UNIPROT:P30044 - FACTA Search

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)

The transgenic mice overexpressing heat shock protein 72 (HSP72) or antioxidants have been reported to be more resistant to myocardial ischemia/reperfusion injury. However, it remains unknown whether whole body heat stress (HS) which may induce HSP72 or endogenous antioxidants affords similar protection in the mouse heart. Adult male mice were treated with either HS (42 degrees C for 15 min) or anesthesia only (SC) against a group of non-stressed controls (NC). At 6 or 24 h later, the hearts were excised and perfused at a constant pressure of 55 mmHg in Langendorff mode. Following 30 min equilibration, hearts were subjected to 20 min of global ischemia and 30 min reperfusion (37 degrees C). Ventricular force was measured by a force-displacement transducer attached to the apex. Leakage of intracellular enzymes (CK, LDH) was measured in coronary efflux. Infarct size was determined by tetrazolium staining. The results showed that no significant differences between HS, SC, and NC groups in ventricular contractile function, CK and LDH release, or infarct size were observed at either time window. HS enhanced the expression of HSP72 in mouse hearts by two- to three-fold, whereas antioxidant enzyme activities (catalase and MnSOD) did not change significantly. We conclude that HS does not precondition the isolated perfused mice hearts against ischemia/reperfusion injury, despite induction of HSP72.
...
PMID:Whole body heat shock fails to protect mouse heart against ischemia/reperfusion injury: role of 72 kDa heat shock protein and antioxidant enzymes. 992 59

The main components of antioxidant enzyme system (AOS) are superoxide dismutase (SOD) and glutathione reductase (GR) catalyses the conversion of the superoxide anion. The important role in AOS belongs to catalase and glutathione peroxidase which perform H2O2 to nontoxic products. Simultaneous determination of AOS activity and malonic dialdehide (MDA) concentration (the index of lipid peroxidation in tissues and blood) characterize cells complex resistance to damage factor. The effect of L-arginine, as a precursor of nitric oxide synthesis and blocator NO-synthase (Nw-nitro-L-arginine) on AOS of rats with different resistance to hypoxia under stress condition is unknown and were subject of our investigation. Experiments were done on liver and blood tissues of white laboratory rats. The experimental animals were divided on two groups depending on hypoxia factor: high resistance (HR) and low resistance (LR). The type of resistance was determined by the time of ability to respire in barocamera with oxygen deficient equal to 12.000 meters over sea level. The animals adaptation to laboratory conditions continue during 14 days after in barocamera presence. All animals were divided dependent on experiment conditions on fourth groups. The first group: intact (HR and LR) animals parentherally injected by 1 ml of 0.9% NaCl solution. The second group was subject of stress condition. The third group: HR and LR animals injected parentherally by 1 ml L-arginine (Sigma, USA) dose (600 mg/kg body weight). The fourth one: rats injected by 1 ml Nw-nitro-L-arginine (L-NNA, Sigma, USA)--the blocator of NO-synthase. The animals were decapitated 30 min after injection and stress condition under ethereal anesthesia. Activity of antioxidant system enzymes superoxide dismutase (SOD), catalase (CAT); glutathione reductase (GR), glutathione peroxidase (GP) were measured spectrophotometrically. Also was investigated the concentration of serum antioxidant ceruloplasmin (CP). Level of lipid peroxidation was estimate by examination of concentration of lipids of hydroperoxides (LHP) and malonic dialdehyde (MDA). Our data confirm suggesting that nitric oxide (NO) is a major regulator in the AOS enzymes activity and limit damage influence of AOF. Action precursor NO L-arginine might be capable of protective role in various disorders which are connected with hypoxia factor. Following thing can be interred the investigation of influence of nitric oxide adaptive answers in stress condition modelling of pathological processes in rats with different resistance to hypoxia and reflect the biological qualities data stady on AOZ and LP.
...
PMID:[Effect of nitric oxide synthase inhibitor L-NNA on the activities of antioxidant enzymes and lipid peroxidation in blood and tissues of rats with different resistance to hypoxia]. 1139 15

We determined the role of p38 mitogen-activated protein kinase (MAPK), 72-kDa heat shock protein (HSP72), and antioxidant enzymes in whole body heat stress (HS)-induced cardioprotection in mouse hearts. Adult male mice were treated with either HS or anesthesia only. At 0.5, 48, 72, or 120 h later, the hearts were subjected to 20 min of global ischemia and 30 min of reperfusion in Langendorff mode. A significant protection against ischemia-reperfusion injury was observed 48 h after HS as demonstrated by: 1) reduction in infarct size; 2) decrease in leakage of lactate dehydrogenase; and 3) enhanced postischemic ventricular contractile function. No such protection was observed at other post-HS time points. HS caused an ~25% increase in phosphorylated c-Jun NH2-terminal kinase (JNK) but not p38 MAPK in the heart during the first 2-h post-HS time period. Cardioprotection was abolished by the MAPK inhibitor SB-203580, which also partially suppressed the HS-induced JNK phosphorylation. The protective effect was associated with a two- to threefold increase in HSP72 protein accumulation, but not antioxidant enzyme activities (catalase and Cu/Zn and Mn SOD) in the myocardium. Although HSP72 levels remained high 72 h after HS, the cardioprotection had already disappeared. We conclude that HS induces a transient delayed cardioprotection at 48 h after thermal stress in mice which appears to be mediated via a MAPK-signaling pathway.
...
PMID:Mitogen-activated protein kinases mediate heat shock-induced delayed protection in mouse heart. 1145 53

Omega-3 (omega-3) is an essential fatty acid (EFA) found in large amounts in fish oil. It contains eicosapentaenoic acid and docosahexaenoic acid (DHA). DHA is one of the building structures of membrane phospholipids of brain and necessary for continuity of neuronal functions. Evidences support the hypothesis that schizophrenia may be the result of increased reactive oxygen species mediated neuronal injury. Recent reports also suggest the protective effect of omega-3 EFA against neuropsychiatric disorders including schizophrenia. This study proposed to assess the changes in antioxidant enzyme and oxidant parameters in the corpus striatum (CS) of rats fed with omega-3 EFA diet (0.4g/kg/day) for 30 days. Eight control rats and nine rats fed with omega-3 were decapitated under ether anesthesia, and CS was removed immediately. Thiobarbituric acid-reactive substances (TBARS) and nitric oxide (NO) levels as well as total superoxide dismutase (t-SOD) and xanthine oxidase (XO) enzyme activities in the CS were measured. Rats treated with omega-3 EFA had significantly lower values of TBARS (P<0.001), NO (P<0.002) and XO (P<0.005) whereas higher values of t-SOD enzyme activity (P<0.002) than the control rats. These results indicate that omega-3 EFA rich fish oil diet reduces some oxidant parameters in CS. This may be revealed by means of reduced CS TBARS levels as an end product of lipid peroxidation of membranes in treated rats. Additionally, reduced XO activity and NO levels may support this notion. On the other hand, although the mechanism is not clear, omega-3 EFA may indirectly enhance the activity of antioxidant enzyme t-SOD. Taken together, this preliminary animal study provides strong support for a therapeutic effect of omega-3 EFA supplemented to classical neuroleptic regimen in the treatment of schizophrenic symptoms and tardive dyskinesia.
...
PMID:Potential role of dietary omega-3 essential fatty acids on some oxidant/antioxidant parameters in rats' corpus striatum. 1290 35

Oxidative stress due to enhanced production of free radicals has been incriminated as one of the several mechanisms involved in arsenic-induced toxic effects in different organs. In the present study, ameliorative potential of certain amino acids like cysteine, methionine and vitamins like ascorbic acid and thiamine on some of the parameters indicative of oxidative stress in liver, kidney and blood and of hepatic and renal infliction was investigated in arsenic exposed rats. Rats were given 0 ppm (group I healthy controls) or 10 ppm arsenic in drinking water ad lib for a period of 12 weeks. During oral exposure to arsenic rats of different groups received daily oral dose of placebo, cysteine, methionine, ascorbic acid or thiamine at 25mg/kg body weight. After the end of the experimental period, animals were sacrificed under light anesthesia and blood, liver and kidney were collected. Samples were processed for estimation of arsenic, biochemical parameters indicative of oxidative stress and hepatic and renal function. Arsenic exposure resulted in significantly (P<0.05) higher accumulation of arsenic in blood, liver and kidney. It was associated with significant (P<0.05) rise in lipid peroxide level and decrease in superoxide dismutase and catalase activities in liver and kidneys. However, alterations in biochemical parameters did not reach statistical (P>0.05) significance. Treatment with vitamins and amino acids resulted in reversal of oxidative stress with significant (P<0.05) decline in tissue arsenic burden. All the treatment produced tissue specific changes in lipid peroxide level, antioxidant enzyme activities and tissue arsenic burden.
...
PMID:Effect of cysteine, methionine, ascorbic acid and thiamine on arsenic-induced oxidative stress and biochemical alterations in rats. 1586 45

The study aim was to investigate the interaction of physical conditioning and chronic ethanol ingestion on blood pressure (BP), heart rate (HR), nitric oxide (NO) and oxidants/antioxidants balance in the plasma of rats. Male Fisher rats were divided into four groups of seven animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks; (2) ethanol (4 g kg(-1), orally) daily for 12 weeks; (3) exercise training on treadmill plus sucrose daily for 12 weeks and (4) exercise training on treadmill followed by ethanol (4 g kg(-1), orally) daily for 12 weeks. The body weight, BP and HR were recorded every week. The animals were sacrificed under ether anesthesia after 12 weeks, blood collected in heparinzed vials, plasma isolated and analyzed. The results show that exercise training significantly lowered the weight gain 6-12 weeks in ethanol treated rats compared to ethanol alone or control rats. The mean arterial BP was significantly elevated 6-12 weeks after ethanol ingestion without significant alterations in HR. Exercise training lowered the BP close to the normal control values in ethanol fed rats. Ethanol significantly decreased the plasma NO levels, reduced to oxidized glutathione ratio (GSH/GSSG) and antioxidant enzymes-superoxide dismutase (CuZn-SOD, and Mn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities while plasma NADPH oxidase activity and malondialdehyde (MDA) levels were significantly elevated compared to control. Exercise training significantly restored the depletion of plasma NO levels, GSH/GSSG ratio, and antioxidant enzyme activities and normalized the MDA levels and NADPH oxidase activity in the plasma of ethanol treated rats. The study concluded that physical conditioning attenuates the chronic ethanol-induced hypertension by augmenting the NO bioavailability and reducing the oxidative stress response in the plasma of rats.
...
PMID:Physiological basis for effect of physical conditioning on chronic ethanol-induced hypertension in a rat model. 1671 71

This study was performed to evaluate the effect of melatonin on methanol-induced liver injury. We evaluated the levels of malondialdehyde (MDA), protein carbonylation (PC), myeloperoxidase (MPO) activities and to assess lipid peroxidation, protein oxidation, neutrophil accumulation and nitrite which is a stable end product of nitric oxide respectively. We also studied superoxide dismutase, catalase, and glutathione peroxidase activities of liver tissue to evaluate the changes in the antioxidant status. Histopathological alterations were also determined. The experiment was performed on Wistar rats, which received intragastric 3 g/kg methanol as a 50% solution in isotonic saline once. After 6 and 24 hr all the drug received and intoxicated rats were killed under anesthesia. Pretreatment with melatonin (10 mg/kg) decreased the MDA levels significantly, restored the PC levels to the control, prevented the increase of nitrite level and MPO activity significantly and reversed to the control levels, prevented the reduction in all of the antioxidant enzyme activities. Additionally in melatonin treated group piecemeal necrosis, lobular lytic necrosis, and portal inflammation returned to normal histologic appearances when compared with methanol administration. In conclusion, melatonin has protective effects against methanol-induced hepatic injury.
...
PMID:Melatonin improves methanol intoxication-induced oxidative liver injury in rats. 1761 34

General anesthesia can impair immunological defense mechanisms while inducing an inflammatory reaction. Generalized inflammatory reactions involve leucocytes which in turn release inflammatory mediators and free oxygen radicals. General anesthetics include a series of gaseous and intravenous sedative-hypnotic agents indicated for induction and maintenance of general anesthesia as well as for sedation of intubated, mechanically ventilated adults in intensive care units (ICU). Some anesthetics, such as propofol, are characterized by a phenolic structure similar to that of alpha-tocopherol, and exhibit antioxidant properties that have been demonstrated both in vitro and in vivo. Similarly, other anesthetics show antioxidant and protective roles but this mechanism is to be related to their ability to induce antioxidant enzyme (i.e., heme oxygenase-1). The aim of the present review is to evaluate the antioxidant properties of anesthetics in various experimental models and if they may be considered efficient therapeutic tools in counteracting oxidative stress during general anesthesia and sedation in ICU.
...
PMID:Antioxidant properties of anesthetics: the biochemist, the surgeon and the anesthetist. 1916 10

Ischaemia/reperfusion (I/R) injury is commonly seen in the field of intestine surgical interventions, shock, trauma, and many other clinical conditions. Simvastatin is known to have antioxidant and anti-inflammatory properties. This study investigated the effect of simvastatin administration in a warm intestinal I/R model on TNF-alpha, antioxidant enzymes and intestinal tissue morphology. Thirty-six male wistar rats underwent laparotomy under general anaesthesia. Simvastatin was administered from four days before ischaemia induction. The rats were divided in to three groups (n = 12): the sham group, the I/R group, and the I/R + simvastatin group. Intestinal ischaemia was induced by superior mesenteric artery ligation with microvascular clamps for 60 minutes, and after ischaemia, blood perfusion was released into the tissue and a reperfusion phase was started, which lasted for 3 hours. After 3 hours, the animals were sacrificed and serum and tissue obtained for biochemical and histological study. In the simvastatin treated group, intestinal tissue injury, TNF-alpha level, and tissue malondealdehyde levels were significantly lower than in the I/R group (p < 0.05). Glutathion peroxidase and superoxide dismutase levels were significantly higher in the simvastatin treated group than in the I/R group (p < 0.05). Simvastatin pretreatment reduced intestinal I/R injury and was associated with down- -regulation of serum TNF-alpha and tissue malondealdehyde level, and simvastatin administration maintained cellular antioxidant enzyme contents compared to the I/R group after 3 hours reperfusion time.
...
PMID:Simvastatin attenuates intestinal ischemia/reperfusion induced injury in rat. 1972 59

Hepatic encephalopathy (HE) is a major neurological complication secondary to severe liver failure. The aim of the present study was to examine the possible neuroprotective effects of caffeic acid phenethyl ester (CAPE) with or without laxative treatment against thioacetamide-induced HE by investigating behavioral and motor activities in rats as well as blood ammonia level and oxidant-antioxidant parameters of cortex, brain stem and cerebellum. After induction of HE by thioacetamide, the rats were treated with lactulose, CAPE (CAPE treatment was started one day before the first dose of thioacetamide) or CAPE plus lactulose. The behavioral and motor scales were measured at the 54th hour after the first thioacetamide injection, the blood samples and brains were taken under anesthesia at the 60th hour for biochemical analysis. The survival rates were 37.5% in HE group, 70% in HE+lactulose group, 80% in HE+CAPE group, and 100% in HE+CAPE+lactulose group. Increased ammonia, ALT and AST levels in blood along with impaired sensory-motor behavior tests were reversed to proximate control values in CAPE+lactulose treated group. There were increased lipid peroxidation and protein oxidation and decreased antioxidant enzyme activities in almost all brain parts of HE group. CAPE or lactulose treatment alone ameliorated those oxidant and antioxidant parameters; however, CAPE treatment together with lactulose reversed them to almost control level. In conclusion, thioacetamide-induced HE injury in rats was reversed almost fully by CAPE and laxative combination. There was no death in CAPE and laxative treated group animals and it may be due to the direct neuroprotective effect of CAPE together with the prevention of the body from ammonia production.
...
PMID:Effects of caffeic acid phenethyl ester on thioacetamide-induced hepatic encephalopathy in rats. 2070 59

1 2 Next >>