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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Lee, In-Chul Ko, Je-Won Lee, Sang-Min Kim, Sung-Hwan Shin, In-Sik Moon, Og-Sung Yoon, Won-Kee Kim, Hyoung-Chin Kim, Jong-Choon |
| Description | Author Affiliation: Lee IC ( College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea.); Ko JW ( College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea.); Lee SM ( College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea.); Kim SH ( College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea); Shin IS ( College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea.); Moon OS ( Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk 363-883, Republic of Korea.); Yoon WK ( Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk 363-883, Republic of Korea.); Kim HC ( Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk 363-883, Republic of Korea.); Kim JC ( College of Veterinary Medicine, Chonnam National University, Gwangju 500-757, Republic of Korea. Electronic address: toxkim@jnu.ac.kr.) |
| Abstract | This 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. |
| File Format | HTM / HTML |
| ISSN | 13826689 |
| Issue Number | 1 |
| Volume Number | 40 |
| e-ISSN | 18727077 |
| Journal | Environmental Toxicology and Pharmacology |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2015-07-01 |
| Publisher Place | Netherlands |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Environmental Health Discipline Pharmacology Liver Drug Effects Alpha-chlorohydrin Analogs & Derivatives Animals Apoptosis Male Oxidative Stress Rats Rats, Sprague-dawley Toxicity Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology |
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