NDLI: In vitro toxicological evaluation of ethyl carbamate in human HepG2 cells

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In vitro toxicological evaluation of ethyl carbamate in human HepG2 cells

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Toxicology Research Vol - 5 Issue - 1

Toxicology Research Vol -4

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

In vitro toxicological evaluation of ethyl carbamate in human HepG2 cells

Content Provider	Royal Society of Chemistry (RSC)
Author	Qiu, Nannan Cui, Xia Wang, Jiayi Wu, Yongning
Copyright Year	2016
Abstract	Ethyl carbamate (EC) is a multi-site carcinogen in experiment animals and probably carcinogenic to humans (IARC group 2A). The present study was designed to investigate the cytotoxicity effect of EC on human hepatoma G2 (HepG2) cells. The results revealed that EC inhibited the viability of HepG2 cells significantly in a dose-dependent manner. Further analysis indicated that high concentration of EC induced cell apoptosis, inhibited the G1 to S phase transition along with increased expression of p53 and p21 and decreased the expression of cyclin E and Cdk 2, but no significant change in p27 expression was observed, which were evidenced by both real time PCR and western blotting analyses. Moreover, the results of the DCFH-DA assay suggested that oxidative stress was involved in the cytotoxic effects of EC. Altogether, the present work indicated that p21, cyclin E and Cdk2, which were regulated by p53, might account for the effect of EC on cell viability and cell cycle arrest, but p27 was not involved in the pathway in HepG2 cells treated with EC.
Starting Page	697
Ending Page	702
Page Count	6
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	5
Issue Number	2
Journal	Toxicology Research
DOI	10.1039/c5tx00453e
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Western blot Oxidative stress Cytotoxicity IARC International Agency for Research on Cancer P21 P53 Polymerase chain reaction Cyclin-dependent kinase 2 Carcinogen Ethyl carbamate Cell cycle Cyclin E Apoptosis Phase transition
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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