shock was observed in cells lacking the CTA1, CTT1, or GPX1 gene encoding catalase A, catalase T, or glutathione peroxidase, respectively. These results suggest that Mpr1 might compensate the function of enzymes that detoxify H(2)O(2). Hence, Mpr1 has promising potential for the breeding of novel ethanol-tolerant yeast strains.
 ...
PMID:N-Acetyltransferase Mpr1 confers ethanol tolerance on Saccharomyces cerevisiae by reducing reactive oxygen species. 1738 67

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.
Alcohol 2006 Nov
PMID:Combined effects of high-fat diet and ethanol induce oxidative stress in rat liver. 1741 98


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