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)

Glutamate-induced excitotoxicity involving the formation of reactive oxygen species (ROS) has been implicated in neuronal dysfunction and cell loss following ischemic and traumatic injury to the central nervous system (CNS). ROS are formed in mitochondria when energy metabolism is compromised, and are inactivated by the ROS scavengers superoxide dismutase (SOD), catalase, and glutathione (GSH). ROS can impair the function of several cellular components including proteins, nucleic acids, and lipids. In the present study, we measured indicators of mitochondrial metabolic activity, ROS formation, lipid peroxidation, and antioxidant enzyme activities in synaptosomes obtained from rat spinal cord at early times following traumatic injury. Mitochondrial metabolic activity was found to significantly decrease as early as 1 h following injury, and continued to be compromised over the remaining postinjury time points. ROS formation was found to be significantly increased at 4 and 24 h following injury, while lipid peroxidation levels were found to be significantly increased in the injured spinal cord at 1 and 24 h, but not 4 h following injury. SOD enzyme activity was unchanged at all postinjury time points, while catalase activity and GSH levels were significantly increased at 24 h following injury. These findings indicate that impaired mitochondrial function, ROS, and lipid peroxidation occur soon after traumatic spinal cord injury, while the compensatory activation of molecules important for neutralizing ROS occurs at later time points. Therapeutic strategies aimed at facilitating the actions of antioxidant enzymes or inhibiting ROS formation and lipid peroxidation in the CNS may prove beneficial in treating traumatic spinal cord injury, provided such treatments are initiated at early stages following injury.
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PMID:Impaired mitochondrial function, oxidative stress and altered antioxidant enzyme activities following traumatic spinal cord injury. 931 1

The effects of primaquine treatment on antioxidant enzyme activities were investigated in rat liver and kidney. Male Sprague-Dawley rats were treated with 0.21 mg/kg daily for two weeks (chronic treatment) or a single dose at 0.21 or 0.63 mg/kg. Antioxidant enzyme activities were determined in liver and kidney cytosolic fractions whereas glutathione (GSH) and malondialdehyde (MDA) levels were determined in tissue samples. Results for the liver showed increases in cytosolic superoxide dismutase (SOD) and glutathione peroxidase (GPX) enzymatic activities after chronic primaquine treatment. Levels of MDA, a marker for lipid peroxidation, were also increased by more than 50% indicating enhanced oxidative damage in the liver. In the single dose study, 0.63 mg/kg primaquine caused a more than 100% increase in liver SOD and a 36% increase in NAD (P) H: quinone oxidoreductase (NQOR) activities. Results for the kidney, however, showed fewer primaquine-induced changes in antioxidant enzyme activities when compared to the liver in both the chronic and single dose studies. Overall, our results indicate that primaquine treatment causes an oxidative stress in the two rat organs. These results are consistent with the known pro-oxidant effects of primaquine in vivo, and supplement current knowledge on the effects of antimalarial drugs on various enzyme systems.
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PMID:Primaquine alters antioxidant enzyme profiles in rat liver and kidney. 935 Apr 21

1. The effect of fish oil administration by gavage (0.4% body weight) on activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-Px) and on content of thiobarbituric acid reactive substances (TBARs) of the lymphoid organs [thymus, spleen and mesenteric lymph nodes (MLN)] and liver was investigated in 21-day pregnant rats. The results were compared with those obtained by administration of soybean oil, cocoa butter and coconut oil. 2. Oil administration did not have any significant effect on antioxidant enzyme activities of the liver, whereas marked changes were found in the lymphoid organs. The MLN presented the most pronounced changes: SOD and catalase activities were increased by the four oils; GSH-Px activity was raised by soybean and fish oils; coconut oil reduced the activity of the three antioxidant enzymes in this organ. 3. Fish oil given by gavage does affect the antioxidant capacity of the lymphoid organs; however, similar effect was also observed for cocoa butter and soybean oil. These changes in the antioxidant enzyme activities were able to prevent the lipid peroxidation process in the lymphoid organs.
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PMID:Changes in the activities of antioxidant enzymes of the lymphoid organs of 21-day pregnant rats due to administration of fish oil by gavage. 935 1

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 present study was designed to investigate and compare the effects of dietary selenium (Se) and vitamin E on some physiological parameters and histological changes in liver, heart, and skin tissues, as well as the blood parameters and the related enzymes. Both sex young rabbits were fed with deficient (9.8 micrograms/kg diet), adequate (225 micrograms/kg diet), and rich (4.2 mg/kg diet) Se and vitamin E diets for 12-15 wk for this purpose. As the plasma Se levels and the erythrocyte glutathione (GSH) peroxidase activity decreased (79.8 +/- 9.4 ng/mL and 2.0 +/- 0.3 U/g Hb, respectively) in the deficient group, these values increased (100.4 +/- 2.7 ng/mL and 14.5 +/- 4.3 U/g Hb) in the rich group significantly with respect to the control group. The other antioxidant enzyme activities and the related element levels did not change significantly in either one of the experimental groups. Although the platelet counts of the two experimental groups were not different from the control values, the collagen and the adenosine diphosphate (ADP) stimulated platelet aggregation rate and intensity increased in the deficient group (p < 0.05) and decreased very significantly (p < 0.001) in the rich group. In both of the experimental groups, as the percentage values of the neutrophils decreased, the lymphocytes and the eosinophils increased significantly. According to the light microscopic investigations, the observed lesions of considerable intensity within the tissues that elicit cell degenerations were more pronounced in the animals fed with the rich diet than in those fed with the deficient diet. The deficiency as well as toxicity of Se and the deficiency of vitamin E caused several alterations in the physiological functions of the tissues, and these alterations were supported by the histological lesions within these tissues.
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PMID:Dietary selenium- and vitamin E-induced alterations in some rabbit tissues. 940 35

We investigated the effect of hemorrhagic shock and reinfusion on the cardiac function and contractility, plasma CK and CK-MB activity and lactate concentration, oxyradical-producing activity of polymorphonuclear leukocytes (PMNL-CL), cardiac chemiluminescence (LV-CL), antioxidant enzyme activity [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX)] and malondialdehyde (MDA) concentration in anesthetized dogs to determine the role of oxyradicals in cardiac depression and cellular injury in hemorrhagic shock and reinfusion. The dogs were assigned into three groups: I (sham), 4 h duration; II (S + R), 2 h of shock followed by reinfusion for 2 h; III (SOD + S + R), as II but pretreated with PEG-SOD. Hemorrhagic shock was produced by withdrawal of blood to maintain the mean arterial pressure at 50 +/- 5 mm Hg. Cardiac function and contractility were depressed during hemorrhagic shock. Plasma CK, CK-MB and lactate increased during shock. Following reinfusion after 2 h of shock hemodynamic parameters and plasma lactate tended to return towards control values. Plasma CK and CK-MB, PMNL-CL and cardiac MDA, total-, Mn- and CuZn-SOD activity increased while LV-CL decreased. In spite of the increase in the antioxidant reserve, there was oxidative damage. Pretreatment with SOD attenuated the deleterious effects of shock and reinfusion on the cardiovascular function, plasma CK, and CK-MB, PMNL-CL, cardiac MDA, SOD, and LV-CL. Protection was incomplete for cardiovascular function and plasma CK and CK-MB. These results suggest that oxyradicals may partly be involved in the deterioration of cardiovascular function and cellular injury during hemorrhagic shock and reinfusion.
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PMID:Cardiac depression and cellular injury in hemorrhagic shock and reinfusion: role of free radicals. 940 75

The activities of rat hepatic subcellular antioxidant enzymes were studied during hepatic ischemia/reperfusion. Ischemia was induced for 30 min (reversible ischemia) or 60 min (irreversible ischemia). Ischemia was followed by 2 or 24 h of reperfusion. Hepatocyte peroxisomal catalase enzyme activity decreased during 60 min of ischemia and declined further during reperfusion. Peroxisomes of normal density (d = 1.225 gram/ml) were observed in control tissues. However, 60 min of ischemia also produced a second peak of catalase specific activity in subcellular fractions corresponding to newly formed low density immature peroxisomes (d = 1.12 gram/ml). The second peak was also detectable after 30 min of ischemia followed by reperfusion for 2 or 24 h. Mitochondrial and microsomal fractions responded differently. MnSOD activity in mitochondria and microsomal fractions increased significantly (p < 0.05) after 30 min of ischemia, but decreased below control values following 60 min of ischemia and remained lower during reperfusion at 2 and 24 h in both organelle fractions. Conversely, mitochondrial and microsomal glutathione peroxidase (GPx) activity increased significantly (p < 0.001) after 60 min of ischemia and was sustained during 24 h of reperfusion. In the cytosolic fraction, a significant increase in CuZnSOD activity was noted following reperfusion in animals subjected to 30 min of ischemia, but 60 min of ischemia and 24 h of reperfusion resulted in decreased CuZnSOD activity. These studies suggest that the antioxidant enzymes of various subcellular compartments respond to ischemia/reperfusion in an organelle or compartment specific manner and that the regulation of antioxidant enzyme activity in peroxisomes may differ from that in mitochondria and microsomes. The compartmentalized changes in hepatic antioxidant enzyme activity may be crucial determinant of cell survival and function during ischemia/reperfusion. Finally, a progressive decline in the level of hepatic reduced glutathione (GSH) and concomitant increase in serum glutamate pyruvate transaminase (SGPT) activity also suggest that greater tissue damage and impairment of intracellular antioxidant activity occur with longer ischemia periods, and during reperfusion.
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PMID:Studies on hepatic injury and antioxidant enzyme activities in rat subcellular organelles following in vivo ischemia and reperfusion. 940 79

In the present study, fresh blood obtained from six healthy adult male donors was investigated for erythrocyte malondialdehyde (MDA) formation and antioxidative enzyme activity. Plasma and erythrocyte membrane lipid peroxidation were measured by MDA formation. Erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels were determined in whole blood stored for transfusion purposes. Erythrocyte and plasma MDA levels increased significantly during the storage period from day 3 to day 19 and, after that, stayed unchanged. Erythrocyte MDA increased 100% on day 7 when compared to day 1. The GSH-Px activity significantly decreased after day 9 and SOD decreased after day 13. The reduction in enzyme activities continued until day 27. Our results showed significant alteration in erythrocyte membrane and plasma MDA formation and intracellular antioxidant enzyme status in whole blood used for transfusion. However, we do not know whether such alterations have clinical importances for the recipient.
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PMID:Investigation of malondialdehyde formation and antioxidant enzyme activity in stored blood. 940 67

Recently there has been growing interest in studying the differences between different classes of antihypertensive drugs in preventing cardiovascular events in diabetic patients. Hypomagnesemia is common in diabetes mellitus, and correlates to its chronic complications and the associated alteration of the antioxidant enzyme activity. Depletion of reduced glutathione (GSH) in the blood has been demonstrated with myocardial injuries associating hypomagnesemia. A previous study has demonstrated a beneficial effect of metformin hydrochloride (Met), an antihyperglycemic drug, on both magnesium (Mg) and GSH levels in diabetic animals. The purpose of this study was to investigate the effect of oral atenolol, metformin (50 and 60 mg kg[-1] day[-1], respectively) and their combination for 14 days on Mg and GSH levels in blood, liver and heart of diabetic male Wistar rats, as these two parameters have been shown to be altered in diabetics and linked to myocardial ischemic injuries. The results of this investigation showed a state of low levels of Mg and GSH in both blood and liver of the diabetic animals. Treatment with atenolol alone did not change these levels significantly, however administration of metformin or atenolol/metformin increased significantly the GSH levels in both liver and blood, and returned the liver Mg content back to normal values.
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PMID:Influence of atenolol and/or metformin on glutathione and magnesium levels in diabetic rats. 941 50

Liver antioxidant enzyme activities, mRNA abundance, and glutathione (GSH) status were investigated in male Sprague-Dawley rats placed in an enclosure module aboard Space Shuttle STS-63 for 8 d (F, n = 6). F animals were compared to rats housed in an enclosure module on the ground (G, n = 9), which simulated the vibration and temperature conditions associated with launch and flight, and rats kept under conventional ground vivarium conditions in individual cages (V, n = 6). Spaceflight significantly decreased catalase, GSH reductase, and GSH sulfur-transferase activities in the liver (p < .05). Neither enzyme activity nor enzyme protein content of Cu-Zn and Mn superoxide dismutase (SOD) was affected by flight. The relative abundance of mRNA for Cu-Zn SOD and catalase was significantly decreased comparing F with G rats (p < .05). Spaceflight resulted in a dramatic decrease of liver GSH, glutathione disulfide, and total GSH contents (p < .01), which were accompanied by a lower gamma-glutamyl transpeptidase activity (p < .05). F rats showed a 47% (p < .05) increase in liver malondialdehyde concentration compared to G and V rats. Liver protein content was not affected by flight. These results indicate that spaceflight can downregulate antioxidant defense capacity and elicit an oxidative stress in the liver.
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PMID:Spaceflight downregulates antioxidant defense systems in rat liver. 943 15


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