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)

The study was conducted to examine the role of free radicals in Indomethacin induced gastric mucosal injury and to evaluate the gastroprotective effects of melatonin and beta-carotene. Gastric mucosal injury was produced in rats by administering indomethacin 30 mg/kg subcutaneously. Melatonin was administered in three different doses of 5, 10 and 20 mg/kg, 30 minutes prior to the administration of indomethacin. Beta-carotene was administered as a single dose of 100 mg/kg. Following parameters were calculated: ulcer index, lipid peroxidation and antioxidant defense enzymes i.e. superoxide dismutase, glutathione peroxidase and catalase. Indomethacin caused gastric mucosal injury in the form of haemorrhages, increased the lipid peroxidation and decreased the levels of the antioxidant defense enzymes. Melatonin (20 mg/kg) and beta-carotene decreased the ulcer index and lipid peroxidation, and reduced the decrease in antioxidant enzyme levels. These findings suggest the melatonin and beta-carotene show protective effect against indomethacin induced gastric injury and this effect is mediated by scavenging of oxygen derived free radicals.
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PMID:Effect of melatonin and beta-carotene on indomethacin induced gastric mucosal injury. 1250 Apr 99

Recently, numerous studies have shown antioxidant actions of melatonin. Melatonin at both physiological and pharmacological levels stimulates glutathione peroxidase, glutathione reductase and superoxide dismutase activities in the brains of rats and chickens. This study was designed to evaluate the effect of melatonin on nephropathy and oxidative stress under constant light exposure. Nephropathy was induced by adriamycin administered in a single dose (25 mg kg(-1) b.w., i.p.). Melatonin was injected i.p. (1,000 microg kg(-1) b.w./day). Malondialdehyde, reduced glutathione, glutathione peroxidase, glutathione reductase, glutathione transferase, catalase and superoxide dismutase were determined in kidney. Urea, creatinine and total proteins in plasma and proteinuria were evaluated and melatonin was determined. Results show a decrease in melatonin levels. Similar effects occurred with the antioxidant enzyme activities and reduced glutathione. Likewise, adriamycin and constant light induced significant enhancement of malondialdehyde. All changes induced both by adriamycin and constant light were reverted to normal by melatonin administration. Constant light exposure was associated with an increase in oxidative stress and nephropathy induced by adriamycin. Treatment with melatonin decreased lipid peroxides, and permitted a recovery of reduced glutathione, scavenger enzyme activity and parameters of renal function.
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PMID:Melatonin effect on renal oxidative stress under constant light exposure. 1257 19

Antioxidant enzymes form the first line of defense against free radicals in organisms. Their regulation depends mainly on the oxidant status of the cell, given that oxidants are their principal modulators. However, other factors have been reported to increase antioxidant enzyme activity and/or gene expression. During the last decade, the antioxidant melatonin has been shown to possess genomic actions, regulating the expression of several genes. Melatonin also influences both antioxidant enzyme activity and cellular mRNA levels for these enzymes. In the present report, we review the studies which document the influence of melatonin on the activity and expression of the antioxidative enzymes glutathione peroxidase, superoxide dismutases and catalase both under physiological and under conditions of elevated oxidative stress. We also analyze the possible mechanisms by which melatonin regulates these enzymes.
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PMID:Regulation of antioxidant enzymes: a significant role for melatonin. 1467 24

Our aim was to examine the effects of melatonin on the testicular tissue of adult rats with experimentally-induced left varicocele, and to determine the relationship between melatonin and apoptosis regular proteins in the anti-oxidant defence system. Forty adult male Wistar rats were divided equally into four groups. A sham operation was performed on the rats in group I, and experimental left varicocele was created in groups II, III and IV. Melatonin was administered intraperitoneally at doses of 5 mg/kg and 10 mg/kg to rats in groups III and IV, respectively. An immunohistochemical analysis of the left testicular tissue was performed to evaluate the expression of Bax and Bcl-2, while tissue malondialdehyde (MDA) and antioxidant enzyme activities were assessed in homogenates to determine the role of the oxygen defence system. The immunohistochemical analysis revealed an increased ratio of pro-apoptotic protein Bax in groups II and III, whereas no significant activity was observed in the sham operated rats ( P<0.05). Similarly, the tissue MDA level increased and a significantly decreased level of antioxidant enzymes was observed in these groups ( P<0.05). Although rats in group IV showed a slightly increased ratio of the pro-apoptotic marker Bax, there was no significant difference between groups I and IV. Similarly, group IV showed decreased levels of MDA and increased levels of anti-oxidant enzyme activity with decreased Bax expression. The close relationship between pro-apoptotic/anti-apoptotic markers, reactive oxygen species and antioxidant agents provided a useful in vivo model for studying the pathophysiology of varicocele and evaluating the role of antioxidants in the prevention testicular damage.
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PMID:The effects of melatonin and the antioxidant defence system on apoptosis regulator proteins (Bax and Bcl-2) in experimentally induced varicocele. 1520 54

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

Studies have shown that ischemia-reperfusion (I/R) produces free radicals leading to lipid peroxidation and to damage of the nervous tissue. Melatonin, a main secretory product of the pineal gland, has free radical scavenging and antioxidant properties and has been shown to diminish I/R injury in many tissues. There are a limited number of studies related to the effects of melatonin on I/R injury in the peripheral nervous system. Therefore, in the present study, the protective effect of melatonin was investigated in rats subjected to 2 hr of sciatic nerve ischemia followed by 3 hr of reperfusion. Following reperfusion, nerve tissue samples were collected for quantitative assessment of malondialdehyde (MDA), an oxidative stress marker, and superoxide dismutase (SOD), a principal antioxidant enzyme. Samples were further evaluated at electron microscopic level to examine the neuropathological changes. I/R elevated the concentration of MDA significantly while there was a reduction at SOD levels. Melatonin treatment reversed the I/R-induced increase and decrease in MDA and SOD levels, respectively. Furthermore, melatonin salvaged the nerve fibers from ischemic degeneration. Histopathologic findings in the samples of melatonin-treated animals indicated less edema and less damage to the myelin sheaths and axons than those observed in the control samples. Our results suggest that administration of melatonin protects the sciatic nerve from I/R injury, which may be attributed to its antioxidant property.
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PMID:Beneficial effects of melatonin on reperfusion injury in rat sciatic nerve. 1535 57

Melatonin, the main secretory product of the pineal gland, is known to collaborate against oxidative stress within cells, but its mechanism of action in terms of stimulating antioxidant enzymes remains unclear. Herein, we propose that melatonin modulates antioxidant enzyme activities via its interaction with calmodulin, which in turn inhibits downstream processes that lead to the inactivation of nuclear RORalpha melatonin receptor. Eventually, this nuclear transcription factor downregulates NF-kappaB-induced antioxidant enzyme expression. Therefore, the increment in antioxidant enzyme activities induced by melatonin involves the inhibition of the RORalpha pathway. Thus, in addition to its direct free radical scavenging activities, melatonin has important actions in oxidative defense by stimulating enzymes which metabolize free radicals and radical products to innocuous metabolites.
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PMID:A proposed mechanism to explain the stimulatory effect of melatonin on antioxidative enzymes. 1609 85

It is generally agreed that one of the major contributors to skin aging is reactive oxygen species. As organisms reach advanced age, free radical generation increases and the activity of tissue antioxidant enzyme system decreases. Melatonin is an antioxidant and free radical scavenger. The present study was first aimed to determine the morphometric and biochemical changes caused by long-term pinealectomy in order to investigate the role of melatonin as skin architecture. Secondly, the effect of exogenous melatonin administration on these changes was determined. Rats were pinealectomized or sham operated (control) for 6 months. Half of the pinealectomized rats were treated with 4 mg/kg melatonin during the last month of the experiment. Pinealectomy resulted in important morphometric and biochemical changes in the back, abdominal and thoracic skin. The thickness of epidermis and dermis and the number of dermal papillae and hair follicles were reduced. Melatonin administration to pinealectomized rats significantly improved these alterations in all body areas (P < 0.005). On the contrary, in pinealectomized rats the levels of antioxidant enzymes, catalase and glutathione peroxidase were decreased. Melatonin restored the levels of these enzymes. The pinealectomy-induced increases in lipid peroxidation in the abdominal and thoracic skin were significantly reduced by melatonin treatment (P < 0.005 and 0.01 respectively). These results suggest that melatonin is highly efficient anti-aging factor and, as melatonin levels decrease with age, melatonin treatment may reduce age-related skin changes.
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PMID:Potent therapeutic effect of melatonin on aging skin in pinealectomized rats. 1615 Jan 2

Quinolinic acid is a well-known excitotoxin that induces oxidative stress and damage. In the present study, oxidative damage to biomolecules was followed by measuring lipid peroxidation and protein carbonyl formation in rat brain tissue culture over a period of 24 hr of exposure to this prooxidant agent at a concentration of 0.5 mm. Quinolinic acid enhanced lipid peroxidation in an early stage of tissue culture, and protein carbonyl at a later stage. These data confirm and extend previous studies demonstrating that quinolinic acid can induce significant oxidative damage. Melatonin, an antioxidant and neuroprotective agent with multiple actions as a radical scavenger and signaling molecule, completely prevented these prooxidant actions of quinolinic acid at a concentration of 1 mm. Morphological lesions and neurotoxicity induced by quinolinic acid were evaluated by light microscopy. Quinolinic acid produced extensive apoptosis/necrosis which was significantly attenuated by melatonin. Cotreatment with melatonin exerted a profound protective effect antagonizing the neurotoxicity induced by quinolinic acid. Glutathione reductase and catalase activities were increased by quinolinic acid and these effects were antagonized by melatonin. Furthermore, melatonin induced superoxide dismutase activity. Quinolinic acid and melatonin acted independently and by different mechanisms in modulating antioxidant enzyme activities. Our findings using quinolinic acid and melatonin clearly demonstrate that such changes should always be seen in the context of oxidative neurotoxicity and antioxidant neuroprotection.
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PMID:Melatonin neutralizes neurotoxicity induced by quinolinic acid in brain tissue culture. 1615 Jan 7

Melatonin plays a role in the prevention of oxidative damage. In the present study, we investigated whether the increased oxidative stress in experimental otitis media with effusion (OME) induced by histamine is reflected in erythrocytes and middle ear effusion fluid. Lipid peroxidation in effusion fluid was measured to determine the effects of melatonin on oxidative stress. Erythrocyte and middle ear effusion malondialdehyde (MDA) levels, erythrocyte glutathione (GSH) levels and glutathione peroxidase (GPx), glutathione reductase (GRd) and glutathione-S-transferase (GST) activities were measured in three groups of six guinea pigs each at 3 hr after the injection of 0.1 mL of histamine (or saline) into the middle ear. In erythrocyte and middle ear effusion samples, MDA levels showed a significant increase in guinea pigs with experimental OME group when compared with the control animals. Erythrocyte GPx, GST, GRd activities and GSH levels significantly reduced in experimental OME guinea pigs when compared with the control and melatonin-treated animals. Erythrocyte GPx activity also significantly increased after melatonin treatment when compared with the control group. These findings suggest that reactive oxygen species play a role in histamine-induced OME. Pretreatment with melatonin increases antioxidant enzyme activities and reduced formation of MDA, an indicator of lipid peroxidation, in histamine-induced OME.
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PMID:Effect of melatonin on lipid peroxidation, glutathione and glutathione-dependent enzyme activities in experimental otitis media with effusion in guinea pigs. 1615 Jan 9


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