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 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.
Highlights
The aniline production worldwide surpassed 5.6 million tons in 2016 [1] and its industrial use is mainly in the manufacture of dyes, pigments, herbicides, fungicides, explosives, isocyanates, hydroquinones, and rubber chemicals
We found that the mitochondrial membrane potential in hepatocytes hepatocytes treated andμg/mL
Aniline induced apoptotic cellof death in a concentration-dependent manner. These findings suggest that hepatocytes undergo apoptosis and growth inhibition after exposure to aniline
Summary
The aniline production worldwide surpassed 5.6 million tons in 2016 [1] and its industrial use is mainly in the manufacture of dyes, pigments, herbicides, fungicides, explosives, isocyanates, hydroquinones, and rubber chemicals. ROS may be involved as specific messengers in the signal-transduction pathway and as inducers of DNA damage in some cases of apoptosis [15]. The results of aniline exposure leading to toxicity of primary cultured hepatocytes and DNA damage have been observed in our [16] and other [17,18] previous studies. Generation of ROS is one of the important biomarkers of cell proliferation and apoptosis [22]. It is unclear whether increasing ROS is a prerequisite for apoptosis and genotoxicity in hepatocytes. The focus of the present study was to investigate the possible involvement of oxidative stress in the effects of aniline exposure in primary cultured hepatocytes
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