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)

Sunflower (Helianthus annuus L. cv. SH222) plants and calli were exposed to KCl stress for three weeks. Calli were more tolerant to KCl than plants. KCl stress decreased NO(-)(3), Mn, Fe and B levels in whole plants and P, Ca and Mg in shoots. NO(-)(3), P, Ca, Mg, Mn, and B levels decreased in 100 mM-stressed calli. Chlorophyll content, F:(m) and (F:(m)-F:(0))/F:(m) ratio decreased in stressed leaves, while F:(0) increased only in leaves exposed to severe stress (100 and 150 mM). Membrane permeability and lipid peroxidation increased in plants under all stress conditions and in 100 and 150 mM stressed calli, but remained unchanged in 25 mM stressed calli. Salt stress also induced changes relating to antioxidant enzymes: plants under all stress conditions showed a decrease in catalase, peroxidase and SOD activities. Calli under moderate stress (25 mM KCl) showed an increase of catalase, peroxidase and SOD activities, but the activities of peroxidase and SOD decreased when calli were exposed to higher KCl concentrations. The decrease of antioxidant enzyme activities is in tune with lipid peroxidation and membrane permeability increases. On the other hand, calli adapted for 6 months to 100 mM KCl showed an increase of these enzyme activities compared to unstressed calli, while MDA production and membrane permeability were not significantly affected.
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PMID:In situ and in vitro senescence induced by KCl stress: nutritional imbalance, lipid peroxidation and antioxidant metabolism. 1128 80

We addressed the hypothesis that in vitro short-term exposure to hematite (Fe(2)O(3)) and polycyclic aromatic hydrocarbons (PAHs) is more deleterious by virtue of their combinations being able to cause higher oxidative stress conditions in human lung cells (A549), than either chemical alone. Lipid peroxidation (malondialdehyde; MDA), antioxidant enzyme activities (superoxide dismutase; SOD, glutathione peroxidase; GPx, glutathione reductase; GR), glutathione status (reduced glutathione; GSH, oxidized glutathione; GSSG) and alpha-tocopherol (alpha-Toc) consumption were studied in cells exposed to Fe(2)O(3), benzo(a)pyrene (B(a)P) or pyrene, alone or in association. We found that increases in GSSG/GSH (P<0.01) and in alpha-Toc consumption (P<0.01) counteracted Fe(2)O(3)-induced lipid peroxidation. Exposure to B(a)P did not induce oxidative injury because of the involvement of non-enzymatic antioxidants in cell homeostasis. Pyrene did not induce free radicals (FR)-induced injury. Exposure to PAHs-coated onto Fe(2)O(3) particles damaged both the enzymatic (i.e. increases in SOD and GR activities; P<0.01) and the non-enzymatic (i.e. increases in GSSG/GSH; P<0.001, alpha-Toc consumption; P<0.01) antioxidant defenses, thereby allowing lipid peroxidation (i.e. MDA production; P<0.05). Exposure to PAHs-coated onto Fe(2)O(3) particles induced not only higher lipid peroxidation (i.e. MDA production; P<0.05) but also higher antioxidant alterations (i.e. SOD and GR activities; P<0.05, GSSH/GSH; P<0.01 or P<0.05) than either chemical alone. Several mechanisms could account for this result, enhanced uptake of Fe(2)O(3) and/or greater availability of PAHs. Hence, our results indicate that exposure to PAHs-coated onto Fe(2)O(3) particles is more deleterious in lungs than either chemical alone.
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PMID:Antioxidant defense disruption by polycyclic aromatic hydrocarbons-coated onto Fe(2)O(3) particles in human lung cells (A549). 1154 9

The aqueous extract from the roots of Rumex patientia L. (Polygonaceae) (D-1) was investigated for its effects on rat liver and erythrocyte antioxidant enzyme systems and lipid peroxidation. Measurements of the GSH-Px, SOD and CAT activities, and MDA levels of liver and erythrocytes in D-1 administered animals showed that there was an increase in GSH-Px and SOD activities when compared to that of controls. No significant decrease was observed in catalase activity and no changes in malondialdehyde levels were observed.
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PMID:The effects of Rumex patientia extract on rat liver and erythrocyte antioxidant enzyme system. 1216 33

Many individuals with cardiovascular diseases undergo periodic physical conditioning with or without medication. Therefore, this study investigated the interaction of exercise training and chronic nitroglycerin treatment on blood pressure (BP) and alterations in nitric oxide (NO), glutathione (GSH), antioxidant enzyme activities and lipid peroxidation in rats. Fisher 344 rats were divided into four groups: (1) sedentary control, (2) exercise training for 8 weeks, (3) nitroglycerin (15 mg/kg, s.c. for 8 weeks) and (4) training + nitroglycerin for 8 weeks. BP, heart rate (HR) and respiratory exchange ratio (RER) were monitored weekly for 8 weeks using tail-cuff method and oxygen/carbon dioxide analyzer, respectively. The animals were sacrificed 24 h after last treatments and plasma isolated and analyzed using HPLC, ELISA and UV-VIS spectrophotometric techniques. The results show that exercise conditioning significantly enhanced NO production (p < 0.001), GSH levels (p < 0.001), GSH/GSSG ratio (p < 0.05) and the up-regulation of the activities of catalase (CAT) (p < 0.05), glutathione peroxidase (GSH-Px) (p < 0.001), and glutathione reductase (GR) (p < 0.05), and depression of lactate levels (p < 0.001) in the plasma of the rat. These biochemical changes were accompanied by a significant increase in RER (p < 0.001) without a significant change in BP and HR. Chronic nitroglycerin administration significantly increased NO levels (p < 0.05), GSH levels (p < 0.001), superoxide dismutase (SOD) activity (p < 0.05), GST activity (p < 0.05), and decreased MDA levels (p < 0.05). These biochemical changes were accompanied by a significant decrease in BP (p < 0.05) and without any significant changes in HR and RER. Interaction of exercise training and chronic nitroglycerin treatment resulted in normalization of plasma NO, MDA, lactate levels, and CAT activity. The combination of exercise and nitroglycerin significantly enhanced GSH levels (p < 0.05), and the up-regulation of SOD (p < 0.001), GSH-Px (p < 0.05), GR (p < 0.05) and GST (p < 0.001) activities. These biochemical changes were accompanied by normalization of BP and a significant increased in RER (p < 0.001). The data suggest that the interaction of physical training and chronic nitroglycerin treatment resulted in the maintenance of BP and the up-regulation of plasma antioxidant enzyme activities and GSH levels in the rat.
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PMID:Interaction of physical training and chronic nitroglycerin treatment on blood pressure and plasma oxidant/antioxidant systems in rats. 1284 29

Recent studies documented that estrogen have antioxidant properties in-vitro, there are conflicting results on the effect of estrogen in vivo. We aimed to investigate the effects of estradiol and Raloxifene on the antioxidant enzyme [superoxide dismutase (SOD) and catalase (CAT)] activities and MDA levels in brain and liver homogenates of ovariectomized female rats. Twelve weeks after ovariectomy, female Sprague-Dawley rats (n = 26) were divided into three groups: (1) Ovariectomized placebo group (n = 6) was given physiologic saline. (2) Estrogen group (n = 10) was given Ethynyl estradiol, 0.1 mg/kg sc. (3) Raloxifene group (n = 10) was given raloxifene, 1 mg/kg sc during 8 weeks. Ten rats were used as naive controls without any treatment (Sham operated group, n = 10). Ovariectomy lead to an increase in the CAT activities in liver tissue samples compared to the sham group (p = 0.056, Mann-Whitney test). While estrogen treatment reversed to normal levels of CAT activities, raloxifene remained as ineffective. Superoxide dismutase activities and MDA levels in liver were remained unchanged in all groups. There was no significant change in the brain tissue SOD and CAT activities between the control ovariectomy, estrogen treated, and raloxifen treated groups. We determined an increase in MDA levels in brain of ovariectmised rat (p = 0.02). While raloxifene treatment reversed to normal levels of MDA (p = estrogen treatment failed. Our data showed that estrogen may play a role in regulation of CAT and SOD activities in liver due to its antioxidative effects. We can suggest estrogen and raloxifene exert their antioxidative effects in brain rather than liver. Since Raloxifene's effect is more clear than estradiol, raloxifene may be suggested primarily for treatment and/or prevention of diseases which can be resulted from oxidative stress in postmenopausal women.
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PMID:The effects of estrogen and raloxifene treatment on antioxidant enzymes in brain and liver of ovarectomized female rats. 1285 5

Total sialic acid levels (TSA), antioxidant enzymes activities such as superoxide dismutase (SOD), catalase (CAT) and lipid peroxidation (LPO) levels were investigated during the developmental period in tadpoles of the predominantly terrestrial amphibian B. viridis and the predominantly aquatic amphibian R. r. ridibunda. Maximum TSA levels were observed in B. viridis and R. r. ridibunda at the fifth and third week of their development, respectively. SOD and CAT activity variations during development in B. viridis were higher than in R. r. ridibunda. Although SOD activity in B. viridis was higher than R. r. ridibunda at the eighth week, SOD activity increased 19.2-fold in R. r. ridibunda and 10.4-fold in B. viridis between the first and eighth week. CAT activity in R. r. ridibunda did not significantly change (p>0.001) until the fifth week then increased, whereas in B. viridis CAT increased after the third week. In contrast to the rise in the antioxidant enzyme activities, LPO levels tended to decrease during the developmental period. Levels of LPO showed a similar trend until the third week for both species. The minimum LPO levels in B. viridis and R. r. ridibunda were 23+/-1.2 and 146+/-7.3 nmol MDA g(-1) tissue, at the eighth week, respectively. While decreasing LPO levels correlated with increasing antioxidant enzyme activities, TSA tended to decrease after reaching a maximum point.
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PMID:The relationship between total sialic acid levels and antioxidant status in the tadpoles of Bufo viridis and Rana ridibunda ridibunda. 1291 Apr 79

Erythrocyte deformability is one of the most important charactheristics of erythrocytes for an effective microcirculatory function and is affected from a number of factors, including the oxidative-damage-induced by nitric oxide (NO). This study was performed to investigate the effects of in vitro melatonin incubation on the antioxidant status and deformability of erythrocytes in sodium nitroprusside (SNP), a nitric oxide donor, induced oxidative stress. 40 blood samples taken from the adult healthy people were divided into 4 groups randomly and incubated with saline, SNP (1 mM), melatonin (MEL, 1 mM), MEL + SNP and SNP + L-NAME (5 mM) respectively. Relative filtration rate (RFR), relative filtration time (RFT) and relative resistance (Rrel) were determined as the indexes of erythrocyte filterability. In addition, malondialdehyde (MDA, as an index of lipid peroxidation) and the antioxidant activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) were also determined in the red blood cells of all groups revealing the oxidant-antioxidant activity. RFT and the Rrel of the erythrocytes incubated with SNP increased significantly (p<0.05) whereas the RFR of the erythrocytes decreased (p<0.05) in comparison to all groups. This reduction in RFR was prevented with both L-NAME or MEL incubation. Furthermore, MEL was found to be significantly efficient in preventing the erythrocytes from lipid peroxidation in these groups. In addition, GSH-Px and SOD activities were elevated with SNP incubation reflecting the oxidative stress in erythrocytes, whereas the CAT activity remained unchanged. Melatonin has no significant effect on the GSH-Px and CAT activity but, it caused a significant decrease in SOD activity (p<0.05). These results reveal that, melatonin can protect the erythrocytes from impaired deformability in SNP-induced oxidative stress due to antioxidant effects as revealed by lipid peroxidation and antioxidant enzyme activities.
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PMID:In vitro effects of melatonin on the filtrability of erythrocytes in SNP-induced oxidative stress. 1525 61

Reactive oxygen species avidly reacts with nitric oxide (NO) producing cytotoxic reactive nitrogen species capable of nitrating proteins and damaging other molecules which leads to the reduction of erythrocyte deformability. The aim of this investigation was to assess the importance of alpha-tocopherol (Vit-E) in the total antioxidant status of the erythrocytes in sodium nitroprusside (SNP), a nitric oxide donor, induced oxidative stress and its relation to erythrocyte deformability. Male Swiss Albino rats were used in 4 groups, comprising of 10 animals in each group. The first group was the control, and the other groups were administered SNP (10 mg/kg, i.p.), Vit-E (10 mg/kg, i.p.) + SNP, and SNP + L-NAME (10 mg/kg, i.p.), respectively. Relative filtration rate (RFR), relative filtration time (RFT) and relative resistance (Rrel) were determined as the indexes of erythrocyte deformability. In addition, malondialdehyde (MDA, as an index of lipid peroxidation) and nitric oxide levels and the antioxidant activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) were also determined in the red blood cells of all groups revealing the oxidant-antioxidant activity. RFT and the Rrel of the erythrocytes of the SNP-treated rats increased significantly (p<0.05) whereas the RFR of the erythrocytes decreased (p<0.05) in comparison to all groups reflecting the impaired deformability. This reduction in RFR was prevented with both L-NAME or Vit-E incubation. Vit-E has also reduced the Rrel of the erythrocyte which reveals that it has improved the erythrocyte deformability. Lipid peroxidation was suppressed by Vit-E and L-NAME significantly, where the red blood cell deformability was improved. Furthermore, SOD and CAT activities were significantly stimulated with SNP treatment (p<0.05), where as GSH-Px remained unchanged. In the contrary, GSH-Px activity was triggered significantly by Vit-E administration, whereas the SOD and CAT activities were reduced (p<0.05). As a result, these data reveal that Vit-E improves the erythrocyte deformability in SNP-induced oxidative stress by its antioxidant effects on the lipid peroxidation and antioxidant enzyme activities.
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PMID:The in vivo antioxidant effectiveness of alpha-tocopherol in oxidative stress induced by sodium nitroprusside in rat red blood cells. 1525 62

Effects of ingesting garlic extract on plasma and erythrocyte antioxidant parameters of atherosclerotic patients were investigated in this study. Eleven patients with atherosclerosis participated in the study. They ingested a dose of 1 ml/kg body weight of garlic extract daily for 6 months (study period). Before and after this period, fasting blood samples were obtained, and oxidant (malondialdehyde, MDA and xanthine oxidase, XO) and antioxidant (superoxide dismutase, SOD and glutathione peroxidase, GSH-Px) parameters were studied in plasma and erythrocytes obtained from the patients. Blood samples obtained from 11 healthy subjects served as the controls. Plasma XO activity and MDA levels were higher, but plasma and erythrocyte GSH-Px activities were lower, in patients with atherosclerosis relative to those of the control group. Our results showed that ingestion of garlic extract leads to significantly lowered plasma and erythrocyte MDA levels in the patients even in the absence of changes in antioxidant enzyme activities. Our results also demonstrated the presence of oxidant stress in blood samples from patients with atherosclerosis, but ingesting garlic extract prevented oxidation reactions by eliminating this oxidant stress. Thus, it is possible that reduced peroxidation processes may play a part in some of the beneficial effects of garlic in atherosclerotic diseases.
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PMID:Effects of garlic extract consumption on plasma and erythrocyte antioxidant parameters in atherosclerotic patients. 1530 63

Docosahexaenoic acid (DHA, 22:6 n-3), a polyunsaturated fatty acid found in fish oil, exerts cytotoxic effects on cancer cells. Although DHA was toxic toward five human cancer cell lines (MCF-7, MDA-MB-231, SiHa, Raji, and DHL-4), the lines were not uniformly sensitive. DHL-4, a bcl-2 overexpressing lymphoid line, was the most sensitive (IC50, 5.2 micromol/L) and the cervical cancer cell line, SiHa, was the most resistant (IC50, >300 micromol/L). Lipid peroxidation has been cited by others as an important component of DHA toxicity, and we confirmed that vitamin E prevents the cytotoxic effects of DHA. Lipid peroxidation was greater following DHA treatment of the sensitive DHL-4 cells than in the resistant SiHa cells, as assessed by thiobarbituric acid reactive substance generation. DHL-4 cells treated with DHA for 20 hours showed a 3.5-fold increase in thiobarbituric acid reactive substances, whereas SiHa cells showed no increase. Reverse transcription-PCR analysis detected a down-regulation of the expression of the major antioxidant enzyme, superoxide dismutase (SOD) 1, in DHL-4 cells but not in SiHa cells after DHA treatment. Knockdown of SOD1 expression in SiHa cells with small interfering RNA significantly enhanced lipid peroxidation and cytotoxicity on exposure to DHA. These results show that DHL-4 cells are highly sensitive to the cytotoxic effect of DHA and that regulation of SOD1 expression may play an important role in determining the sensitivity of different tumor cells to the cytotoxic effects of DHA.
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PMID:Differential sensitivity of cancer cells to docosahexaenoic acid-induced cytotoxicity: the potential importance of down-regulation of superoxide dismutase 1 expression. 1536 5


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