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Article: Effects of sperm DNA damage on the levels of RAD51 and p53 proteins in zygotes and 2-cell embryos sired by golden hamsters without the major accessory sex glands
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TitleEffects of sperm DNA damage on the levels of RAD51 and p53 proteins in zygotes and 2-cell embryos sired by golden hamsters without the major accessory sex glands
 
AuthorsChen, H
Liao, S
Cheung, MPL
Chow, PH
Cheung, A
O, WS
 
Issue Date2012
 
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
 
CitationFree Radical Biology & Medicine, 2012, v. 53 n. 4, p. 885-892 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.freeradbiomed.2012.06.007
 
AbstractWe previously reported that the male accessory sex gland (ASG) secretion is the main source of antioxidants to safeguard sperm genomic integrity and functional competence. Removal of all ASGs in the golden hamster can reduce male fertility by increasing embryo wastage. This study aims to investigate whether the oxidative DNA-damaged sperm from hamsters without all ASGs (TX) could successfully fertilize oocytes and to qualify the status of DNA repair by the expression of RAD51 and p53 proteins. Here we demonstrated a significantly higher DNA-base adduct formation (8-hydroxy-2'-deoxyguanosine) in sperm from TX males than those from sham-operated males. Comet assays demonstrated that all female pronuclei in both zygotes were intact, but single- and double-strand DNA damage was found in decondensed sperm in TX males only. DNA damage could also be detected in both nuclei of the TX 2-cell embryos. RAD51, a DNA repair enzyme, was found to be evenly distributed in the cytoplasm and nuclei in oocytes/zygotes, while at the 2-cell stage, a strong expression of p53 protein and a larger clear perinuclear area without RAD51 expression were found in TX embryos. In conclusion, we demonstrated for the first time DNA damage in decondensed sperm of zygotes and blastomeres of 2-cell stage embryos sired by TX males, resulting in the activation of DNA repair. Sperm DNA damage could induce the increase in p53 expression and the reduction of RAD51 expression in the TX 2-cell stage embryos.
 
ISSN0891-5849
2013 Impact Factor: 5.710
2013 SCImago Journal Rankings: 2.220
 
DOIhttp://dx.doi.org/10.1016/j.freeradbiomed.2012.06.007
 
ISI Accession Number IDWOS:000307920100024
 
DC FieldValue
dc.contributor.authorChen, H
 
dc.contributor.authorLiao, S
 
dc.contributor.authorCheung, MPL
 
dc.contributor.authorChow, PH
 
dc.contributor.authorCheung, A
 
dc.contributor.authorO, WS
 
dc.date.accessioned2012-08-16T05:47:37Z
 
dc.date.available2012-08-16T05:47:37Z
 
dc.date.issued2012
 
dc.description.abstractWe previously reported that the male accessory sex gland (ASG) secretion is the main source of antioxidants to safeguard sperm genomic integrity and functional competence. Removal of all ASGs in the golden hamster can reduce male fertility by increasing embryo wastage. This study aims to investigate whether the oxidative DNA-damaged sperm from hamsters without all ASGs (TX) could successfully fertilize oocytes and to qualify the status of DNA repair by the expression of RAD51 and p53 proteins. Here we demonstrated a significantly higher DNA-base adduct formation (8-hydroxy-2'-deoxyguanosine) in sperm from TX males than those from sham-operated males. Comet assays demonstrated that all female pronuclei in both zygotes were intact, but single- and double-strand DNA damage was found in decondensed sperm in TX males only. DNA damage could also be detected in both nuclei of the TX 2-cell embryos. RAD51, a DNA repair enzyme, was found to be evenly distributed in the cytoplasm and nuclei in oocytes/zygotes, while at the 2-cell stage, a strong expression of p53 protein and a larger clear perinuclear area without RAD51 expression were found in TX embryos. In conclusion, we demonstrated for the first time DNA damage in decondensed sperm of zygotes and blastomeres of 2-cell stage embryos sired by TX males, resulting in the activation of DNA repair. Sperm DNA damage could induce the increase in p53 expression and the reduction of RAD51 expression in the TX 2-cell stage embryos.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationFree Radical Biology & Medicine, 2012, v. 53 n. 4, p. 885-892 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.freeradbiomed.2012.06.007
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.freeradbiomed.2012.06.007
 
dc.identifier.epage892
 
dc.identifier.hkuros205573
 
dc.identifier.isiWOS:000307920100024
 
dc.identifier.issn0891-5849
2013 Impact Factor: 5.710
2013 SCImago Journal Rankings: 2.220
 
dc.identifier.issue4
 
dc.identifier.pmid22705368
 
dc.identifier.spage885
 
dc.identifier.urihttp://hdl.handle.net/10722/159273
 
dc.identifier.volume53
 
dc.languageeng
 
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
 
dc.publisher.placeUnited States
 
dc.relation.ispartofFree Radical Biology & Medicine
 
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in Free Radical Biology & Medicine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Free Radical Biology & Medicine, [VOL 53, ISSUE 4, 2012] DOI 10.1016/j.freeradbiomed.2012.06.007
 
dc.titleEffects of sperm DNA damage on the levels of RAD51 and p53 proteins in zygotes and 2-cell embryos sired by golden hamsters without the major accessory sex glands
 
dc.typeArticle
 
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<item><contributor.author>Chen, H</contributor.author>
<contributor.author>Liao, S</contributor.author>
<contributor.author>Cheung, MPL</contributor.author>
<contributor.author>Chow, PH</contributor.author>
<contributor.author>Cheung, A</contributor.author>
<contributor.author>O, WS</contributor.author>
<date.accessioned>2012-08-16T05:47:37Z</date.accessioned>
<date.available>2012-08-16T05:47:37Z</date.available>
<date.issued>2012</date.issued>
<identifier.citation>Free Radical Biology &amp; Medicine, 2012, v. 53 n. 4, p. 885-892</identifier.citation>
<identifier.issn>0891-5849</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/159273</identifier.uri>
<description.abstract>We previously reported that the male accessory sex gland (ASG) secretion is the
      main source of antioxidants to safeguard sperm genomic integrity and functional
      competence. Removal of all ASGs in the golden hamster can reduce male fertility
      by increasing embryo wastage. This study aims to investigate whether the
      oxidative DNA-damaged sperm from hamsters without all ASGs (TX) could
      successfully fertilize oocytes and to qualify the status of DNA repair by the
      expression of RAD51 and p53 proteins. Here we demonstrated a significantly higher
      DNA-base adduct formation (8-hydroxy-2&apos;-deoxyguanosine) in sperm from TX males
      than those from sham-operated males. Comet assays demonstrated that all female
      pronuclei in both zygotes were intact, but single- and double-strand DNA damage
      was found in decondensed sperm in TX males only. DNA damage could also be
      detected in both nuclei of the TX 2-cell embryos. RAD51, a DNA repair enzyme, was
      found to be evenly distributed in the cytoplasm and nuclei in oocytes/zygotes,
      while at the 2-cell stage, a strong expression of p53 protein and a larger clear 
      perinuclear area without RAD51 expression were found in TX embryos. In
      conclusion, we demonstrated for the first time DNA damage in decondensed sperm of
      zygotes and blastomeres of 2-cell stage embryos sired by TX males, resulting in
      the activation of DNA repair. Sperm DNA damage could induce the increase in p53
      expression and the reduction of RAD51 expression in the TX 2-cell stage embryos.</description.abstract>
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<rights>NOTICE: this is the author&#8217;s version of a work that was accepted for publication in Free Radical Biology &amp; Medicine. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Free Radical Biology &amp; Medicine, [VOL 53, ISSUE 4, 2012] DOI 10.1016/j.freeradbiomed.2012.06.007</rights>
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