Time-course and molecular mechanism of hepatotoxicity induced by 1,3-dichloro-2-propanol in rats

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dc.contributor.authorIn Chul Lee-
dc.contributor.authorJ W Ko-
dc.contributor.authorS M Lee-
dc.contributor.authorS H Kim-
dc.contributor.authorI S Shin-
dc.contributor.authorOg Sung Moon-
dc.contributor.authorWoon Kee Yoon-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorJ C Kim-
dc.date.accessioned2017-04-19T10:07:44Z-
dc.date.available2017-04-19T10:07:44Z-
dc.date.issued2015-
dc.identifier.issn13826689-
dc.identifier.uri10.1016/j.etap.2015.06.011.ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12696-
dc.description.abstractThis study investigated the time-course of 1,3-dichloro-2-propanol (1,3-DCP)-induced hepatotoxicity and the molecular mechanism of its oxidative stress and apoptotic changes in rats. Thirty-six male rats were randomly assigned to six groups of six rats each and were administered a single oral dose of 1,3-DCP (90 mg/kg) or its vehicle. 1,3-DCP caused acute hepatic damage, as evidenced by marked increases in serum aminotransferase, alkaline phosphatase, and histopathological alterations. These functional and histopathological changes in the liver peaked at 12h after administration and then decreased progressively. Oxidative stress indices were increased significantly at 6h, peaked at 12h, and then decreased progressively. The number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)- and caspase-3-positive cells increased after 6h, peaked at 12 and 24h, and then decreased. The protein levels of phosphorylated mitogen-activated protein kinases (MAPKs) including p-Erk1/2 and p-JNK showed a similar trend to the numbers of TUNEL- and caspase-3-positive cells. These results indicate that 1,3-DCP increases oxidative stress, nuclear translocation of Nrf2, and expression of Nrf2-targeted genes, followed by increased functional and histopathological alterations in the liver. The increase in hepatocellular apoptosis induced by 1,3-DCP may be related to oxidative stress-mediated MAPK activation.-
dc.publisherElsevier-
dc.titleTime-course and molecular mechanism of hepatotoxicity induced by 1,3-dichloro-2-propanol in rats-
dc.title.alternativeTime-course and molecular mechanism of hepatotoxicity induced by 1,3-dichloro-2-propanol in rats-
dc.typeArticle-
dc.citation.titleEnvironmental Toxicology and Pharmacology-
dc.citation.number1-
dc.citation.endPage198-
dc.citation.startPage191-
dc.citation.volume40-
dc.contributor.affiliatedAuthorIn Chul Lee-
dc.contributor.affiliatedAuthorOg Sung Moon-
dc.contributor.affiliatedAuthorWoon Kee Yoon-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName이인철-
dc.contributor.alternativeName고제원-
dc.contributor.alternativeName이상민-
dc.contributor.alternativeName김성환-
dc.contributor.alternativeName신인식-
dc.contributor.alternativeName문옥성-
dc.contributor.alternativeName윤원기-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName김종춘-
dc.identifier.bibliographicCitationEnvironmental Toxicology and Pharmacology, vol. 40, no. 1, pp. 191-198-
dc.identifier.doi10.1016/j.etap.2015.06.011-
dc.subject.keyword1,3-Dichloro-2-propanol-
dc.subject.keywordHepatotoxicity-
dc.subject.keywordMechanism of action-
dc.subject.keywordTime-course-
dc.subject.local1,3-Dichloro-2-propanol-
dc.subject.localHepatotoxicity-
dc.subject.localMechanism of action-
dc.subject.localTime-course-
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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