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)

High dosage of fructose induces insulin resistance, glucose intolerance and alterations in plasma lipid profile in normal rats. Recently, it has been shown that these rats also develop oxidative stress, which plays a prominent role in diabetic pathology. We now report the effect of taurine on the susceptibility of the aorta to lipid peroxidation and also on the activities of enzymic and non-enzymic antioxidants in rats fed a high fructose-diet for 4 weeks. Fructose-fed rats were more susceptible to lipid peroxidation as measured by thiobarbituric acid reactivity, and antioxidant status was significantly lower. Taurine supplementation caused a significant reduction in the production of thiobarbituric acid--reactive substances and significant rises in antioxidant enzyme activities. The levels of lipid peroxides, diene conjugates, lipofuscin and hydroperoxides were significantly higher in fructose-fed rats. When these rats received taurine in drinking water, no peroxidative changes were observed. Increased aorta lipid peroxidation could play a role in the pathology associated with fructose-feeding, and taurine reduces the lipid peroxidation by inducing antioxidant enzymes.
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PMID:Taurine modulates antioxidant potential and controls lipid peroxidation in the aorta of high fructose-fed rats. 1218 69

Selenium is essential for normal mammalian development. Being a component of antioxidant enzyme, glutathione peroxidase, it plays a major role in protecting the cells from free radical damage. The level of glutathione peroxidase was directly related to the amount of selenium present in various tissues and organs. A decrease in selenium leads to various pathological changes in humans as well as in various laboratory animals. The aim of the present study was to understand whether there is an increase in the level of selenium in different brain regions of rat pups whose mothers were supplemented with selenium, either 2 or 4 mg/l of their drinking water throughout the period of their pregnancy. There was a significant increase in the level of selenium in the cerebellum, cortex and hypothalamic and hippocampal tissues of selenium supplemented mothers as compared with those of non-supplemented mothers. The brain stem of these animals did not show any significant difference in the level of selenium. Furthermore, the differences in the level of selenium between the rat pups of 2 mg/l selenium supplemented mothers and 4 mg/l selenium supplemented mothers were not statistically significant. These studies suggest that supplementation of selenium to mothers during the period of their pregnancy can selectively increase the level of this trace element in different brain regions. Further studies are necessary to understand the significance of selective accumulation of selenium in specific brain regions on brain development and function.
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PMID:Brain selenium accumulation in rat pups of selenium supplemented mothers. 1219 65

Catalase, Mn-superoxide dismutase (MnSOD) and Cu,Zn-superoxide dismutase (CuZnSOD) activities were studied in rat liver and kidney 6-48 h after CdCl(2) intraperitoneal administration or 10-30 days daily oral CdCl(2) intake in drinking water. This approach provided some indications as to the sensitivity of each enzyme to cadmium toxicity. These experiments showed that the formation of thiobarbituric acid reactive substance (TBARS) did not strictly depend on how well the antioxidant enzyme worked. From in vitro experiments it appeared that TBARS removal by vitamin E did not restore the three enzyme activities at all. As for cadmium's inhibitory mechanism on catalase activity, our data, obtained in the pH range 6.0-8.0, are a preliminary indication that the negative effect of this metal is probably due to imidazole residue binding of His-74 which is essential in the decomposition of hydrogen peroxide. Cadmium inhibition of liver mitochondrial MnSOD activity was completely removed by Mn(2+) ions, suggesting that the reducing effect on this enzyme is probably due to the substitution of cadmium for manganese. We also observed the antioxidant capacity of Mn(2+) ions, since they were able to normalize the increased TBARS levels occurring when liver mitochondria were exposed to cadmium. The reduced activity of CuZnSOD does not seem to be due to the replacement of Zn by Cd, nor to the peroxides formed. As this enzyme activity was almost completely recovered after 48 h, we hypothesize that the momentary inhibition is imputable to a cadmium/enzyme interaction. This causes some perturbation in the enzyme topography which is critical for its catalytic activity. The pathological implications linked to antioxidant enzyme disorders induced by cadmium toxicity are discussed.
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PMID:Molecular inhibitory mechanisms of antioxidant enzymes in rat liver and kidney by cadmium. 1220 41

The possible repercussions of osmoregulatory processes on some indicators of classical and oxidative stress were examined during gradual acclimation of sturgeons (Acipenser naccarii) to full seawater (35% salinity) and after a period of 20 approximately days at this salinity. Erythrocyte constants and levels of cortisol, protein and glucose in the plasma were determined. In addition, plasma osmolality and muscle-hydration values, as well as liver and heart protein, were determined. Catalase, glutathione peroxidase and superoxide dismutase activities and lipidperoxidation levels were measured in blood (plasma and red blood cells) and tissue (liver and heart). A number of physiological responses, such as disturbance in body fluid, activation of osmoregulatory mechanisms, augmented antioxidant defences in blood and alteration of energy metabolites, were detected with increasing environmental salinity. After 20 days at 35% salinity, plasma osmolality, erythrocyte constants and muscle water content all returned to values usual for low environmental salinity, indicating that osmoregulatory processes have achieved their objective. However, cortisol values, antioxidant enzyme activities in the blood (plasma and red blood cells), lipid peroxidation in plasma, and hepatic proteins did not return to initial values, showing that osmoregulatory processes cause major physiological changes in the fish.
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PMID:Physiological changes of sturgeon Acipenser naccarii caused by increasing environmental salinity. 1240 96

Effects of cobalt on the antioxidant status of control and streptozotocin diabetic rat heart and aorta were examined at the second, fourth and sixth week of treatment. Rats were divided into four groups: control, diabetic, control treated with cobalt chloride and diabetic treated with cobalt chloride. Diabetes was induced by tail vein injection of streptozotocin (STZ). Cobalt treatment groups were given 0.5 mM of CoCl(2) in drinking water. The rats in both groups were further subdivided into three groups of six rats each. Rats in these subgroups were studied at 2-week intervals up to 6 weeks. At the end of the experiment, all animals were sacrificed by decapitation, heart and aorta samples were removed for determination of thiobarbituric acid reactive substance (TBARS) level and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities. It was found that lipid peroxidation levels and antioxidant enzyme activities were increased in the streptozotocin-induced diabetic rats at all times studied. Cobalt treatment of diabetic rats (0.5 mM in drinking water) resulted in attenuation of the increased levels of TBARS and antioxidant enzyme activities in heart and aorta. Thus, the effect of oral administration of cobalt at this dose during the early stage of experimental diabetes can be considered as a consequence of altered endogenous defence mechanisms in heart and aorta.
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PMID:Effect of cobalt on the oxidative status in heart and aorta of streptozotocin-induced diabetic rats. 1257 18

Large amounts of d-2-hydroxyglutaric acid (DGA) accumulate in d-2-hydroxyglutaric aciduria (D-2-OHGA), an inherited neurometabolic disorder characterized by severe neurological dysfunction and cerebral atrophy. Despite the significant brain abnormalities, the neurotoxic mechanisms of brain injury in this disease are virtually unknown. In this work, the in vitro effect of DGA on various parameters of oxidative stress was investigated; namely chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS), total radical-trapping antioxidant potential (TRAP), total antioxidant reactivity (TAR) and the activities of the antioxidant enzymes catalase, glutathione peroxidase and superoxide dismutase in cerebral cortex from 30-day-old-rats. DGA significantly increased chemiluminescence and TBA-RS and decreased TAR values in the cortical supernatants. In contrast, TRAP and the antioxidant enzyme activities were not altered by the metabolite. Furthermore, the DGA-induced increase of TBA-RS was fully prevented by the free radical scavengers ascorbic acid plus Trolox (water-soluble alpha-tocopherol) and attenuated by the inhibitor of nitric oxide synthase Nomega-nitro-L-arginine methyl ester (L-NAME), suggesting the role of superoxide, hydroxyl and nitric oxide radicals in this action. The data indicate a stimulation of lipid peroxidation through the production of free radicals and a reduction of the brain capacity to efficiently modulate the damage associated with the enhanced generation of free radicals by DGA. In the case that these findings also occur in human D-2-OHGA, it is feasible that oxidative stress may be involved in the pathophysiology of the brain injury observed in patients with this disease.
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PMID:D-2-hydroxyglutaric acid induces oxidative stress in cerebral cortex of young rats. 1278 67

We investigated morphological and photosynthetic responses of current-year seedlings of oak (Quercus crispula Blume) under high-light conditions. Quercus crispula seedlings were grown from seed in a relative photosynthetically active photon flux density (RPPFD) of 100, 10 or 2%. There was no difference in total dry mass between 100 and 10% RPPFD. At the end of the growing season, plants grown in 2% RPPFD had a lower total dry mass than those grown in 100 or 10% RPPFD. Seedlings grown in 100% RPPFD showed morphological acclimation, i.e., high root/shoot ratios and high leaf mass per area. De-epoxidation level in the xanthophyll cycle and activity of an antioxidant enzyme were highest in 100% RPPFD, but total chlorophyll concentration and photosynthetic rate were highest in 10% RPPFD. These results indicate that excess photons were generated in 100% RPPFD, leading to increased capacities for dissipation of received light energy through the xanthophyll cycle and for scavenging of reactive oxygen species through the water-water cycle. Nevertheless, a midday decrease in dark-adapted quantum yield of photosystem II (F(v)/F(m)) indicated that seedlings grown in 100% RPPFD were suffering from photoinhibition. We conclude that Q. crispula current-year seedlings have high morphological acclimation to high light but that photosynthetic efficiency cannot be maintained under high-light conditions even with a photoprotection system.
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PMID:Morphological and photosynthetic responses of Quercus crispula seedlings to high-light conditions. 1283 30

Chronic exposure of humans to inorganic arsenic, mainly pentavalent arsenate (iAsV), results in drinking water-induced oxidative stress (Pi et al., 2002). Thioredoxin reductase (TR) and glutathione reductase (GR) are the two critical enzymes in the response to oxidative stress in vivo. In the present study we examined alterations in enzyme activities of hepatic TR and GR from prolonged exposure of male New Zealand white rabbits to iAsV. Exposure of rabbits to iAsV in drinking water (5 mg/L) for 18 weeks caused a significant suppression of hepatic TR and GR activities, of approximately 30% and 20%, respectively, below controls. In vitro experiments suggested that trivalent inorganic arsenic (iAsIII) but not pentavalent arsenicals including iAsV, monomethylarsonic acid (MMAsV), and dimethylarsinic acid (DMAsV) affected the hepatic TR activity of rabbit. So it was suggested that in the present study iAsV ingested via drinking water was metabolized to reactive trivalent arsenicals, such as iAsIII, which may play an important role in the decreased TR and GR activities from prolonged exposure to iAsV observed in vivo.
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PMID:Decreased enzyme activity of hepatic thioredoxin reductase and glutathione reductase in rabbits by prolonged exposure to inorganic arsenate. 1450 82

The effects of aqueous extracts of Celastrus paniculatus (CP) seeds were shown to have antioxidant properties in rats. In the study reported here, we have investigated the free radical scavenging capacity of three aqueous extracts (WSEs) obtained from CP seeds: a room temperature extract (WF); a hot water extract (HF); an acid extract (AF). All the WSEs exhibited a dose-dependent free radical scavenging capacity for 1,1-diphenyl-2-picryl-hydrazyl radical (DPPH) and also for superoxide-generated assays (in vitro assays). In addition, we used enriched forebrain primary neuronal cell (FBNC) cultures to evaluate the neuroprotective effects of the three CP-WSE extracts on H(2)O(2)-induced toxicity. FBNC were pre-treated with the CP-WSE and then with H(2)O(2) to evaluate the protection afforded against H(2)O(2)-induced toxicity. The criteria for neuroprotection by the WSEs were based on a mitochondrial function test following the H(2)O(2)-induced neurotoxicity. All the WSEs significantly attenuated H(2)O(2)-induced neuronal death, and AF was the most effective in protecting the neuronal cells against oxidative injury caused by H(2)O(2). In 10 day FBNC, cellular superoxide dismutase activity was not affected by the WSEs or H(2)O(2), but catalase activity was decreased and levels of malondialdehyde were increased by H(2)O(2) treatment. When the neuronal cells were treated with WSEs prior to H(2)O(2) exposure, catalase activity was increased and levels of malondialdehyde were decreased significantly. The data presented here suggest that CP seed WSEs protected neuronal cells in part by their free radical scavenging properties, by reducing lipid peroxidation, and also by their ability to induce the antioxidant enzyme catalase. Our results indicate that WSEs might exert neuroprotective effects against increased oxidative stress resulting from free radical damage that is associated with a number of neurodegenerative diseases.
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PMID:Celastrus paniculatus seed water soluble extracts protect cultured rat forebrain neuronal cells from hydrogen peroxide-induced oxidative injury. 1463 Jan 70

Chloroacetonitrile (CAN) is a disinfection by-product of chlorination of drinking water. Epidemiological studies indicate that it might present a potential hazard to human health. The present work provides an evidence for CAN activation to cyanide (CN-) by myeloperoxidase (MPO)/hydrogen peroxide (H2O2)/chloride (Cl-) system in vitro. Optimum conditions for the oxidation of CAN to CN- were characterized with respect to pH, temperature and time of incubation as well as CAN, MPO, H2O2 and KCl concentrations in incubation mixtures. The kinetic parameters governing the reaction; maximum velocity (Vmax) and Michaelis-Menten constant (Km) were assessed. Oxidation of CAN to CN- by NaOCl alone was shown. Addition of the MPO inhibitors; sodium azide (NaN3), 4-amino benzoic acid hydrazine (ABAH) or indomethacin to the reaction mixtures resulted in a significant decrease in the rate of CAN oxidation. Inclusion of the antioxidant enzyme catalase (CAT) in the incubation mixtures resulted in a significant decrease in the rate of CAN oxidation and CN- formation. Addition of the sulfhydryl compounds; glutathione (GSH), N-acetyl-L-cysteine (NAC), L-cysteine or D-penicillamine significantly enhanced the rate of CN- release. In conclusion, MPO/H2O2/Cl- system has the ability of oxidizing CAN to CN-. The present results represent a novel pathway for CAN activation and might be important in explaining CAN-induced toxicity.
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PMID:Myeloperoxidase-catalyzed oxidation of chloroacetonitrile to cyanide. 1468 62


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