Journal
JOURNAL OF APPLIED TOXICOLOGY
Volume 43, Issue 7, Pages 1083-1094Publisher
WILEY
DOI: 10.1002/jat.4445
Keywords
apoptosis; benzo[b]fluoranthene; bronchial epithelial cells; cell cycle; human lung epithelial cells; mitochondrial membrane potential
Categories
Ask authors/readers for more resources
This study investigated the cytotoxicity of BbF on human lung epithelial cells and bronchial epithelial cells, and found that BbF inhibited cell growth and induced apoptosis through the ROS-mediated mitochondria disruption pathway.
Benzo[b]fluoranthene (BbF) is a common constituent of polycyclic aromatic hydrocarbons (PAHs). While numerous studies revealed adverse effects of PAHs on human health, the health effects of individual PAHs differ, and few investigations were performed on BbF. Therefore, the present study established cytotoxicity models of human lung epithelial cells (BEAS-2B cells) and bronchial epithelial cells (16HBE cells) exposed to BbF (10, 20, and 40 mu M) for 24 h to reveal the mechanisms. Results from cytotoxicity and proliferation studies demonstrated that BbF inhibited cell growth in a dose-dependent manner. Flow cytometric analysis showed that BbF induced the appearance of a sub G1 peak, S-phased arrest, and apoptosis in both cells. Mechanistic investigations illustrated that BbF promoted reactive oxygen species (ROS) production, altered the expression of oxidative stress indicators, and decreased mitochondrial membrane potential. BbF also interfered with the expression of regulators associated with mitochondria disruption pathway. Taken together, these results strongly suggested that BbF inhibited cell growth and induced apoptosis in human airway epithelial cells via ROS-mediated mitochondria disruption.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available