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)

Senescence marker protein 30 (SMP30), an important aging marker molecule, has been identified functionally as a calcium regulatory protein. Recent evidence showed its new assumed role as an effective anti-oxidative property. However, the role of SMP30 in the brain has not been explored. To delineate its role in the brain, we utilized SMP30 knock-out (SMP30 KO) mice in the current study. We focused on the oxidative status of the brain by examining selected oxidative markers in brains of SMP30 KO mice. Results showed that the generation of reactive species (RS) and NADPH oxidase activities were significantly elevated in SMP30 deficient brain. The increased oxidative status in these mice was further confirmed by increased oxidatively modified proteins such as dityrosine formation and carbonylation in the cortex of SMP30 KO mice. Moreover, SMP30 deficient brain showed the increased Mac-1 protein and myeloperoxidase (MPO) activity in the brain, supporting the putative anti-oxidative action of SMP30. Interestingly, the activities of major antioxidant enzymes, superoxide dismutase, catalase and reduced glutathione peroxidase in the brain were not affected by SMP30 depletion. Our results documented that brain SMP30 has a protective action against oxidative damage, without influencing antioxidant enzyme status.
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PMID:SMP30 deficiency causes increased oxidative stress in brain. 1650 Jun 93

Hepatic ischemia-reperfusion (I/R) injury may be developed in some conditions, such as trauma, major hepatic resection, hemorrhagic shock or liver transplantation. I/R injury of the liver causes hepatocellular damage that may lead to hepatic failure. A considerable body of evidence indicates that reactive oxygen species (ROS) and inflammation may contribute to hepatocellular injury in liver I/R. Leflunomide is an isoxazole derivative, and a unique immunomodulatory agent. In the present study, we examined the effects of leflunomide on the neutrophil activation with oxidative stress and some antioxidant enzymes in the reperfusion following I/R in the rat liver. Thirty-two rats divided into four groups: group 1 (control); was given leflunomide 10 mg/kg, i.g.; group 2 (SHAM), animals were only laparotomized; group 3 (liver I/R), and group 4 (liver I/R + Leflunomide). In group 4, rats were pretreated with leflunomide (10 mg/kg, i.g.) two doses prior to experiment. In groups 3 and 4, occluding the hepatic pedicel for 60 min induced ischemia and reperfusion was allowed thereafter for 60 min. At the end of the reperfusion period, rats were sacrificed. superoxide dismutase, catalase, nitric oxide, xanthine oxidase, malondialdehyde, protein carbonyl and myeloperoxidase levels were determined in hepatic tissue as well as histological examination with H and E staining. Group 3 animals demonstrated severe deterioration of liver morphology and a significant liver oxidative stress. Pretreatment of animals with leflunomide markedly attenuated morphological alterations and neutrophil activation, reduced elevated oxidative stress products levels and restored the depleted hepatic antioxidant enzyme. The findings imply that ROS play a causal role in I/R-induced hepatic injury, and leflunomide exerts hepatoprotective effects probably by the anti-inflammatory effect with radical scavenging and antioxidant activities.
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PMID:Protective effects of leflunomide against ischemia-reperfusion injury of the rat liver. 1655 9

This study was performed to evaluate the effect of melatonin on methanol-induced liver injury. We evaluated the levels of malondialdehyde (MDA), protein carbonylation (PC), myeloperoxidase (MPO) activities and to assess lipid peroxidation, protein oxidation, neutrophil accumulation and nitrite which is a stable end product of nitric oxide respectively. We also studied superoxide dismutase, catalase, and glutathione peroxidase activities of liver tissue to evaluate the changes in the antioxidant status. Histopathological alterations were also determined. The experiment was performed on Wistar rats, which received intragastric 3 g/kg methanol as a 50% solution in isotonic saline once. After 6 and 24 hr all the drug received and intoxicated rats were killed under anesthesia. Pretreatment with melatonin (10 mg/kg) decreased the MDA levels significantly, restored the PC levels to the control, prevented the increase of nitrite level and MPO activity significantly and reversed to the control levels, prevented the reduction in all of the antioxidant enzyme activities. Additionally in melatonin treated group piecemeal necrosis, lobular lytic necrosis, and portal inflammation returned to normal histologic appearances when compared with methanol administration. In conclusion, melatonin has protective effects against methanol-induced hepatic injury.
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PMID:Melatonin improves methanol intoxication-induced oxidative liver injury in rats. 1761 34

The aim of the present study is to investigate whether the antioxidant mechanisms are involved in epidermal growth factor (EGF)-mediated protection from ethanol-induced gastric damage. Twenty four female Sprague-Dawley rats were assigned into 3 groups; control (C) group (n=8) was given physiologic saline by gavage; ethanol (E) group (n=8) was given 1 ml of 80% ethanol (v/v) in distilled water by gavage and EGF group (n=8) was given EGF (100 mg/kg-body wt.) intraperitonealy half an hour before the administration of ethanol. The protein carbonyl content was significantly higher in the E group than the C group (p<0.01). On the other hand, EGF decreased the protein carbonyl content in the EGF group (p<0.01). Gastric myeloperoxidase activity increased significantly after the administration of ethanol (p<0.01). The administration of EGF decreased significantly the myeloperoxidase activity (p<0.01). Although ethanol caused a slight decrease in the catalase activity, no statistical significance was observed between groups E and C. The catalase activity increased significantly after EGF treatment (p<0.01). The superoxide dismutase activity decreased significantly in the E group when compared to the C group (p<0.05) while it was found to be increased significantly in the EGF group in comparison with the E group (p<0.01). In summary, the present results indicate that the gastroprotective effect of EGF in the experimental lesions induced by ethanol could be attributed to its property such as to augment the antioxidant enzyme activities.
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PMID:Epidermal growth factor increases tissue antioxidant enzyme activities in ethanol-induced gastric injury in rat. 1761 49

We studied the effects of intense exercise on the neutrophil antioxidant enzyme activities and gene expression. Blood samples were taken from seven cyclists in basal conditions and 3 h after two competition stages of 165 km. Serum creatine kinase (CK) activity, plasma carbonyl derivatives and uric acid levels increased after exercise. The cycling stage induced neutrophilia and increased myeloperoxidase (MPO) activity and reactive oxygen species (ROS) production. Antioxidant enzyme activities (catalase, glutathione peroxidase and superoxide dismutase) decreased after exercise, although gene expression increased. Immunocytochemistry showed catalase (CAT) enzyme equally distributed between the cytoplasm and organelles before exercise, and after exercise the cytoplasmic CAT levels were reduced and were absent in the compartments. After in vitro stimulation with opsonized zymosan (OZ) the extracellular CAT levels increased. This suggests a CAT secretion in order to avoid neutrophil-induced oxidative damage at a local level or to regulate the function of ROS as extracellular signalling molecules.
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PMID:Intense physical activity enhances neutrophil antioxidant enzyme gene expression. Immunocytochemistry evidence for catalase secretion. 1765 44

Erdosteine is a mucolytic agent having antioxidant properties through its active metabolites in acute injuries induced by pharmacological drugs. This study was designed to investigate the renoprotective potential of Erdosteine against gentamicin (GM)-induced renal dysfunction by using Technetium-99 m dimercaptosuccinic acid (Tc-99 m DMSA) uptake and scintigraphy in rats. For this purpose, male Wistar rats were randomly allotted into one of the four experimental groups: Control, Erdosteine, GM, and GM + Erdosteine groups. GM and GM + Erdosteine groups received 100 mg/kg GM intramuscularly for 6 days. In addition, Erdosteine and GM + Erdosteine groups received 50 mg/kg Erdosteine orally for 6 days. Renal function tests were assessed by serum blood urea nitrogen (BUN), creatinine levels, as well as scintigraphic and tissue radioactivity measurements with Tc-99 m DMSA. Renal oxidative damage was determined by renal malondialdehyde (MDA) levels, by antioxidant enzyme activities; superoxide dismutase (SOD) and catalase (CAT) and activities of oxidant enzymes; xanthine oxidase (XO) and myeloperoxidase (MPO). GM administration resulted in marked renal lipid peroxidation, increased XO and MPO activities and decreased antioxidant enzyme activities. GM + Erdosteine group significantly had lower MDA levels, higher SOD and CAT activities and lower XO and MPO activities, when compared to GM. Also GM + Erdosteine had lower levels of serum BUN, creatinine and higher renal tissue Tc-99 m DMSA uptake and radioactivity with respect to GM. In conclusion, our results supported a protective role of Erdosteine in nephrotoxicity associated with GM treatment.
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PMID:Renoprotective effect of erdosteine in rats against gentamicin nephrotoxicity: a comparison of 99mTc-DMSA uptake with biochemical studies. 1789 18

Injection of D-galactosamine and lipopolysaccharide (DGaIN/LPS) is useful as an experimental model of acute hepatic damage. Juvenile rats were used for investigation. The hepatoprotective activity of aqueous garlic (Allium sativum) extract (AGE) at a dose of 300 mg/kg body weight for 14 days, intraperitoneal (i.p.) prior to the induction of DGalN/LPS, was investigated against DGalN/LPS-induced hepatitis in rats. DGalN/LPS (300 mg/kg body weight/30 microg/kg body weight, i.p.), induced hepatic damage that was manifested by a significant increase in the activities of marker enzymes [alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and gamma glutamyl transferase (gamma GT)], bilirubin, lipid peroxides (LPO), tumor necrosis factor (TNF-alpha) and myeloperoxidase (MPO) activity level in serum. Also, the lipid profile in serum and liver homogenate including total cholesterol, triglycerides, free fatty acids and phospholipids were significantly deteriorated. The antioxidant enzyme activities (superoxide dismutase, SOD; reduced glutathione, GSH; catalase, CAT and glutathione peroxidase, GPX) in liver homogenate were significantly decreased in the DGalN/LPS. Pretreatment of rats with AGE reversed these altered parameters near to normal control values. Results of this study revealed that AGE could afford a significant protection in the alleviation of DGalN/LPS-induced hepatic damage.
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PMID:Aqueous garlic extract attenuates hepatitis and oxidative stress induced by galactosamine/lipoploysaccharide in rats. 1857 Feb 25

Overweight and physical inactivity are associated with elevated reactive oxygen species and chronic low-grade inflammation. Exercise training studies have measured changes in systemic inflammatory and oxidative/antioxidative biomarkers but predominantly at moderate-high intensities. Few low-intensity, lifestyle-based physical activity (PA) studies have been conducted. The purpose of this study was to determine whether improvements in lifestyle-oriented PA resulting from a 16-wk Internet-delivered PA program [Active Living Every Day-Internet (ALED-I)] elicit cardioprotective improvements in measures of inflammation, oxidation, or antioxidant enzyme capacity. Forty-one men and women (age 23-62 yr) were randomized to either the ALED-I intervention [n = 19; age = 40.4 +/- 1.9 yr; body mass index (BMI) = 31.4 +/- 1.1 kg/m(2)] or a delayed intent-to-treat control condition (n = 22; age = 46.6 +/- 1.3 yr; BMI = 31.0 +/- 0.7 kg/m(2)). TNF-alpha, C-reactive protein, myeloperoxidase, superoxide dismutase, catalase, total antioxidative capacity, change in PA, and other cardiometabolic disease risk factors were measured at baseline and postintervention. The ALED-I group increased PA and decreased central adiposity without changes in the control group. There was no change in the control group for any inflammation, oxidation, or antioxidant biomarkers. TNF-alpha decreased (P = 0.01) in the intervention group but was not statistically different from the control group. In conclusion, modest improvements in daily low-intensity ambulatory PA as a result of an Internet-delivered lifestyle PA intervention may be cardioprotective in sedentary and overweight adults through reductions in central adiposity and inflammation. However, the absence of favorable changes in other inflammation, oxidation, and antioxidant biomarkers highlights the need for further attention to the dose response of lifestyle-structured PA promotion strategies for health maintenance/improvement.
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PMID:Internet-delivered lifestyle physical activity intervention: limited inflammation and antioxidant capacity efficacy in overweight adults. 1900 91

It has been well established that diet high in cholesterol and saturated fatty acids could significantly elevate plasma cholesterol levels and also increase the risk of cardiovascular diseases. We hypothesize that repeated systemic Escherichia coli (E. coli) in conjunction with hypercholesterolemia, leads to development of oxidative stress that may affect the development and progression of inflammatory CVD. Swiss albino mice (4 weeks old) were randomly assigned to high cholesterol diet (HCD) or normal laboratory diet (NLD) groups. At 10 weeks of age, mice were inoculated intravenously with E. coli or vehicle for 24 weeks. Serum cholesterol, low density lipoprotein, C reactive protein levels, blood glucose level and selective antioxidant enzymes throughout the systemic infection period in murine aorta, heart and liver during hypercholesterolemia, were examined. Serum cholesterol levels were elevated in HCD-fed mice, compared to NLD. The blood colony forming units (CFU) of E. coli suggested persistence of systemic infection. The antioxidant enzyme levels were elevated in E. coli infected groups as compared to controls. The myeloperoxidase content of aortic tissue was significantly higher in all groups infected with E. coli. Our study suggests that during hypercholesterolemia, repeated systemic E. coli infection induces an endogenous antioxidant response that serves to modulate vascular inflammation leading to cardiovascular diseases.
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PMID:Repeated systemic Escherichia coli infection enhances anti-oxidant response in hypercholesterolemic mice inducing cardiovascular inflammation. 1922 70

The effects of the water extracts of Millettia reticulata Benth (WEMRB) and its active compound (protocatechuic acid [PCA]) on acute hepatic injury and inflammation in CCl(4)-induced Sprague-Dawley rats were investigated. Sprague-Dawley rats were orally treated with WEMRB or PCA for 28 consecutive days, and then the rats were given an intraperitoneal injection with CCl(4). Pretreatment with WEMRB or PCA significantly lowered the CCl(4)-induced serum levels of hepatic enzyme markers (aspartate and alanine aminotransferases). Liver histopathology showed that WEMRB reduced the incidence of cytoplasmic vacuolization and necrosis induced by CCl(4) in rats. Pretreatment with WEMRB also showed anti-inflammation on the expression of cyclooxygenase-2, inducible nitric oxide synthase, and myeloperoxidase, as well as nitrite and nitrate levels in the CCl(4)-induced Sprague-Dawley rats. The results suggest that oral administration of WEMRB decreases the hepatotoxic effects by increasing glutathione-dependent antioxidant enzyme activity, thereby reducing oxidative stress and inflammation in CCl(4)-induced Sprague-Dawley rats.
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PMID:Protective effect of Millettia reticulata Benth against CCl(4)-induced hepatic damage and inflammatory action in rats. 1973 83


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