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)

Recently, it has been suggested that bilirubin may act as a potent biological chain-breaking antioxidant. To observe the effects of free bilirubin on antioxidant reactions in cumene hydroperoxide-treated erythrocytes (15 g hemoglobin/dl), we added bilirubin at four different concentrations (0.5, 1, 5, and 10 mg/dl). We measured the thiobarbituric acid-reactive substance and reduced glutathione levels, and some antioxidant enzyme activities, namely superoxide dismutase, catalase, and glucose-6-phosphate dehydrogenase. Thiobarbituric acid-reactive substance and chemiluminescent signals decreased during the incubation. Superoxide dismutase activities also decreased but not as much as in the control group. Glucose-6-phosphate dehydrogenase activities and reduced glutathione levels increased, but catalase activities remained the same as the control group. Our results suggest that bilirubin--in the concentrations we have used--partially prevented the oxidant effects of cumene hydroperoxide.
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PMID:The effect of bilirubin on lipid peroxidation and antioxidant enzymes in cumene hydroperoxide-treated erythrocytes. 987 96

Ionizing radiation induces the production of reactive oxygen species, which play an important causative role in radiation damage. NADP+-dependent isocitrate dehydrogenase (ICDH) in Escherichia coli produces NADPH, an essential reducing equivalent for the antioxidant system. The protective role of ICDH against ionizing radiation in E. coli was investigated in wild-type and ICDH-deficient strains. Upon exposure to ionizing radiation, the viability was lower and the lipid peroxidation was higher in mutant cells compared to wild-type cells. Activities of key antioxidant enzymes such as superoxide dismutase, catalase, glutathione reductase, and glucose-6-phosphate dehydrogenase were decreased by irradiation in both cells. Results suggest that ICDH plays an important role as an antioxidant enzyme in cellular defense against ionizing radiation.
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PMID:Radiation sensitivity of an Escherichia coli mutant lacking NADP+-dependent isocitrate dehydrogenase. 992 Jul 94

Of all the clinical disciplines, radiotherapy probably has the most secure and scientific foundations. In oral cancer, radiotherapy may be used as the sole treatment or in combination with other modalities of treatment. Blood samples were collected from stage III oral cancer patients attending the Oncology Department, Bernard Institute of Radiation and Oncology, Chennai Medical College, Chennai, India, before initiating radiotherapy and after the sixth week of radiotherapy. The effect of radiation on oral cancer patients has been studied using activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPX), glutathione reductase (GR), glutathione-S-transferase (GST), glucose-6-phosphate dehydrogenase (G6PDH) and levels of malondialdehyde (MDA). The levels of MDA showed a significant increase in untreated and radiation oral cancer patients when compared with normal subjects. The activities of red blood cell (RBC) hemolysate antioxidant enzymes such as SOD, catalase, GPX, GR, GST and G6PDH showed a significant decrease, representing the lack of antioxidant defense. Radiation induces lipid peroxidation by inactivating the antioxidant enzymes, thereby rendering the system inefficient in management of the free radical attack. Thus, the degree of radiation affects the extent of the depression of the antioxidant enzyme activities and increases lipid peroxidation.
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PMID:Oxidant and antioxidant activity changes in patients with oral cancer and treated with radiotherapy. 1062 47

To investigate the effects of repeated exposure to nitrogen dioxide (NO2) on antioxidant enzymes in lung tissue and isolated lung cells, rats were continuously exposed to 20 mg/m3 NO2 (10.6 ppm) for 4 days. The activities of glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), and glutathione peroxidase (GSHPx) were measured in the cytosolic fraction of lung tissue of both control and NO2-exposed rats as well as in isolated alveolar macrophages (AMs) and type II cells. Qualitative and quantitative changes in AM and type II cells were studied by electron microscopy and by morphometric analyses using enzyme and immunohistochemistry. NO2 exposure resulted in significantly increased pulmonary activities of G6PDH, GR, and GSHPx, both expressed per lung and per gram of lung weight. Morphometric data show that NO2 exposure significantly increased the number of type II cells, predominantly in the centriacinar region, indicating proliferation of epithelium following cellular injury. Type II cells in lungs of NO2-exposed rats had a squamous, less cuboidal appearance with more lamellar bodies compared to type II cells in lungs of control rats. Compared to control lungs, a higher number of macrophages could be isolated from NO2-exposed lungs, while numbers of type II cells isolated from lungs of control and NO2-exposed rats were the same. Isolated type II cells from control and NO2-exposed rats were polymorphic, with a small number of lamellar bodies and without polarity. Isolated macrophages were rounded and contained many filopodia. NO2 exposure caused increases in the activities of G6PDH and GSHPx in isolated type II cells and of GSHPx in isolated macrophages, when expressed per number of cells. Macrophages and type II cells isolated from control and NO2-exposed rats and re-exposed in vitro to NO2, showed no differences in phagocytosis and viability features. Our results indicate that NO2-induced increases in pulmonary antioxidant enzymes are also reflected in isolated AM and type II cells. Since these lung cells do not display a decreased sensitivities toward an in vitro NO2 exposure, overall increase in antioxidant enzyme activities do not seem to play the most pivotal role in controlling cellular NO2 sensitivity and oxidant defence. Combined data from biochemical, morphological, and morphometric analyses of lungs and lung cells suggest that lung cell and tissue oxidant sensitivity and defence largely depends on the cell and tissue organisation, i.e., cell numbers and morphology as well as the ratio of surface area to cytoplasmic volume.
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PMID:Biochemical and morphological changes in lung tissue and isolated lung cells of rats induced by short-term nitrogen dioxide exposure. 1100 89

This study aims to investigate the effects of the herbicide 2,4-D and the insecticide azinphosmethyl on hepatic antioxidant enzyme activities and lipid peroxidation in tilapia. Fish were exposed to 27 ppm 2,4-D, 0.03 ppm azinphosmethyl and to a mixture of both for 24, 48, 72 and 96 h. Activities of catalase (EC 1.11.1.6), glutathione-S-transferase (GST, EC 2.5.1.18) and the level of malondialdehyde (MDA) in the liver of Oreochromis niloticus exposed to 2,4-D and azinphosmethyl, both individually and in combination, were not affected by the pesticide exposures. However, glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) and glutathione reductase (GR, EC 1.6.4.2) activities in individual and combined treatments, increased significantly compared to controls. Furthermore, glutathione peroxidase (GPx, EC 1.11.1.9) activity increased in individual treatment, while the same enzyme activity decreased in combination. 2,4-D did not affect the activity of superoxide dismutase (SOD, EC 1.15.1.1), but the activity of this enzyme in azinphosmethyl treatment decreased, while its activity increased in combination. Combined treatment of the pesticides exerted synergistic effects in the activity of SOD, while antagonistic effects were found in the activities of G6PD, GPx, GR. The results indicate that O. niloticus resisted oxidative stress by antioxidant mechanisms and prevented increases in lipid peroxidation.
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PMID:Combined effects of 2,4-D and azinphosmethyl on antioxidant enzymes and lipid peroxidation in liver of Oreochromis niloticus. 1124

We have reported that melatonin protects against alpha-naphthylisothiocyanate (ANIT)-induced acute liver injury in rats by preventing enhanced lipid peroxidation. Herein, we examine the effect of melatonin on hepatic antioxidant enzyme activities in rats with a single i.p. injection of ANIT (75 mg/kg body weight) in order to clarify the protective mechanism of the indoleamine against ANIT-induced acute liver injury. Rats received a single oral administration of melatonin (10 or 100 mg/kg body weight) at 12 hr after ANIT treatment. Hepatic Cu,Zn-superoxide dismutase (Cu,Zn-SOD), Mn-superoxide dismutase (Mn-SOD), catalase (CAT), Se-glutathione peroxidase (Se-GSH-Px), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PDH) activities and reduced glutathione (GSH) concentration were determined 12 and 24 hr after ANIT treatment. ANIT-treated rats showed decreases in hepatic Cu,Zn-SOD and GSSG-R activities at 24 hr after treatment, transient increases in hepatic CAT and Se-GSH-Px activities at 12 hr, and no changes in hepatic Mn-SOD and G-6-PDH activities at 12 or 24 hr. Only the high dose of melatonin attenuated the decrease in hepatic Cu,Zn-SOD activity, while both doses of the indoleamine almost completely attenuated the decrease in hepatic GSSG-R activity. Neither dose of melatonin affected hepatic CAT, Se-GSH-Px, and G-6-PDH activities. ANIT-treated rats showed an increase in hepatic GSH concentration at 24 hr after treatment. Neither dose of melatonin affected the increase in hepatic GSH concentration. These results indicate that orally administered melatonin prevents decreases in Cu,Zn-SOD and GSSG-R activities in the liver of ANIT-treated rats, and suggest that the indoleamine may protect against ANIT-induced acute liver injury by attenuating the disruption of hepatic antioxidant defense systems.
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PMID:Effect of melatonin on changes in hepatic antioxidant enzyme activities in rats treated with alpha-naphthylisothiocyanate. 1170 68

The aim of this study was to test the hypothesis that exposure of red blood cells (RBC) to low-power laser energy can modulate their metabolism and deformability. The effects of exposure to a He-Ne (lambda=632.8 nm), GaAlAs (lambda=780 nm) and GaAs (lambda=904 nm) lasers have been examined. Red cells diluted to a hematocrit of 45% were incubated in a humidified atmosphere of 95% air and 5% CO(2) at 37 degrees C, and exposed to three different laser beams held 5 cm from the target area to yield a spot surface area of 2 cm(2). Three red cell suspensions belonging to the experimental groups were treated with each laser beam by 5, 15 and 30 minutes, respectively. The temperature was constant during the exposure's time. Three control suspensions of RBC were kept for the same time as sham-irradiated groups. The erythrocyte elongation index (EEI) was evaluated using a Rheodyn SSD (Myrene, Roetgen, Germany). The enzyme activities of glucose-6-phosphate dehydrogenase (G-6-PD), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) were assayed in each sample spectrophotometrically. Adenosine triphosphate (ATP) and diphosphoglicerate (2,3-DPG) levels were also assessed. No statistical differences were observed in the erythrocyte elongation index at shear stresses of 0.30, 0.60, 1.20, 3.00, 6.00, 12.00, 30.00 and 60.00 Pa after being irradiated for 5 and 15 minutes as compared to not irradiated ones. At 30.00 and 60.00 Pa a decrease (p<0.03 and p<0.05, respectively) in EEI has been observed after 30 min exposure to all three wavelengths of laser light when compared to the control. The antioxidant enzyme activities showed no significant changes following 5, 15 and 30 min of irradiation by all three laser wavelengths laser tested. Similarly, erythrocyte organic phosphate levels (ATP and 2,3-DPG) showed no significant changes following treatment by laser radiation. This study revealed that the low-power laser at 632.8, 780 and 904 nm wavelengths have little biological effects on red blood cells in vitro.
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PMID:The influence of low-power laser energy on red blood cell metabolism and deformability. 1184 17

The aim of this study was to investigate the alterations in lipid peroxidation and antioxidant enzyme defences in the blood of patients with malignant breast tumour and benign breast disease. Forty patients with malignant breast tumour, 20 patients with benign breast disease and also 20 healthy control subjects were recruited for the study. Malondialdehyde levels in plasma and erythrocytes, and the activities of erythrocyte CuZn-superoxide dismutase, catalase, glutathione peroxidase and glucose-6-phosphate dehydrogenase were measured. Malondialdehyde levels were higher in patients with both benign breast disease and malignant breast tumour compared with control subjects. The activities of all antioxidant enzymes were higher in patients with malignant breast tumour, while only glutathione peroxidase and CuZn-superoxide dismutase activities were higher in patients with benign breast disease. Except for glucose-6-phosphate dehydrogenase, the antioxidant enzymes studied correlated positively with the malondialdehyde levels in patients with malignant breast tumour. On the other hand, only glucose-6-phosphate dehydrogenase activity was increased by the level of malignancy. The activity increases in erythrocyte antioxidant enzymes may be a compensatory upregulation in response to increased oxidative stress especially in patients with malignant breast tumour.
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PMID:Oxidant/antioxidant status in blood of patients with malignant breast tumour and benign breast disease. 1241 67

Free radicals are now well known to damage cellular components. To investigate whether age and thyroid level affect peroxidation speed, we examined the levels of malondialdehyde and antioxidant enzyme activities in different age groups of hypothyroid rats. Hypothyroidism was induced in 30- and 60-day-old Wistar Albino rats by the i.p. administration of propylthiouracil (10 mg kg(-1) body weight) for 15 days. While malondialdehyde levels of 30- or 60-day-old hypothyroid rats were increased in liver, they were decreased in the tissues of the heart and thyroid. While glucose-6-phosphate dehydrogenase activity levels did not change in heart, brain and liver tissues of 30-day-old rats, they increased in brain and heart tissues of 60-day-old experimental groups, but decreased in the liver. Catalase activities decreased in the liver and heart of rats with hypothyroidism, but increased in erythrocytes. In control groups while malondialdehyde levels increased in brain, heart and thymus with regard to age, they decreased in plasma. Glucose-6-phosphate dehydrogenase and catalase activities were not affected by age in tissues of the thymus, thyroid and brain, but they were decreased in the heart tissue. The changes in the levels of lipid peroxidation and antioxidant enzyme activities which were determined in different tissues of hypothyroid rats indicate a cause for functional disorder of these tissues. Moreover, there may be changes depending on age at lipid peroxidation and antioxidant enzyme activity levels.
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PMID:Oxidative damage and antioxidant enzyme activities in experimental hypothyroidism. 1462 70

We have studied the activities of enzymes (glucose-6-phosphate dehydrogenase (G-6-PD), copper, zinc-superoxide dismutase (Cu,Zn-SOD), catalase (CAT), selenium-dependent glutathione peroxidase (Se-GSH-Px) and glutathione-S-transferase (GST)), and the levels of reduced glutathione (GSH), oxidized glutathione (GSSG) and thiobarbituric acid-reactive substances (TBARS) in rat erythrocytes and estimated the ratio of GSH/GSSG and the redox index. Male Wistar rats at ages of 1, 6 and 12 months were used. The activities of G-6-PD and Cu,Zn-SOD, the levels of GSSG and TBARS were increased, while the activity of Se-GSH-Px and the level of GSH were decreased with age. GSH/GSSG ratio was significantly decreased with age. We found a positive correlation between age and G-6-PD (r=0.476, p<0.01), Cu,Zn-SOD (r=0.291, p<0.01), CAT (r=0.254, p<0.01) and GST activities (r=0.250, p<0.05), and GSSG (r=0.708, p<0.05) and TBARS levels (r=0.802, p<0.01), whereas the correlation between age and Se-GSH-Px activity (r=-0.376, p<0.05), GSH level (r=-0.603, p<0.01) and GSH/GSSG ratio (r=-0.685, p<0.05) were negative. We found age-related differences in erythrocyte antioxidant enzyme activities, GSH, GSSG, total GSH and TBARS levels, GSH/GSSG ratio and the redox index.
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PMID:Changes in glucose-6-phosphate dehydrogenase, copper, zinc-superoxide dismutase and catalase activities, glutathione and its metabolizing enzymes, and lipid peroxidation in rat erythrocytes with age. 1503 14


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