Dimethylacetamide-induced Hepatic Injury in Vitro: Mechanism and Potential Preventive Strategy.

Author: Xin LIU ¹ ; Wei GONG ¹ ; Yan Qiong XU ¹ ; Bao Li ZHU ¹
Author Information

1. Institute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing 210028, Jiangsu, China.
Publication Type:Journal Article
MeSH: Acetamides; toxicity; Apoptosis; drug effects; Cell Line; Chemical and Drug Induced Liver Injury; etiology; prevention & control; Glutathione; therapeutic use; Humans; Liver; drug effects
From: Biomedical and Environmental Sciences 2016;29(2):153-157
CountryChina
Language:English
Abstract: N,N-Dimethylacetamide (DMAc) is a widely used organic solvent in modern chemical industry with low to moderate hepatotoxicity to occupational health of employees. But so far, there are fewer and less conclusive data concerning its pathogenic mechanism in detail. In current study, the toxicity of DMAc was firstly investigated on human normal hepatocytes (LO-2), using a series of molecular biology measurements to ananlyze the effect and mechanism of DMAc-induced hepatic cell injury and explore effective prophylactic measures. We found that DMAc triggered LO-2 apoptosis in a obviously dose-dependent manner, caused by increased ROS generation and activation of Bcl-2 pathway. Significantly, glutathione (GSH) rather than vitamin C (Vit C) could partially inhibit DMAc-induced apoptosis thus showing potential as a effective precaution for workers.