Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the effect of combination of vitamin C (ascorbic acid), vitamin E (alpha -tocopherol), and selenium (sodium selenate) on ethanol-induced liver and intestine injury in rats was investigated. The ethanol-induced injury was produced by the administration of 1 ml of absolute ethanol to each rats. Animals received vitamin C (250 mg/kg), vitamin E (250 mg/kg), and sodium selenate (Se) (0.5 mg/kg) for 3 days; 1 h after the final antioxidant administration, they were sacrificed. Lipid peroxidation and glutathione levels, catalase (CAT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GP(x)) activities were determined in liver and intestine tissues. Myeloperoxidase (MPO), aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) were determined in liver tissue. Also, CAT activity, urea, creatinine, uric acid, and total lipid levels were determined in serum samples. In the ethanol group, serum urea, creatinine, uric acid, and total lipid levels; liver and intestine LDH; liver MPO, AST, ALP, ALT, and GGT activities; and liver and intestine LPO levels increased, whereas serum CAT activity, liver and intestine GSH levels, and CAT, SOD, and GP(x) activities decreased. On the other hand, treatment with vitamin C, vitamin E, and Se reversed these effects. As a result of these findings, we can say that the combination of vitamin C, vitamin E, and selenium has a protective effect on ethanol-induced changes in lipid peroxidation, glutathione levels, and antioxidant enzyme activities in liver and intestine tissues, and in some serum parameters of rats.
 ...
PMID:Combined effects of vitamin C, vitamin E, and sodium selenate supplementation on absolute ethanol-induced injury in various organs of rats. 1806 67

Recent studies revealed that the herb Andrographis paniculata possesses cardioprotective activities. Using neonatal rat cardiomyocytes, the cardioprotective actions of several diterpene lactones derived from A. paniculata including andrographolide, 14-deoxyandrographolide, 14-deoxy-11,12-didehydroandrographolide, and sodium 14-deoxyandrographolide-12-sulfonate were investigated. Pretreatment with andrographolide but not with the other compounds protected the cardiomyocytes against hypoxia/ reoxygenation injury and up-regulated the cellular-reduced glutathione (GSH) level and antioxidant enzyme activities. The cardioprotective action of andrographolide was found to coincide in a time-dependent manner with the up-regulation of GSH, indicating the important role of GSH. The cardioprotective action of andrographolide was also completely abolished by buthionine sulfoximine, which acts as a specific gamma-glutamate cysteine ligase (GCL) inhibitor to deplete cellular GSH level. It was subsequently found that the mRNA and protein levels of the GCL catalytic subunit (GCLC) and modifier subunit (GCLM) were up-regulated by andrographolide. Luciferase reporter assay also demonstrated that andrographolide activated both the GCLC and the GCLM promoters in the transfected rat H9C2 cardiomyocyte cell line. The 12-O-tetradecanoylphorbo-13-acetate response element or the antioxidant response element may be involved in the transactivating actions of andrographolide on the GCLC and GCLM promoters. The present study pinpoints andrographolide as a cardioprotective principle in A. paniculata and reveals its cytoprotective mechanism.
 ...
PMID:Andrographolide up-regulates cellular-reduced glutathione level and protects cardiomyocytes against hypoxia/reoxygenation injury. 1817 84

The aim of the study was to determine the selenium (Se) requirement of guinea pigs as a species unable to synthesize ascorbic acid. Forty-nine male guinea pigs (average weight 208 +/- 3.5 g) were divided into an initial status group and six experimental groups. The animals received a Se deficient Torula yeast based basal diet (<0.02 mg Se and 26 mg alpha-tocopherol/kg) or a Se addition of 0.05, 0.10, 0.15, 0.20 and 0.25 mg/kg diet as sodium selenate for 10 weeks. There was no significant difference in weight gain (final weight 643 +/- 21 g) between the groups and no clinical symptoms of Se deficiency occurred. With the exception of the testes, there was an increasing Se concentration in liver, plasma and haemolysate dependent on supplementation level. Glutathione peroxidase was determined in the plasma and Se dependent glutathione peroxidase (GPx1) in haemolysate, liver, kidney, heart and lung. Thioredoxin reductase (TR) activity was measured in liver, kidney and heart and deiodinase activity in the liver. A phospholipid hydroperoxide reducing activity with Se influence was determined in liver, kidney, heart, testes and brain. With the exception of GPx1 activity in heart and haemolysate and TR activity in the kidney, all enzymes already reached their maximal activity at 0.05 mg Se/kg diet. The activities of GPx1 and TR were used as parameters for broken line analysis and a Se requirement of 0.080 mg Se/kg diet was derived as sufficient for growing guinea pigs adequately supplied with vitamin E.
 ...
PMID:Estimation of the selenium requirement of growing guinea pigs (Cavia porcellus). 1866 58

The study is carried out on Wistar white rats non-adapted to oxygen deficit and on semiaquatic rodents muskrats adapted to periodic arrest of respiration during diving under conditions of Nembutal narcosis. It has been revealed that 1 h after a subcutaneous injection of sodium nitrite (3 mg/100 g body mass), intensification of lipid peroxidation (LPO) in the muskrat brain is absent, the activity of the antioxidant enzyme catalase increasing 16 times (p < 0/01) as compared with control injected with equivalent saline volume. In heart and liver, a statistically significant decrease of the content of LPO products active in the test with 2-thionarbituric acid; in the femoral muscle tissue, the LPO intensity does not change. In rats, unlike muskrats, after injection of sodium nitrite, an increase of LPO is recorded in brain, while a decrease of the LPO product content in the femoral muscle; in liver the LPO intensity did not change. In muskrats, the sodium nitrite administration leads to a decrease of the leukocyte spontaneous mobility, of lymphocyte cytokine-producing activity, and ofneutrophil bactericidal activity (by the content of cationic proteins in neutrophilic phagocytes), whereas in rats the leukocyte mobility does not change, only the blood neutrophil bactericidal activity decreases. The ability of neutrophils to produce the superoxide anion during the nitrite intoxication does not change both in rats and in muskrats. The obtained data allow concluding that under conditions of Nembutal narcosis the leukocyte functional activity on the background of nitrite intoxication is suppressed to the greater degree in the muskrats genotypically adapted to oxygen deficit than in immunocompetent cell of the rodents not adapted to hypoxia.
 ...
PMID:[Comparative-physiological study of leukocyte participation in initiation of lipid peroxidation during nitrite intoxication in rats and muskrats]. 1876 57

Salt stress induced an increase in endogenous carbon monoxide (CO) production and the activity of the CO synthetic enzyme haem oxygenase (HO) in wheat seedling roots. In addition, a 50% CO aqueous solution, applied daily, not only resulted in the enhancement of CO release, but led to a significant reversal in dry weight (DW) and water loss caused by 150 mm NaCl treatment, which was mimicked by the application of two nitric oxide (NO) donors sodium nitroprusside (SNP) and diethylenetriamine NO adduct (DETA/NO). Further analyses showed that CO, as well as SNP, apparently up-regulated H(+)-pump and antioxidant enzyme activities or related transcripts, thus resulting in the increase of K/Na ratio and the alleviation of oxidative damage. Whereas, the CO/NO scavenger haemoglobin (Hb), NO scavenger or synthetic inhibitor methylene blue (MB) or N(G)-nitro-l-arginine methyl ester hydrochloride (l-NAME) differentially blocked these effects. Furthermore, CO was able to mimic the effect of SNP by strongly increasing NO release in the root tips, whereas the CO-induced NO signal was quenched by the addition of l-NAME or cPTIO, the specific scavenger of NO. The results suggested that CO might confer an increased tolerance to salinity stress by maintaining ion homeostasis and enhancing antioxidant system parameters in wheat seedling roots, both of which were partially mediated by NO signal.
 ...
PMID:Carbon monoxide enhances salt tolerance by nitric oxide-mediated maintenance of ion homeostasis and up-regulation of antioxidant defence in wheat seedling roots. 1881 35

In order to study effects of different salinity levels on antioxidant enzyme activities, catalase (CAT), ascorbate peroxidase (APX) and guaiacol peroxidase (GPX) associated with compatible solutes, proline and carbohydrate and mineral nutrient content in shoots, sodium and potassium, in three wheat cultivars an experiment was conducted as completely randomized 3 x 4 factorial design with three replicates in a greenhouse. Three wheat cultivars (Pishtaz, Kavir and Hamon), that differ in their salt tolerances, were grown in four different salinity levels (S0 = control, S1 = 100, S2 = 200 and S3 = 300 mM NaCl). Twenty days after wheat cultivars subjected to salt stress, data showed salinity stress induced increase in the antioxidant enzyme activities. Among the cultivars, salinity stress decreased leaf-APX but increased the activities of leaf-GPX in Pishtaz cultivar. Our results showed a positive correlation between praline accumulation and Leaf-APX (r2 = 0.56), Leaf-GPX (r2 = 0.63) and Leaf-CAT (r2 = 0.73). In these cultivars, in their shoots Na+ showed an increase in concentration with salinity that approximately matches a decrease in K+ concentration. It seems that Na+ concentrations in the shoot may have had a more significant effect on plant antioxidant enzyme activities and compatible solutes such as proline and carbohydrates. These results indicated which in wheat under salinity stress antioxidant enzymes and compatible solutes help to plant adaptation. In this study we found a positive correlation between Na+ concentration in the shoots and the antioxidant enzyme activities and compatible solutes in the leaves.
 ...
PMID:Salinity effects on compatible solutes, antioxidants enzymes and ion content in three wheat cultivars. 1881 74

Herbicides present in the environment induce oxidative stress in plants. We investigated the roles of exogenous NO-regulated chlorophyll synthesis, antioxidant enzyme activity and gene expression in herbicide-treated unicellular green algae Chlorella vulgaris. Atrazine (100 microg/L) or glufosinate (10 mg/L) treatment alone or in combination with 20 microM sodium nitroprussiate (SNP, 10 microM with glufosinate) was administered to algae for a short time period of 48 h to observe changes in physiology and gene transcription and expression. Supplementation of atrazine or glufosinate with low SNP significantly reduced H2O2, reactive oxygen species (ROS) and malondialdehyde (MDA) induction by herbicides. Supplementation also increased chlorophyll content and antioxidant enzymes, superoxide dismutase (SOD), peroxidase (POD) and catalase (CAT) activity, as compared to herbicide treatment alone. This trend suggests an effect of NO on the scavenging of ROS. Furthermore, the expression of photosynthesis genes (psbC, psaB, chlB and rbcL) was also upregulated by supplementation of low SNP, thus maintaining the normal photosynthetic function. However, high concentration of SNP (100 microM) in combination with herbicides aggravated damage to algae, including increases in H2O2, ROS and MDA and decreases in chlorophyll content, antioxidant enzyme activity and photosynthesis genes transcription. 2-Phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (PTIO), the NO scavenger, was also examined in this study; the results showed that PTIO could neutralise the effect of low SNP. Data also showed that an exogenous supply of NO protects Chlorella vulgaris against the toxicity of herbicides by protecting against oxidant substances and increasing the transcription of related genes.
 ...
PMID:The effect of exogenous nitric oxide on alleviating herbicide damage in Chlorella vulgaris. 1929 32

We tested two hypotheses, first that exercise training reverses age-related decrements in endothelium-dependent dilation in soleus muscle feed arteries and second that this improved endothelium-dependent dilation is the result of increased nitric oxide (NO) bioavailability due to increased content and phosphorylation of endothelial NO synthase (eNOS) and/or increased antioxidant enzyme content. Young (2 mo) and old (22 mo) male Fischer 344 rats were exercise trained (Ex) or remained sedentary (Sed) for 10-12 wk, yielding four groups of rats: 1) young Sed (4-5 mo), 2) young Ex (4-5 mo), 3) old Sed (24-25 mo), and 4) old Ex (24-25 mo). Soleus muscle feed arteries (SFA) were isolated and cannulated with two glass micropipettes for examination of endothelium-dependent (ACh) and endothelium-independent [sodium nitroprusside (SNP)] vasodilator function. To determine the mechanism(s) by which exercise affected dilator responses, ACh-induced dilation was assessed in the presence of N(omega)-nitro-l-arginine (l-NNA; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), and l-NNA + Indo. Results indicated that ACh-induced dilation was blunted in old Sed SFA relative to young Sed SFA. Exercise training improved ACh-induced dilation in old SFA such that vasodilator responses in old Ex SFA were similar to young Sed and young Ex SFA. Addition of l-NNA, or l-NNA + Indo, abolished the exercise effect. Immunoblot analysis revealed that extracellular superoxide dismutase (SOD) protein content was increased by training in old SFA, whereas eNOS and SOD-1 protein content were not altered. Addition of exogenous SOD, or SOD + catalase, improved ACh-induced dilation in old Sed SFA such that vasodilator responses were similar to young Sed SFA. Addition of l-NNA abolished the effect of exogenous SOD in old Sed arteries. Collectively, these results indicate that exercise training reverses age-induced endothelial dysfunction in SFA by increasing NO bioavailability and that increases in vascular antioxidant capacity may play an integral role in the improvement in endothelial function.
 ...
PMID:Exercise training reverses age-related decrements in endothelium-dependent dilation in skeletal muscle feed arteries. 1929 69

In Alzheimer's disease (AD), oxidative stress is present early and contributes to disease pathogenesis. We previously reported that in Tg19959 transgenic AD mice, partial deficiency of the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD) exacerbated amyloid pathology. We therefore asked whether MnSOD overexpression would prove beneficial against AD pathogenesis, by studying the offspring of Tg19959 mice crossed with MnSOD-overexpressing mice. At 4 mo of age, there was a 2- to 3-fold increase in MnSOD protein levels in Tg19959-MnSOD mice compared to Tg19959 littermates. Tg19959-MnSOD mice also had a 50% increase in catalase protein levels, a 50% decrease in levels of oxidized protein, and a 33% reduction in cortical plaque burden compared to Tg19959 littermates. Spatial memory was impaired and synaptophysin levels were decreased in Tg19959 mice compared to wild-type littermates, but memory and synaptophysin levels were restored to wild-type levels in Tg19959-MnSOD littermates. These benefits occurred without changes in sodium dodecyl sulfate-soluble or formic acid-soluble Abeta pools or Abeta oligomers in Tg19959-MnSOD mice compared to Tg19959 littermates. These data demonstrate that facilitation of the mitochondrial antioxidant response improves resistance to Abeta, slows plaque formation or increases plaque degradation, and markedly attenuates the phenotype in a transgenic AD mouse model.
 ...
PMID:Reduction of oxidative stress, amyloid deposition, and memory deficit by manganese superoxide dismutase overexpression in a transgenic mouse model of Alzheimer's disease. 1934 95

The aim of this study is to investigate the improving effects of selenium (Se) on cerebrum and cerebellum impairments induced by methimazole (MMI) in suckling rats. Animals were randomly divided into four groups of six each: group I served as control which received standard diet; group II received only MMI (250 mg L(-1)(,) orally); group III received both MMI (250 mg L(-1), orally) and Se (0.5 mg kg(-1) of diet); group IV served as a positive control and received Se (0.5 mg kg(-1) of diet) as sodium selenite (Na(2)SeO(3)). Treatments were started from the 14th day of pregnancy until day 14 after delivery. In the MMI-treated group, plasma-free thyroid hormone levels (FT(3) and FT(4)), protein, DNA and RNA contents in cerebrum and cerebellum decreased when compared to control. Co-treatment with Se ameliorated these parameters. In the MMI-treated group, antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) significantly decreased, while malonaldialdehyde (MDA) levels in cerebrum and cerebellum increased. Co-administration of Se through the diet restored these parameters to near normal values. The biochemical modifications are correlated histologically with the abnormal development of an external granular layer, indicating a delay of granular cells migration towards the molecular layer in the MMI-treated group. Our results showed that Se improved cerebrum and cerebellum MMI-induced damages in suckling rats. Moreover, we concluded that Se is an important neuroprotective element that may be used as a dietary supplement against brain impairments.
 ...
PMID:Dietary selenium addition improves cerebrum and cerebellum impairments induced by methimazole in suckling rats. 1961 34


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>