Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.9 (glutathione peroxidase)
22,002 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peroxisome proliferator-activated receptor gamma (PPAR-gamma) is a nuclear hormone receptor super family that has recently been implicated in atherosclerosis, inflammation, cancer, infertility, and demyelination. Oxidative stress, neutrophil infiltration, proinflammatory cytokines, and the exhibition of luminal acid play a role in the pathogenesis of gastric injury induced by ischemia-reperfusion. Rosiglitazone, a specific PPAR-gamma ligand, has been shown to have antiinflammatory activity, but its effects on experimental ischemia-reperfusion gastric injury remain unknown. We have investigated the effects of the rosiglitazone on gastric injury caused by ischemia following reperfusion in rats. Tumour necrosis factor-alpha (TNF-alpha) levels and changes in enzymatic activities of myeloperoxidase, as a marker of neutrophils infiltration, xanthine oxidase, superoxide dismutase, and glutathione peroxidase, were determined. Histological analysis of the lesions was also carried out. Pretreatment with 1 or 4 mg/kg of rosiglitazone ameliorated the gastric damage induced by clamping the celiac artery for 30 min followed by 60 min of reperfusion. It significantly (P<0.05) reduced the index of neutrophil infiltration and the levels of the cytokine. Rosiglitazone did not revert the reduced glutathione peroxidase activity but enhanced significantly (P<0.01) the decreased xanthine oxidase and superoxide dismutase activities in gastric mucosa of ischemic rats. In conclusion, rosiglitazone reduces the damage in ischemia-reperfusion gastric injury and alleviates the inflammatory response and the oxidative events.
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PMID:Rosiglitazone, an agonist of peroxisome proliferator-activated receptor gamma, protects against gastric ischemia-reperfusion damage in rats: role of oxygen free radicals generation. 1555 53

Testicular torsion is a serious problem in male children and, if not treated at the right time, can lead to subfertility and infertility. The main reason for testicular damage is ischemia-reperfusion injury. A number of chemical substances have been used to protect testes against ischemia-reperfusion injury in experimental animals. The possible protective effect of N-acetylcysteine on testicular tissue after testicular detorsion was examined in the current study. Twenty-four rats were divided into four groups: sham operation, torsion, detorsion, and NAC + detorsion groups (n = 6 for each group). Excluding sham operation group, the rats were subjected to unilateral torsion (720-degree rotation in clockwise direction). After torsion (5 h) and detorsion (2 h), unilateral orchidectomy was performed. Malondialdehyde levels and superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities were determined in testicular tissue. Administration of N-acetylcysteine caused a decrease in malondialdehyde levels and an increase in glutathione peroxidase levels compared to detorsion group. The results suggest that N-acetylcysteine may be a potential protective agent for preventing the negative biochemical changes related to oxidative stress in testicular injury caused by testis torsion.
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PMID:The effects of N-acetylcysteine on antioxidant enzyme activities in experimental testicular torsion. 1641 70

Microbial infections, localized as well as systemic, are known to cause transitive or permanent male infertility. However, the mechanisms of infection-induced infertility are largely unknown. Earlier reports showed that steroidogenesis and spermatogenesis are affected during bacterial lipopolysaccharide (LPS)-induced acute inflammation. The present study used an LPS rat model to investigate the role of oxidative stress in spermatogenesis. Intraperitoneal administration of bacterial LPS (5mg/kg body weight) to adult male albino rats elevated testicular malondialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE), and decreased the activities of testicular antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. The GSH/GSSG ratio also decreased significantly. Time series analysis revealed transitory oxidative stress and expression of inflammatory mediators such as interleukin-1beta (IL-1beta), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) from 3h to 12h after LPS. Testicular expression of steroidogenic acute regulatory (StAR) protein decreased to 24h, in correlation with damage to spermatogenesis. These data are consistent with oxidative stress as a major causal factor in altered steroidogenesis, spermatogenesis, and perhaps male infertility during endotoxin-induced acute inflammation.
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PMID:Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats. 1664 80

Successful spermatogenesis is dependent on the proper attachment of developing germ cells to Sertoli cells. Manipulation of these interactions by drugs like Adjudin can hamper the development of germ cells and lead to conditions of temporary infertility. Although studies have shown the contraceptive potential of Adjudin, much is not known about its action in the testis. In this study, we sought to investigate the effect of Adjudin on the oxidative status of mammalian testis. Adult male rats were administered with a single dose of Adjudin (50 mg/kg body weight) by oral gavage and were killed at 1, 2, 4, 7, 15, or 30 days of treatment. Adjudin caused a significant increase in the production of hydrogen peroxide and lipid peroxidation from 4 to 7 days after treatment. There was a significant decrease in the activities of anti-oxidant enzymes superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase from 4 to 7 days after treatment with Adjudin. However, the state of oxidative stress was less pronounced from 15 to 30 days after Adjudin treatment. The level of androgen binding protein (ABP) remained unchanged following Adjudin treatment. These results show that there is an induction of oxidative stress accompanying adherens junction restructuring which suggests a role for reactive oxygen species in the regulation of these testicular junctions. However, transient elevation in reactive oxygen species levels did not affect androgen transport.
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PMID:Adjudin-mediated germ cell depletion alters the anti-oxidant status of adult rat testis. 1844 95

The aim of this study was to assess seminal reactive oxygen species (ROS)-antioxidants relationship in fertile and infertile men with and without varicocele. One hundred and seventy six males were studied; fertile healthy volunteers (n = 45), fertile men with varicocele (n = 45), infertile oligoasthenozoospermia (OA, n = 44) without varicocele and infertile OA with varicocele (n = 42). In their seminal plasma, two ROS parameters (malondialdehyde, hydrogen peroxide) and five antioxidants (superoxide dismutase, catalase, glutathione peroxidase, vitaminE, vitaminC) were estimated. Compared with fertile healthy men, in all other studied groups, estimated seminal ROS were significantly higher and estimated antioxidants were significantly lower. Infertile men with varicocele showed the same relationship as infertile men without varicocele. Sperm concentration, total sperm motility as well as sperm normal forms were negatively correlated with seminal malondialdehyde and were positively correlated with vitaminC. It is concluded that varicocele has an oxidative stress (OS) in fertile normozoospermic bearing conditions. This may allow understanding that, within men with varicocele, there is a threshold value of OS over which male fertility may be impaired.
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PMID:Seminal reactive oxygen species-antioxidant relationship in fertile males with and without varicocele. 1926 Aug 50

The oxidative stress imposed by nutritional variations in selenium (Se) has plausible role in reproductive toxicology and affects the reproductive potential. Also, the expression of heat shock proteins (HSPs) is a highly regulated event throughout the process of spermatogenesis and is modulated by stressful stimuli. This prompted us to investigate the possibility that Se-induced oxidative stress may affect the fertility status by altering the expressions of the constitutive and inducible HSP70 proteins, having crucial role in spermatogenesis. Different Se status-deficient, adequate, and excess, male Balb/c mice were created by feeding yeast-based Se-deficient diet (group I) and deficient diet supplemented with Se as sodium selenite at 0.2 and 1 ppm Se (group II and III) for a period of 8 weeks. After completion of the diet-feeding schedule, a significant decrease in the Se and glutathione peroxidase (GSH-Px) levels was observed in the Se-deficient group (I), whereas Se-excess group (III) demonstrated an increase. Increased levels of reactive oxygen species, malondialdehyde, and alterations in the redox status in both groups I and III indicated oxidative-stressed conditions. There was an overall reduced fertility status in mice supplemented with Se-deficient and Se-excess diet. The mRNA and protein expression of HSP70 was found to be elevated in these two groups, whereas the expression patterns of HSP70-2 and MSJ-1 demonstrated a reverse trend. In vitro CDC2 kinase assay showed reduced kinase activity in group I and group III. These findings suggest that Se-induced oxidative stress by differentially regulating various HSP70s can affect its downstream factors having crucially important role in differentiation of germ cells and completion of spermatogenesis. Therefore, it can provide an insight into the mechanism(s) by which the oxidative stress-induced reproductive toxicity can lead to increased apoptosis/growth arrest and infertility. This will thus add new dimensions to the molecular mechanism underlying the human male infertility and open new vistas in the development of various chemo-preventive methods.
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PMID:Diminished reproductive potential of male mice in response to selenium-induced oxidative stress: involvement of HSP70, HSP70-2, and MSJ-1. 1936 46

Testicular torsion is a common syndrome that could lead to infertility. We investigated the therapeutic effects of lycopene, an antioxidant caretenoid, on testicular ischemia/reperfusion (IR) injury that resembles testicular torsion. Male Wistar albino rats were divided into three groups: sham (n = 6), IR (n = 18), and ischemia/reperfusion with lycopene (IRL, n = 18). Left testicular artery and vein was occluded for 1 h, followed by reperfusion of 3 h, 24 h or 30 days in IR and IRL animals. Either corn oil (vehicle) or lycopene (4 mg/kg) was administrated once daily by gavage to IR or IRL animals, respectively, 5 min after ischemia. Sham-operated animals were treated with vehicle by gavage 5 min after the operation. IR decreased sperm motility and concentration in both ipsilateral and contralateral testes and increased abnormal sperm rate in ipsilateral testis after 30 days of reperfusion. Treatment with lycopene increased the motility in bilateral testes and decreased the rate of abnormal sperm in ipsilateral testis to the sham level, but did not increase sperm concentration in bilateral testes. IR increased the activities of catalase and glutathione peroxidase and the level of reduced glutathione by 24 h of reperfusion, but malondialdehyde remained unchanged. Lycopene treatment restored the enzyme activities but not the reduced glutathione level. Lycopene treatment also ameliorated the IR-induced tissue damage in bilateral testes. In conclusion, the therapeutic antioxidant effect of lycopene on germ cells could serve as a promising intervention to oxidative stress-associated infertility problems, such as testicular torsion.
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PMID:Lycopene, an antioxidant carotenoid, attenuates testicular injury caused by ischemia/reperfusion in rats. 1947 70

Physiological function of reactive oxygen species (ROS) has been known since a long, but recently toxic effects of ROS on spermatozoa have gained much importance in male infertility. Mitochondrial DNA (mtDNA) is believed to be both source and target of ROS. mtDNA unlike nuclear DNA is not compactly packed and hence more susceptible to oxidative stress (OS) than nuclear DNA. In the present study, the role of OS in mitochondrial genome changes was studied in men with idiopathic infertility. The study included 33 infertile oligo-asthenozoospermic (OA) men and 30 fertile controls. Semen analyses were performed and OS was measured by estimating the level of malondialdehye (MDA) in the seminal plasma and ROS in the sperm. Sperm mtDNA was sequenced by standard PCR-DNA sequencing protocol for ATPase and nicotinamide adenine dinucleotide dehydrogenase (ND) groups of genes. Sperm count and progressive motility were found to be significantly lower in infertile group than the fertile controls. Semen MDA and ROS levels of infertile group were significantly higher (p<0.0001), when compared to the control group. However, catalase and glutathione peroxidase (GPx) levels were significantly lower in infertile group, compared to controls, but no significant difference in superoxide dismutase (SOD) activity was observed between control and cases. This might be due to higher expression of SOD alone in order to overcome OS in the semen. mtDNA analysis showed significant and high frequency of nucleotide changes in the ATPase (6 and 8), ND (2, 3, 4 and 5) genes of infertile cases compared to the controls. Hence excess ROS and low antioxidant levels in the semen might cause mtDNA mutations and vice versa in OA men that might impair the fertilizing capacity of spermatozoa. Thus, it is important to understand the etiology of mitochondrial genome mutations in idiopathic OA cases for better diagnostic and prognostic value in infertility treatment/assisted reproductive technique.
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PMID:Oxidative stress and sperm mitochondrial DNA mutation in idiopathic oligoasthenozoospermic men. 1951 95

In mammals, posttesticular epididymal sperm maturation is considered an essential step in the transformation of immature testicular gametes to mature spermatozoa capable of fertilization. Reactive oxygen species (ROS) have been shown to be key actors in this maturation process, and it is now clear that ROS are central for sperm physiology in processes such as sperm maturation and capacitation. However, during epididymal maturation and storage and until the onset of fertilization, oxidative damage is a threat spermatozoa must face more than any other cells. Spermatozoa were found to be extremely sensitive to oxidative attacks correlated with lipid peroxidation, DNA damage, and impaired sperm motility, all affecting fertilization. To control the quantity of H(2)O(2) in the vicinity of male gametes, mammalian epididymis uses a panel of nonenzymatic and enzymatic scavengers, among which the glutathione peroxidase (GPx) family is largely represented. Among the various GPx proteins expressed in the mammalian epididymis, GPx4 and GPx5 occupy unique positions and functions that are reviewed in this paper. This paper underlines the importance of the GPx protein family in determining the fertilizing potential of mammalian spermatozoa. This is particularly relevant in the field of mammalian fertility and infertility as well as in the development of assisted medical procreation technologies and male gamete preservation techniques that are extensively used in human and animal reproduction programs.
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PMID:Mammalian glutathione peroxidases control acquisition and maintenance of spermatozoa integrity. 2004 49

Oxidative stress due to chronic hyperglycemia is known to cause infertility in diabetic patients. Pioglitazone (PIO), a PPAR-gamma ligand is known to possess the antioxidant property however, its role on the oxidative stress mediated germinal damage in Type-2 diabetes mellitus (T2DM) is poorly studies in the literature. In this study, the effect of PIO (1 and 10 mg/kg, p.o. daily for 4 weeks) was evaluated against the nicotinamide (NA- 230 mg/kg, ip) and streptozotocin (STZ-65 mg/kg, ip) induced changes in sperm abnormality and antioxidant status in Wistar rats. The effect of PIO on the male reproductive cells was studied by determining the sperm shape abnormality and sperm count in the experimental T2DM. The antioxidant profile was studied by estimating the serum lipid peroxidation (LPO), glutathione (GSH) and glutathione peroxidase (GPx) levels. The higher dose of PIO (10 mg/kg) significantly (p<0.001) reduced the sperm shape abnormality and increased the sperm count (p<0.001), besides decreasing (p<0.05) the LPO and enhancing the GSH and GPx levels in the diabetic rats. However, the lower dose of PIO (1 mg/kg) produced inhibitory (p<0.05) effect against the changes induced by T2DM in the sperm shape abnormality and GSH levels. alpha-tocopherol tested as an standard antioxidant agent prevented (p<0.001) the NA-STZ mediated alterations in sperm abnormalities and antioxidant enzyme levels. The results suggest that the inhibitory effect of PIO against the T2DM induced sperm abnormality could be related to its antioxidant property.
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PMID:Pioglitazone, a PPAR-gamma ligand inhibited the nicotinamide-streptozotocin induced sperm abnormalities in type-2 diabetic Wistar rats. 2056 48


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