Oxidative stress and sperm mitochondrial DNA mutation in idiopathic oligoasthenozoospermic men.

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dc.contributor.authorKumar, R
dc.contributor.authorVenkatesh, S
dc.contributor.authorKumar, M
dc.contributor.authorTanwar, M
dc.contributor.authorShasmsi, M B
dc.contributor.authorKumar, R
dc.contributor.authorGupta, N P
dc.contributor.authorSharma, R K
dc.contributor.authorTalwar, P
dc.contributor.authorDada, Rima
dc.date.accessioned2011-11-09T05:48:38Z
dc.date.available2011-11-09T05:48:38Z
dc.date.issued2009-04
dc.description.abstractPhysiological 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 techniqueen_US
dc.identifier.citationKumar R, Venkatesh S, Kumar M, Tanwar M, Shasmsi M B, Kumar R, Gupta N P, Sharma R K, Talwar P, Dada Rima. Oxidative stress and sperm mitochondrial DNA mutation in idiopathic oligoasthenozoospermic men. Indian Journal of Biochemistry & Biophysics. 2009 Apr; 46(2): 172-177.en_US
dc.identifier.urihttps://imsear.searo.who.int/handle/123456789/135191
dc.language.isoenen_US
dc.source.urihttps://nopr.niscair.res.in/bitstream/123456789/4054/1/IJBB%2046%282%29%20172-177.pdfen_US
dc.subjectReactive oxygen speciesen_US
dc.subjectOxidative stressen_US
dc.subjectInfertilityen_US
dc.subjectAntioxidant enzymesen_US
dc.subjectmtDNA mutationsen_US
dc.subjectAssisted reproductive techniqueen_US
dc.subjectSpermen_US
dc.subjectOligoasthenozoospermicen_US
dc.subject.meshAdult
dc.subject.meshAntioxidants --metabolism
dc.subject.meshAsthenozoospermia --genetics
dc.subject.meshAsthenozoospermia --metabolism
dc.subject.meshCase-Control Studies
dc.subject.meshDNA, Mitochondrial --genetics
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshMutation
dc.subject.meshNucleotides--metabolism
dc.subject.meshOligospermia --genetics
dc.subject.meshOligospermia --metabolism
dc.subject.meshOxidative Stress
dc.subject.meshSemen --metabolism
dc.subject.meshSpermatozoa --metabolism
dc.subject.meshSpermatozoa --pathology
dc.subject.meshSpermatozoa --ultrastructure
dc.titleOxidative stress and sperm mitochondrial DNA mutation in idiopathic oligoasthenozoospermic men.en_US
dc.typeArticleen_US
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