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)

Oxidative damage due to free radical production is increased in uraemic patients and has been suggested as a possible factor contributing to the anaemia of chronic renal failure (CRF) and the pathogenesis of atherosclerosis. Oxidative stress was assessed in 40 patients with CRF maintained by either haemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD) and in 18 healthy controls. Lipid peroxidation (assessed as malondialdehyde, MDA), total glutathione (TG), antioxidant enzyme (glutathione reductase (GSHRx), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD)) activity and antioxidant associated trace metal (selenium, copper, zinc) levels were studied. Erythrocyte membrane fluidity was examined using the fluorescent probe 1,6 diphenyl-1,3,5-hexatriene (DPH). The results indicate increased levels of oxidative stress and altered erythrocyte membrane fluidity in patients treated with CAPD compared with controls and patients treated with HD. Only minor changes were observed in patients treated with HD. Altered free radical activity, oxidative stress and altered erythrocyte membrane fluidity observed in patients with CRF may contribute to the increase in vascular disease in such patients and to the anaemia of CRF.
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PMID:Oxidative stress and erythrocyte membrane fluidity in patients undergoing regular dialysis. 755 72

Free radical-initiated lipid peroxidation (LP) following intestinal ischemia/reperfusion (I/R) may disrupt mucosal integrity. It is unknown if inhibition of LP prevents this injury. We analyzed rat ileum, subjected to I/R, for evidence of LP inhibition and structural damage following treatment with the 21-aminosteroid, U74389F, a potent LP inhibitor. Four groups of Lewis rats were studied after superior mesenteric artery occlusion with ligation of collateral arcades: (i) no ischemia, (ii) 10 min ischemia, (iii) 10 min ischemia + 1 hr reperfusion, (iv) 10 min ischemia + 1 hr reperfusion + U74389F (6 mg/kg i.v. prior to clamp removal and reperfusion). Ileal mucosa was analyzed for: 9i0 superoxide dismutase (SOD; U/mg protein), a key antioxidant enzyme, (ii) myeloperoxidase (MPO; U/mg protein), an index of PMN stimulation, (iii) malondialdehyde (MDA; pmole/mg), an end product of LP, and (iv) routine histology. MDA rose from 2.09 +/- 0.44 (mean +/- SE) in Group 1 to 15.10 +/- 2.22 in Group 3 following I/R (P < 0.01). In Group 2 and Group 4, MDA remained unchanged at 3.25 +/- 1.38 and 1.73 +/- 0.15, respectively. MPO, likewise, rose during I/R from 0.59 +/- 0.17 in Group 1 to 1.10 +/- 0.13 in Group 3 (P = 0.08) and 1.49 +/- 0.24 in Group 4 (P < 0.05). SOD did not vary significantly in the four groups studied. Despite PMN stimulation indicated by increased MPO with reperfusion, no PMN infiltration was seen histologically. U74389F normalized MDA, indicating effective inhibition of LP; however, similar epithelial sloughing and edema and hemorrhage in the lamina propria were seen in treated and untreated rats. These data implicate MDA-independent or possibly LP-independent pathways in intestinal morphologic damage occurring with I/R.
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PMID:Inhibition of intestinal lipid peroxidation does not minimize morphologic damage. 823 Nov 75

Experiments on rats with experimental streptosotocin-induced diabetes have shown intensification of the lipid peroxidation processes and reduction of activity of antioxidant defensive enzymes. The content of G-SH and glutathione peroxidase activity has decreased in comparison with the normal rate by 69% and 28%, respectively. Glutathione reductase activity has risen by 20%. Activity of the antioxidant enzymes (superoxide dismutase, catalase) has reduced and the amount of the final product of lipid peroxidation, MDA has increased. Injection of nicotinamide to diabetic rats (200 mg/1 kg of weight) for 14 days normalized activity of the antioxidant enzyme system and the content of the lipid peroxidation products.
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PMID:[The effect of nicotinamide on the enzymatic activity of the antioxidant defense in experimental diabetes]. 900 53

The purpose of this study was to measure resting muscle and blood antioxidant status in untrained (n = 8) and jump-trained (n = 8) humans and to evaluate free radical-mediated muscle damage after a strenuous jump test consisting of six bouts of 30-s continuous jumping separated by 2 min of rest. Resting muscle antioxidant activities [superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reductase (GR), and manganese SOD] were significantly higher in jump-trained compared with untrained subjects. Blood antioxidant enzyme activities and muscle catalase, however, were not different between the two groups. Creatine kinase activities increased significantly (P < 0.0001) after the jump test in untrained individuals, but remained unchanged in the jump trained. Plasma and muscle malonaldehyde (MDA) after the jump test were not significantly different from rest. These data suggest that jump training is associated with elevated activities of SOD and the coupled enzymes GPX and GR in muscle tissue, but other antioxidants remain unchanged. High-intensity jump exercise induces muscle enzyme leakage in untrained humans, but muscle lipid peroxidation, measured as changes in MDA, was not different in the two groups despite the varied muscle antioxidant enzyme levels.
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PMID:Antioxidant status and lipid peroxidation after short-term maximal exercise in trained and untrained humans. 914 28

Recent evidence has shown that alcohol as well as exercise induces oxidative stress. However, the combination of both on the cardiac antioxidant system is not known. This study investigates the interactive effects of exercise training and chronic ethanol consumption on the antioxidant system of the rat heart. Male Fisher-344 rats were treated as follows: 1) sedentary control (SC); 2) exercise training (ET) for 6.5 weeks; 3) ethanol (2 g/kg, PO) for 6.5 weeks, and 4) ET plus ethanol for 6.5 weeks. Rats were sacrificed and hearts were isolated. Glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and lipid peroxidation (MDA) were determined in heart tissues. SOD and GSH-Px activities were significantly increased 118% and 148% of SC, respectively, due to ET. GSH level increased 118% of SC in ET rats. GSH-Px activity increased 118% of SC whereas SOD activity and CuZn-SOD protein level and GR activity decreased 87%, 71%, and 90% of SC due to chronic ethanol administration. GSH level decreased 87% of SC and lipid peroxidation increased 149% of SC due to ethanol consumption. GSH-Px activity and GSH levels increased 143% and 130% of SC due to combination of ET and ethanol. This study suggests that ET and chronic ethanol ingestion augments the antioxidant enzyme activity and GSH levels in the heart. This combination reduced the extent of ethanol-induced lipid peroxidation. The data suggest that ET may reduce the extent of the damage caused by ethanol consumption on the myocardium.
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PMID:Response of cardiac antioxidant system to alcohol and exercise training in the rat. 916 Aug 8

This study was undertaken in order to determine the changes in auditory brainstem-evoked responses relationship with the changes in the levels of GSH, lipid peroxidation and antioxidant enzymes activity in cisplatin-induced ototoxicity and otoprotection by 4-methylthiobenzoic acid (MTBA). Male Wistar rats in different groups were treated as follows: 1) saline control; 2) cisplatin (16 mg/kg, intraperitoneally); 3) MTBA (250 mg/kg, intraperitoneally), and 4) cisplatin plus MTBA. Post-treatment auditory brainstem-evoked responses were performed after three days and the rats were sacrificed and cochleae harvested. The cochleae were analyzed for glutathione (GSH), antioxidant enzyme activity, and malondialdehyde levels. The cisplatin injected rats showed a threshold elevation of 31.9 +/- 16.0 dB above the pretreatment thresholds using click stimulus. Rats treated with MTBA plus cisplatin did not show significant elevation of hearing threshold. Cisplatin plus MTBA administration showed a higher levels of cochlear GSH (5.59 +/- 0.35 nmoles/mg protein) compared to cisplatin alone (4.46 +/- 0.13 nmoles/mg protein). Cisplatin treated rats showed a decrease in superoxide dismutase, catalase, glutathione peroxidase (GSH-peroxidase), and glutathione reductase (GSH-reductase) activities (57%, 83%, 78% and 58% of control). Cochlear superoxide dismutase, catalase and GSH-reductase activities and MDA levels were restored in the rats injected with cisplatin plus MTBA, compared to cisplatin alone. It is concluded that the protection conferred by MTBA against cisplatin ototoxicity is associated with sparing of the cochlear antioxidant system.
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PMID:Protection by 4-methylthiobenzoic acid against cisplatin-induced ototoxicity: antioxidant system. 935 48

The objective of the study was to determine the influence of blood loss volume on lipid peroxidation (LP) process and antioxidant system (AOS) state in the patients with a heavy combined trauma. The studies were proceeded in 36 patients with a heavy combined trauma. The mean age of the patients was 40 +/- 2. A craniocerebral trauma was associated with trauma of both thorax and abdominal cavities and locomotor system. Blood loss reached 75% of circulating blood volume (CBV), mean value was 28 +/- 3%. Blood samples for the studies were obtained at admission of the patients by emergency medical service teams, and--after 4; 24 hours, 3 and 7 days after the trauma. CBV determination was made by dradioisotope method. LP and AOS state was judged from serum level of primary (conjugated dienes), secondary (malonic dialdehyde, MDA) LP products and extracellular antioxidant enzyme ceruloplasmin (CP). K coefficient, an integral indicator was used for LP-AOS system imbalance assessment. According to the obtained data, in the studied patients intensification of the LP processes manifesting in CD and MDA contents increase was most expressed from 1 to 3 days after trauma (2.0-2.6-fold, p < 0.05) and rise of TP content maximally in the 3 day 2.28-fold (p < 0.05) was observed in the there patients. At the admission of decrease (1.6-fold, p < 0.05) was registered which normalized to the 3 day. K coefficient time course study permitted to establish that as early as at the admission of the patients into the clinic its value was substantially higher than the normal one, and to the 4 hour the imbalance in the LP-AOS system increased 5.0-fold (p < 0.05). An expression of LP processes and AOS disturbances in the patients with heavy combined trauma depended on the blood loss volume. The revealed imbalance in the LP-AOS system is indicative of a necessity of inclusion antioxidants into the complex therapy.
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PMID:[Dynamics of lipid peroxidation and antioxidant system in patients with severe combined trauma]. 991 65

This study investigated the alterations in levels of glutathione, lipid peroxidation, and antioxidant enzyme activity in the liver, lung, and kidney of rats treated with acute doses of ethanol. Male Fisher-344 rats were randomly divided into four groups, and were treated as follows: (1) vehicle (saline) control; (2) ethanol 2 g/kg, p.o.; (3) ethanol 4g/kg, p.o.; and (4) ethanol 6 g/kg, p.o. The animals were sacrificed 1 h after treatment, and tissues were isolated and analyzed. The hepatic GSH levels significantly decreased (73, 68, and 66% of control) due to ethanol ingestion at 2, 4, and 6g/kg, respectively. The hepatic GSH/GSSG ratio also decreased with increasing doses indicating stress response due to ethanol. The hepatic SOD activity significantly decreased (70, 75 and 71% of control) with graded doses of ethanol ingestion. The hepatic CAT/SOD and GSH-Px+CAT/SOD ratios significantly increased (147, 169 and 177% of control) and (140, 167 and 178% of control), respectively with increasing doses of ethanol. In the lung, graded doses of ethanol increased GSH-Px activity (120, 114 and 141% of control) and decreased GR activity (98, 89 and 89% of control), respectively. The MDA concentrations in the lung also increased after higher ethanol ingestion. Most of the antioxidant enzyme ratios increased with increasing doses of ethanol in the lung. In the kidney, GSH-Px activity increased (139, 119 and 151% of control), whereas GR activity decreased (84, 85 and 83% of control). GSH-Px/SOD and GSH-Px+CAT/SOD ratios increased whereas GR/GSH-Px ratio decreased after graded doses of ethanol. GSH levels in the kidney decreased after ethanol ingestion. MDA concentrations increased with increasing dose of ethanol in the kidney. These results showed the dose dependant and tissue specific changes in the antioxidant system after ethanol ingestion. Ethanol exerts oxidative stress on antioxidant systems of liver, lung and kidney in proportion to the amount of ethanol ingestion.
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PMID:Dose response of ethanol on antioxidant defense system of liver, lung, and kidney in rat. 1082 82

The lipid peroxidation (as malondialdehyde, MDA), activities of superoxide dismutase (SOD) and catalase (CAT), and benzo[a]pyrene (BaP) metabolites were investigated in sera and erythrocytes of male Sprague-Dawley rats treated with BaP (20 mg per rat). MDA levels were significantly increased in sera (16.98+/-3.29 nmol/ml serum, P<0.05) 12 h after BaP treatment and persisted up to 96 h (13.80+/-1. 65 nmol/ml serum, P<0.05), but no significant change in NIDA levels was observed in erythrocytes. SOD and CAT activities were significantly increased in erythrocytes shortly after BaP exposure, and they were slightly decreased in sera, indicating an inverse correlation between lipid peroxidation and antioxidant enzyme activity. BaP and BaP-quinones (BaP-1,6-quinone and BaP-3,6-quinone) were measured in sera during the study period. A rapid increase of unmetabolized BaP was observed in sera (41.27+/-4.14 pmol/ml serum) 3 h after BaP treatment, reaching a peak at 6 h (48.56+/-4.62 pmol/ml serum) followed by a sharp decrease. Formation of the BaP-1, 6-quinone and BaP-3,6-quinone started in sera 3 h after BaP treatment, reached a peak at 24 h (7.23+/-1.02 pmol/ml serum) and 12 h (9.20+/-0.98 pmol/ml serum), respectively, and then decreased gradually. The time-dependent pattern of serum lipid peroxidation and the level of erythrocyte antioxidant enzymes were shown to be related to the concentrations of the BaP-quinone metabolites. These results suggest that BaP treatment, probably via the formation of BaP-quinones, oxidatively altered lipids and antioxidant enzymes in the blood, and might be associated with BaP-related vascular toxicity including carcinogenesis.
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PMID:Lipid peroxidation, antioxidant enzymes, and benzo[a]pyrene-quinones in the blood of rats treated with benzo[a]pyrene. 1093 29

Present study was carried out to evaluate oxidant-antioxidant status and effect of hemodialysis in acute and chronic renal failure. Serum MDA levels increased while serum SOD found decreased significantly. This study indicates the existence and increased production of an oxidizing stress resulting from hemodialysis and disturbance in antioxidant enzyme system.
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PMID:Oxidant-antioxidant status in acute and chronic renal failure. 1122 21


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