Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cellular protection against free radical reactions was measured in myocardium from ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. The activities of Cu,Zn-superoxide dismutase (SOD) and glutathione-S-transferase were higher in ethanol-fed rats than in controls, whereas Mn-SOD, catalase and glutathione peroxidase activities were not altered by ethanol treatment. Myocardial zinc was higher and selenium concentration lower in ethanol-fed rats than in controls. Ethanol consumption, which failed to modify the myocardial vitamin E level, did not result in increased lipid peroxidation, but decreased cytosolic and membraneous protein thiols.
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PMID:Effects of chronic ethanol administration on free radical defence in rat myocardium. 141 73

Recent studies have demonstrated that intracolonic administration of trinitrobenzenesulfonic acid (TNB) dissolved in ethanol produces chronic colitis in rats, and that this model shares many features of human inflammatory bowel disease (IBD), particularly Crohn's disease. We investigated the role of free radicals in the pathogenesis of this colitis model. In the early stage of this colitis, antioxidant enzymes (such as superoxide dismutase, glutathione peroxidase) and an antioxidant, alpha-tocopherol, were significantly decreased with the severity of colonic damage. Mn-SOD at a dose of 50000 U/kg attenuated this colitis when preadministered subcutaneously one hour before the induction of colitis. These results suggest that oxygen-derived free radicals may play an important role in this colitis.
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PMID:Possible role of free radicals in the chronic inflammation of the gut. 145 May 97

An acute dose of ethanol was used to investigate the biochemical response of tissues with a compromised antioxidant defense system to a surge of oxygen radical production. The copper (Cu)-deficient rat served as the animal model for this study based on its compromised antioxidant defense system. Rats were fed control (10 micrograms Cu/g) or Cu-deficient (0.2 microgram Cu/g) diet for 14 days. In order to minimize secondary effects associated with chronic Cu deficiency, the chelator triethylenetetramine was added to the Cu-deficient diet to shorten the time required for the induction of Cu deficiency. On day 14, rats were gavaged with ethanol (4.5 g/kg b.wt.) or saline and killed 9 hours postgavage. Rats fed the Cu-deficient diets had lower liver superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities than controls. Ethanol treatment had no effect on liver CuZnSOD or Gpx activity, while MnSOD activity was higher than saline control levels following EtOH treatment. Despite low GPx and SOD activity, Cu-deficient rats did not exhibit higher hepatic thiobarbituric acid reacting substances (TBARS) than controls; in fact, hepatic microsomal TBARS were lower in saline-treated Cu-deficient rats relative to Cu-sufficient rats. Ethanol treatment resulted in higher whole homogenate and mitochondrial TBARS than in saline-gavaged rats. Copper status did not influence hepatic TBARS production in response to an acute EtOH load. These data suggest that compensatory mechanisms contribute to the protection of the liver from excessive free radical production in this model of Cu deficiency.
Alcohol
PMID:Influence of copper status on the response to acute ethanol exposure in rats. 178 25

Cu,Zn superoxide dismutase (Cu,Zn-SOD; EC 1.15.1.1) is known to be inhibited slowly by H2O2. Using EPR and the spin traps 5,5-dimethyl-1-pyrroline 1-oxide (DMPO) and N-tert-butyl-alpha-phenylnitrone (PBN), we have shown that Cu,Zn-SOD catalyzes the formation of "free" .OH radicals from H2O2 in pH 7.6 bicarbonate buffer. Supporting evidence includes the following: (i) H2O2 and active Cu,Zn-SOD are required to yield significant signals from spin-trap-OH adducts. (ii) With O2-., Cu,Zn-SOD causes the appearance of intense resonance signals due to DMPO-OH adducts. These signals were inhibited strongly by catalase. (iii) With H2O2, Cu,Zn-SOD, and DMPO, radical scavengers formate and azide, but not ethanol, decrease DMPO-OH signals while causing new intense signals due to their corresponding DMPO-radical adducts. Failure of ethanol to quench DMPO-OH signals is discussed in light of the positively charged active channel of the enzyme. (iv) With PBN as a spin trap, ethanol quenches .OH radical signals and yields PBN-trapped hydroxyethyl radical signals. (v) Mn-SOD does not catalyze "free" .OH radical formation and it also exerts no effect on the signals of DMPO-OH adducts when added together with the Cu,Zn-SOD. The capacity of Cu,Zn-SOD to generate "free" .OH radicals from H2O2 may in part explain the biological damage associated with elevated intracellular SOD activity.
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PMID:Copper, zinc superoxide dismutase catalyzes hydroxyl radical production from hydrogen peroxide. 216 16

A series of investigations was conducted to trace serum superoxide dismutase (SOD) activities by ELISA and localizations of hepatic tissue SOD by the indirect method using peroxidase conjugated antibody, and the diagnostic and physiological significance of SOD in 19 alcoholics was studied. The values increased significantly both in serum Cu, Zn-SOD to 136 +/- 18 ng/ml (normally 33 +/- 9 ng/ml) and in serum Mn-SOD to 859 +/- 686 ng/ml(normally 84 +/- 30 ng/ml) respectively when polyclonal antibody was used (P less than 0.001). The increase in serum Mn-SOD was higher than that in serum Cu, Zn-SOD, fluctuations of these values showed similar tendencies. Meanwhile, serum Cu, Zn-SOD (94 +/- 50 ng/ml) identified by monoclonal antibody, also, showed higher values than that of normal subjects (37 +/- 7 ng/ml) (P less than 0.001). On the other hand, localization of hepatic tissue Cu, Zn-SOD in alcoholics varied, being 63.2% in the cytoplasmic diffuse type, 42.0% in the nuclear diffuse type, 42.1% in the vacuolated membrane type, and 15.8% in the small granular type respectively. Participation of Cu, Zn-SOD in ethanol oxidation, protective roles played by cell membrane, lysosome membrane and nucleic acid of Cu, Zn-SOD to harmful free radicals was presumed. In addition, localization of hepatic tissue Mn-SOD was mostly of the cytoplasmic diffuse type (52.7%) and was extremely variable. From such results, relative or absolute reductions of hepatic tissue SOD in alcoholics was suggested to act on the development of tissue injuries acceleratingly.
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PMID:Serum activity and hepatic localization of superoxide dismutase in alcoholics. 266 7

The chemiluminescence level and superoxide dismutase (SOD) activity were determined in the plasma of patients with alcoholic and non-alcoholic liver injuries. Chemiluminescence level was significantly higher in alcoholics than in non-alcoholics. It increased significantly in patients with fatty livers and had a tendency to increase with the progression of alcoholic liver injury from a fatty liver to liver cirrhosis. Mn-SOD activity was elevated in patients with alcoholic liver injuries. Furthermore, there was a positive correlation between the levels of plasma chemiluminescence and plasma Mn-SOD activity. The increases in chemiluminescence and Mn-SOD activity suggests that the generation of a large amount of activated oxygen is associated with the pathogenesis and progression of alcoholic liver injury in humans.
Alcohol
PMID:Chemiluminescence and superoxide dismutase in the plasma in patients with alcoholic and non-alcoholic liver injuries. 402 67

1. The activity of manganese-superoxide dismutase (EC 1.15.1.1; SOD) was increased in the livers and kidneys of adult rats after exposure to aqueous ethanol (200 ml/1) for 32 weeks. 2. The concentration of Mn in the livers and kidneys was significantly higher after 24 weeks, and by 32 weeks liver copper and zinc levels were lower. 3. The activity of foetal (day 19) liver superoxide dismutase was appreciably higher in offspring from dams receiving ethanol during pregnancy. Quantitatively the response appeared to be almost entirely due to the Mn-SOD form of the enzyme. 4. Maternal alcoholism during pregnancy had no effect on the levels of Cu, Mn or Zn in foetal (day 19) livers.
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PMID:Superoxide dismutase (EC 1.15.1.1), manganese and the effect of ethanol in adult and foetal rats. 688 37

Saccharomyces cerevisiae aBR10 cells are able to develop resistance to lethal ethanol concentrations (14%, v/v), by preexposure to a sublethal heat shock (37 degrees C) or ethanol stress (8%, v/v). Heat shock and 8% ethanol stress had no effect on the concentrations of glutathione [reduced (GSH) and oxidized (GSSG) forms] and on glutathione reductase and CuZn superoxide dismutase (SOD) activities, suggesting that the development of resistance to lethal ethanol concentrations is independent of these antioxidant defenses. In fact, a S. cerevisiae mutant, deficient in CuZnSOD, had an even higher ethanol tolerance, compared to the wild-type strain, and this mutation did not impair a further acquisition of ethanol tolerance. In contrast to CuZnSOD, the MnSOD activity seems to play a more important role in ethanol resistance. The MnSOD activity of the S. cerevisiae aBR10 cells increased upon exposure to heat shock or 8% ethanol. The higher tolerance to 14% ethanol in CuZnSOD deficient cells was also associated to a higher MnSOD activity, as compared to the aBR10 cells; this activity decreased during both stress pretreatments (while still higher than that observed in the wild-type strain). The results obtained suggest that maximum ethanol tolerance is attained with a MnSOD activity close to 1.0 U/mg protein. On either side of this value, the increased sensitivity of S. cerevisiae cells to 14% ethanol might be due to an inability to prevent either superoxide radical- or hydrogen peroxide-induced damages, respectively. These results are supported by the fact that a MnSOD deficiency renders yeast cells more ethanol sensitive.
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PMID:Acquisition of ethanol tolerance in Saccharomyces cerevisiae: the key role of the mitochondrial superoxide dismutase. 843 41

Alcohol damage to the liver can, among other factors, be mediated through the action of toxic oxygen radicals generated by ethanol. Major antioxidants in the liver are copper/zinc and manganese superoxide dismutases (Cu/Zn- and Mn-SODs). In order to test whether SODs may be differentially expressed in alcoholic liver disease (ALD), biopsies from 45 patients with ALD were analyzed for qualitative and quantitative immunoreactivity of Cu/Zn- and Mn-SOD in hepatocytes. The overall amount of Cu/Zn-SOD reactivity was significantly lower in ALD than in control biopsies, whereas no difference was found for Mn-SOD. Staining for both enzymes was decreased in ballooned hepatocytes. Low Cu/Zn-SOD was correlated with advanced lattice-like perisinusoidal fibrosis. In hepatocytes forming cirrhotic nodules, SOD reactivity was similar to that of control cells. The results suggest that SODs may be differentially regulated in ALD, and that Mn-SOD, an inducible enzyme, may be involved in recovery and cell protection in ALD.
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PMID:Copper/zinc and manganese superoxide dismutases in alcoholic liver disease: immunohistochemical quantitation. 893 Jun 33

Oxidative stress-associated parameters [concentrations of lactoferrin, Cu,Zn-superoxide dismutase (SOD) and Mn-SOD] were determined in sera of 20 patients suffering from alcohol dependence immediately after detoxification and in 15 non-dependent healthy subjects as controls. In the patient group, the mean Mn-SOD concentration reached almost double the values of those from the control group (142.9 vs 76.0 ng/ml, P < 0.01). The other parameters tended to be increased in patients, but did not differ significantly between index and control groups. The findings are consistent with increased oxidative stress due to chronic alcohol intake, which might be responsible for secondary diseases such as brain atrophy, peripheral polyneuropathy and liver fibrinogenesis.
Alcohol Alcohol
PMID:Increased concentrations of manganese superoxide dismutase in serum of alcohol-dependent patients. 913 93


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