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)

Aspirin is widely used as an antiinflammatory drug especially in children with rheumatic fever arthritis. The diminishing effects of aspirin on antioxidant enzymes and hepato-renal systems at high doses are well-known. It is now evident that the damage at antioxidant system worsens the clinical picture of the disease and prolongs the treatment time. Thus, we investigated the effect of antioxidant enzyme cofactors-zinc and selenium-supplementation on superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels (erythrocyte and liver) and hepato-renal toxicity during aspirin treatment at therapeutic doses. The rats were divided into five groups. The first and second groups were given aspirin 75 mg/kg/day and aspirin plus selenium (Selenium 200, selenium 200 mg tablet as selenium yeast, GNC) and zinc (Zinc 100, zinc 100 mg tablet as zinc gluconate, GNC), respectively, the third and fourth take 50 mg/kg/day aspirin and aspirin plus selenium and zinc twice a day, respectively. The fifth group was control. The rats were treated with aspirin for 5 weeks as in the treatment of rheumatic fever arthritis in children. Erythrocyte SOD and MDA levels were preserved with supplementation, whereas there was no change for GSH-Px levels. Liver SOD, GSH-Px, and MDA levels were not changed. In zinc- and selenium-supplemented groups, the levels of serum alanine aminotransferase, uric acid, and direct bilirubin levels were found statistically decreased compared with nonsupplemented groups. There was no significant histopathologic change in specimens of hepatic and renal tissues. Trace element supplementation may prevent free radical damage and shorten treatment time in children using long-term aspirin treatment.
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PMID:Do zinc and selenium prevent the antioxidant, hepatic and renal system impairment caused by aspirin in rats? 1830 10

Mice lacking the 66 kDa isoform of the adapter molecule shcA (p66(shcA)) display increased resistance to oxidative stress and delayed aging. In cultured cell lines, p66 promotes formation of Reactive Oxygen Species (ROS) in mitochondria, and apoptotic cell death in response to a variety of pro-oxidant noxious stimuli. As mitochondrial ROS and oxidative cell damage are clearly involved in alcohol-induced pathology, we hypothesized that p66 may also have a role in ethanol. In vivo, changes observed in p66+/+ mice after 6-week exposure to ethanol in the drinking water, including elevated serum alanine aminotransferase (ALT), liver swelling and evident liver steatosis, were significantly attenuated in p66-/- mutant mice. Biochemical analysis of liver tissues revealed induction of the p66 protein by ethanol, whereas p66-deficient livers responded to alcohol with a significant upregulation of the mitochondrial antioxidant enzyme MnSOD, nearly absent in control mice. Evidence of an inverse correlation between expression level of p66 and protection from alcohol-induced oxidative stress was also confirmed in vitro in primary hepatocytes and in HepG2-E47 cells, an ethanol-responsive hepatoma cell line. In fact, MnSOD upregulation by exposure to ethanol in vitro was much more pronounced in p66KO versus wild-type isolated liver cells, and blunted in HepG2 cells overexpressing p66shc. p66 overexpression also prevented the activation of a luciferase reporter gene controlled by the SOD2 promoter, indicating that p66 repression of MnSOD operates at a transcriptional level. Finally, p66 generated ROS in HepG2 cells and potentiated oxidative stress and mitochondrial depolarization by ethanol. Taken together, the above observations clearly indicate a role for p66 in alcohol-induced cell damage, likely via a cell-autonomous mechanism involving reduced expression of antioxidant defenses and mitochondrial dysfunction.
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PMID:Role of the life span determinant P66(shcA) in ethanol-induced liver damage. 1849 Aug 96

This study was undertaken to assess the risk of poisoning due to consumption of the puffer fish Lagocephalus lagocephalus collected along the Tunisian coast. Wistar rats were daily intraperitoneally injected, for 10 days, with acidic extracts of liver or flesh (muscles + skin) of L. lagocephalus. Control rats received injections of NaCl (0.9%). No mortality and no evident signs of neurotoxicity were recorded in treated rats. Conversely, treatment led to: (1) diarrhoea and body and organ (liver, kidney) weights loss; (2) oxidative stress evidenced by an increase in lipid peroxidation (TBARS) and conversely a decrease in antioxidant enzyme activities (SOD, catalase, GSH-Px) in tissues (blood cells, liver, kidneys); (3) a decrease in alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities in blood plasma.
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PMID:Toxicity assessment of the puffer fish Lagocephalus lagocephalus from the Tunisian coast. 1860 90

The protective effect of a fermented substance from Saccharomyces cerevisiae (FSSC) on liver injury caused by acetaminophen (AAP) was studied in mice. Mice were pretreated with FSSC (0.5-2.0 g/kg, p.o.) for 4 d, and on the fourth day, the mice received an overdose of AAP (500 mg/kg, i.p.). Subsequently, they were sacrificed at 7 h, and blood was drawn from the abdominal vein and liver samples were collected. Histological and biochemical examinations revealed that the administration of AAP caused liver injury in the mice, including increases in plasma alanine aminotransferase and asparate aminotransferase activities and decreases in the hepatic reduced form of glutathione (GSH) content and antioxidant enzyme activities. Prior to AAP treatment, the mice pretreated with FSSC showed significantly reduced levels of alanine aminotransferase (ALT) and aspirate aminotransferase (AST) activity. Liver histology in the FSSC-pretreated mice was significant. In these mice, pretreatment with FSSC also served to reduce hepatic GSH depletion and the inhibition of antioxidant enzyme activity caused by AAP overdose. In conclusion, oral administration of FSSC significantly reduced AAP-induced hepatic injury in the mice.
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PMID:Protective effect of a fermented substance from Saccharomyces cerevisiae on liver injury in mice caused by acetaminophen. 1883 23

In the present study, we evaluated the beneficial effect of mulberry extracts (ME), which are rich in phenolics and anthocyanins, on the induction of antioxidant enzymes and on the promotion of cognition in senescence-accelerated mice (SAMP). Six-month old SAMP8 and SAMR1 mice were fed a basal diet supplemented with 0.18% and 0.9% ME for consecutive 12 weeks. The results showed that the mice fed the ME supplement demonstrated significantly less amyloid beta protein and showed improved learning and memory ability in avoidance response tests. ME-treated mice showed a higher antioxidant enzyme activity and less lipid oxidation in both the brain and liver, as compared to the control mice. Furthermore, treatment with ME decreased the levels of serum aspartate aminotransferase, alanine aminotransferase, triglyceride and total cholesterol that increase with ageing. The hepatoprotective effect of ME appeared to occur through a mechanism related to regulation of the mitogen-activated protein kinases and activation of the nuclear factor-erythroid 2 related factor 2, where the latter regulates the induction of phase 2 antioxidant enzymes and reduction of oxidative damage. Overall, supplementation of ME might be advantageous to the induction of an antioxidant defense system and for the improvement of memory deterioration in ageing animals.
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PMID:Antioxidant and cognitive promotion effects of anthocyanin-rich mulberry (Morus atropurpurea L.) on senescence-accelerated mice and prevention of Alzheimer's disease. 1944 93

This study examined the effects of beta-carotene on antioxidant status in rats with chronic alcohol consumption. At the beginning of experiment (week 0), according to both the plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, rats (n = 24) were divided into 3 groups and fed with a standard diet (group C), a diet containing ethanol (group E), or a diet containing ethanol and beta-carotene (group E+B). After 10 weeks, plasma AST and ALT, fat accumulation in the liver, antioxidant enzyme activities in erythrocytes and the liver, malondialdehyde (MDA), and alpha-tocopherol and retinol in plasma and hepatic samples were analyzed. The chronic alcohol diet significantly increased AST and ALT levels in plasma, and these changes were prevented by supplementing the diet with beta-carotene. Glutathione (GSH) in erythrocytes and in the liver was significantly elevated in rats fed with a diet containing beta-carotene. The results indicate that beta-carotene supplementation can prevent ethanol-induced liver damage and increase GSH concentrations in erythrocytes and the liver.
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PMID:Effects of beta-carotene on antioxidant status in rats with chronic alcohol consumption. 1963 86

Changes in water temperature and salinity are responsible for a variety of physiological stress responses in aquatic organisms. Stress induced by these factors was recently associated with enhanced reactive oxygen species (ROS) generation, which caused oxidative damage. In the present study, we investigated the time-related effects of changes in water temperature and salinity on mRNA expression and the activities of antioxidant enzymes (SOD and CAT) and lipid peroxidation (LPO) in the gills and digestive glands of the ark shell, Scapharca broughtonii. To investigate physiological responses, hydrogen peroxide (H(2)O(2)), lysozyme activity, aspartate aminotransferase (AspAT), and alanine aminotransferase (AlaAT) were measured in the hemolymph. Water temperature and salinity changes significantly increased antioxidant enzyme mRNA expression and activity in the digestive glands and gills in a time-dependent manner. H(2)O(2) concentrations increased significantly in the high-temperature and hyposalinity treatments. LPO, AspAT and AlaAT levels also increased significantly in a time-dependent manner, while lysozyme activity decreased. These results suggest that antioxidant enzymes play important roles in reducing oxidative stress in ark shells exposed to changes in water temperature and salinity.
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PMID:Activity of antioxidant enzymes and physiological responses in ark shell, Scapharca broughtonii, exposed to thermal and osmotic stress: effects on hemolymph and biochemical parameters. 1978 26

Liver ischemia/reperfusion (I/R) injury, which is mainly caused by the generation of reactive oxygen species (ROS) during the reperfusion, remains an important clinical problem associated with liver transplantation and major liver surgery. Therefore, ROS should be detoxified to prevent hepatic I/R-induced injury. Delivery of antioxidant genes into liver is considered to be promising for prevention of hepatic I/R injury; however, therapeutic effects of antioxidant gene transfer to the liver have not been fully examined. The aim of this study was to examine whether adenovirus (Ad) vector-mediated catalase gene transfer in the liver is an effective approach for scavenging ROS and preventing hepatic I/R injury. Intravenous administration of Ad vectors expressing catalase, which is an antioxidant enzyme scavenging H(2)O(2), resulted in a significant increase in catalase activity in the liver. Pre-injection of catalase-expressing Ad vectors dramatically prevented I/R-induced elevation in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and hepatic necrosis. The livers were also protected in another liver injury model, CCl(4)-induced liver injury, by catalase-expressing Ad vectors. Furthermore, the survival rates of mice subjected to both partial hepatectomy and I/R treatment were improved by pre-injection of catalase-expressing Ad vectors. On the other hand, control Ad vectors expressing beta-galactosidase did not show any significant preventive effects in the liver on the models of I/R-induced or CCl(4)-induced hepatic injury described above. These results indicate that hepatic delivery of the catalase gene by Ad vectors is a promising approach for the prevention of oxidative stress-induced liver injury.
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PMID:Prevention of hepatic ischemia-reperfusion injury by pre-administration of catalase-expressing adenovirus vectors. 1995 28

Physical training induces beneficial adaptations; however, exhausting exercise increases reactive oxygen species generation, resulting in damage to DNA and tissues. Pequi (Caryocar brasiliense), a fruit of the Brazilian Cerrado, contains a carotenoid-rich oil. We investigated whether pequi oil had antioxidant effects in runners. Evaluations were made after outdoor races before and after ingestion of 400 mg pequi-oil capsules for 14 days. Blood samples were taken after races and submitted to comet and TBARS assays and biochemical analyses of creatine kinase (CK), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). To determine if the protective effects of pequi-oil were influenced by antioxidant enzyme genotypes, MnSOD (-Val9Ala), CAT (-21A/T) and GPX1 (Pro198Leu) gene polymorphisms were also investigated. Pequi oil was efficient in reducing tissue injuries evaluated for AST and ALT, particularly in women, and in reducing DNA damages in both sexes. Except for CK levels, the results were influenced by MnSOD genotypes; heterozygous excess was related to less DNA damage, tissue injury and lipid peroxidation, besides presenting a better response to pequi oil against exercise-induced damage.
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PMID:Dietary carotenoid-rich pequi oil reduces plasma lipid peroxidation and DNA damage in runners and evidence for an association with MnSOD genetic variant -Val9Ala. 2008 61

Recent studies reported that 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors have pleotropic effects independent of their lipid-lowering properties. The present study was undertaken to determine whether treatment with rosuvastatin (RO) would be beneficial in a rat model of bile duct ligation (BDL). Animals were divided into three groups: a sham group (group I), a BDL group treated with vehicle (group II), and a BDL group treated with RO (10 mg/kg) (group III). Serum levels of total bilirubin, gamma-glutamyl transpeptidase, alanine aminotransferase, and aspartate aminotransferase decreased significantly in group III when compared to group II. Lipid peroxides and NO levels of group III were found to be significantly lower than those of group II. Antioxidant enzymes (superoxide dismutase, glutathione-S-transferase, and catalase) activity in liver tissues markedly decreased in group II, whereas treatment with RO preserved antioxidant enzyme activity. DT-diaphorase activity in group II was significantly higher than that in group III. The histopathological results showed multiple numbers of newly formed bile ductules with inflammatory cells infiltration in group II. These pathological changes were improved in group III. Our data indicate that RO ameliorates hepatic injury, inflammation, lipid peroxidation and increases antioxidant enzymes activity in rats subjected to BDL. RO may have a beneficial effect on treatment of cholestatic liver diseases.
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PMID:Effect of rosuvastatin on cholestasis-induced hepatic injury in rat livers. 2014 76


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