Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes
Yue Wang,
Hong Gao,
Xiao-Lin Na,
Shu-Ying Dong,
Hong-Wei Dong,
Jia Yu,
Li Jia and
Yong-Hui Wu
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Yue Wang: Department of Occupational Health, College of Public Health, Harbin Medical University, Harbin 150086, China
Hong Gao: Department of Sanitary Microorganisms, College of Public Health, Harbin Medical University, Harbin 150086, China
Xiao-Lin Na: Department of Environmental Health, College of Public Health, Harbin Medical University, Harbin 150086, China
Shu-Ying Dong: Department of Environmental Health, College of Public Health, Harbin Medical University, Harbin 150086, China
Hong-Wei Dong: Department of Occupational Health, College of Public Health, Harbin Medical University, Harbin 150086, China
Jia Yu: Department of Environmental Health, College of Public Health, Harbin Medical University, Harbin 150086, China
Li Jia: Department of Environmental Health, College of Public Health, Harbin Medical University, Harbin 150086, China
Yong-Hui Wu: Department of Occupational Health, College of Public Health, Harbin Medical University, Harbin 150086, China
IJERPH, 2016, vol. 13, issue 12, 1-11
Abstract:
The toxicity and carcinogenicity of aniline in humans and animals have been well documented. However, the molecular mechanism involved in aniline-induced liver toxicity and carcinogenesis remains unclear. In our research, primary cultured hepatocytes were exposed to aniline (0, 1.25, 2.50, 5.0 and 10.0 ?g/mL) for 24 h in the presence or absence of N -acetyl- l -cysteine (NAC). Levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH), activities of superoxide dismutase (SOD) and catalase (CAT), mitochondrial membrane potential, DNA damage, cell viability, and apoptosis were detected. Levels of ROS and MDA were significantly increased and levels of GSH and CAT, activity of SOD, and mitochondrial membrane potential in hepatocytes were significantly decreased by aniline compared with the negative control group. The tail moment and DNA content of the tail in exposed groups were significantly higher than those in the negative control group. Cell viability was reduced and apoptotic death was induced by aniline in a concentration-dependent manner. The phenomena of ROS generation, oxidative damage, loss of mitochondrial membrane potential, DNA damage and apoptosis could be prevented if ROS inhibitor NAC was added. ROS generation is involved in the loss of mitochondrial membrane potential and DNA injury, which may play a role in aniline-induced apoptosis in hepatocytes. Our study provides insight into the mechanism of aniline-induced toxicity and apoptosis of hepatocytes.
Keywords: aniline; apoptosis; reactive oxygen species; hepatocytes (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:gam:jijerp:v:13:y:2016:i:12:p:1188-:d:84133
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