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Title 

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

Authors 

I C LeeJ W KoS M LeeS H KimI S ShinOg Sung MoonWoon Kee YoonHyoung-Chin KimJ C Kim

Publisher 

Elsevier

Issue Date 

2015

Citation 

Environmental Toxicology and Pharmacology, vol. 40, no. 1, pp. 191-198

Keywords 

1,3-Dichloro-2-propanolHepatotoxicityMechanism of actionTime-course

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.

ISSN 

1382-6689

Link 

http://dx.doi.org/10.1016/j.etap.2015.06.011.

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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