Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes

Autor: Yong-Hui Wu, Jia Yu, Li Jia, Yue Wang, Shu-Ying Dong, Xiao-Lin Na, Hong Gao, Hong-Wei Dong
Rok vydání: 2016
Předmět:
Male
0301 basic medicine
Cell Survival
DNA damage
Health
Toxicology and Mutagenesis

lcsh:Medicine
medicine.disease_cause
Article
Rats
Sprague-Dawley

Superoxide dismutase
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Malondialdehyde
medicine
Animals
Humans
aniline
Viability assay
Cells
Cultured

Membrane Potential
Mitochondrial

reactive oxygen species
chemistry.chemical_classification
Reactive oxygen species
Aniline Compounds
biology
Superoxide Dismutase
lcsh:R
apoptosis
Public Health
Environmental and Occupational Health

Glutathione
Catalase
Molecular biology
hepatocytes
Acetylcysteine
Rats
Oxidative Stress
030104 developmental biology
chemistry
Apoptosis
030220 oncology & carcinogenesis
Hepatocytes
biology.protein
Environmental Pollutants
Oxidation-Reduction
Oxidative stress
Zdroj: International Journal of Environmental Research and Public Health
International Journal of Environmental Research and Public Health, Vol 13, Iss 12, p 1188 (2016)
International Journal of Environmental Research and Public Health; Volume 13; Issue 12; Pages: 1188
ISSN: 1660-4601
DOI: 10.3390/ijerph13121188
Popis: 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 μg/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.
Databáze: OpenAIRE