Apoptotic cell death in rat epididymis following epichhlorohydrin treatment

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dc.contributor.authorIn Chul Lee-
dc.contributor.authorK H Kim-
dc.contributor.authorS H Kim-
dc.contributor.authorH S Baek-
dc.contributor.authorC Moon-
dc.contributor.authorS H Kim-
dc.contributor.authorWoon Kee Yoon-
dc.contributor.authorKi Hoan Nam-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorJ C Kim-
dc.date.accessioned2017-04-19T09:45:18Z-
dc.date.available2017-04-19T09:45:18Z-
dc.date.issued2013-
dc.identifier.issn09603271-
dc.identifier.uri10.1177/0960327112467042ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11581-
dc.description.abstractEpichlorohydrin (ECH) is an antifertility agent that acts both as an epididymal toxicant and an agent capable of directly affecting sperm motility. This study identified the time course of apoptotic cell death in rat epididymides after ECH treatment. Rats were administrated with a single oral dose of ECH (50 mg/kg). ECH-induced apoptotic changes were evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and its related mechanism was confirmed by Western blot analysis and colorimetric assay. The TUNEL assay showed that the number of apoptotic cells increased at 8 h, reached a maximum level at 12 h, and then decreased progressively. The Western blot analysis demonstrated no significant changes in proapoptotic Bcl-2-associated X (Bax) and anti-apoptotic Bcl-2 expression during the time course of the study. However, phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and phospho-c-Jun amino-terminal kinase (p-JNK) expression increased at 8-24 h. Caspase-3 and caspase-8 activities also increased at 8-48 h and 12-48 h, respectively, in the same manner as p-p38 MAPK and p-JNK expression. These results indicate that ECH induced apoptotic changes in rat epididymides and that the apoptotic cell death may be related more to the MAPK pathway than to the mitochondrial pathway.-
dc.publisherSage-
dc.titleApoptotic cell death in rat epididymis following epichhlorohydrin treatment-
dc.title.alternativeApoptotic cell death in rat epididymis following epichhlorohydrin treatment-
dc.typeArticle-
dc.citation.titleHuman & Experimental Toxicology-
dc.citation.number6-
dc.citation.endPage646-
dc.citation.startPage640-
dc.citation.volume32-
dc.contributor.affiliatedAuthorIn Chul Lee-
dc.contributor.affiliatedAuthorWoon Kee Yoon-
dc.contributor.affiliatedAuthorKi Hoan Nam-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName이인철-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName윤원기-
dc.contributor.alternativeName남기환-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName김종춘-
dc.identifier.bibliographicCitationHuman & Experimental Toxicology, vol. 32, no. 6, pp. 640-646-
dc.identifier.doi10.1177/0960327112467042-
dc.subject.keywordapoptosis-
dc.subject.keywordEpichlorohydrin-
dc.subject.keywordepididymis-
dc.subject.keywordreproductive dysfunction-
dc.subject.localapoptosis-
dc.subject.localApoptosis-
dc.subject.localEpichlorohydrin-
dc.subject.localepididymis-
dc.subject.localreproductive dysfunction-
dc.description.journalClassY-
Appears in Collections:
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > 1. Journal Articles
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