Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 87, Issue -, Pages 80-88Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2012.09.028
Keywords
Selenite toxicity; PLHC-1; Apoptosis; Reactive oxygen species; Mitochondrial membrane potential
Categories
Funding
- NIH [5P20RR016477]
- HRSA grants Center for Bioengineering and Biomanufacturing Commercialization
Ask authors/readers for more resources
Elevated concentration of selenium poses a toxic threat to organisms inhabiting aquatic ecosystems influenced by excessive inputs from anthropogenic sources. Selenium is also an essential micronutrient in living things, particularly in fish, and provides antioxidant properties to tissues. Whole fish and hepatocytes in primary culture show selenite toxicity above threshold levels. The present study was designed to investigate the process by which selenite exposure causes cellular toxicity and apoptotic and necrotic cell death in fish hepatoma cell line PLHC-1. PLHC-1 cells were exposed to various selenite concentrations (1, 10, 50 and 100 mu M) for 10, 20 and 40 h intervals. The 24 h inhibitory concentration 50 (IC50) of selenite in PLHC-1 cell line was found to be 237 mu M. Flow cytometery data showed that selenite exposed cells promote apoptotic and necrotic mediated cell death when selenite concentrations were >= 10 mu M compared to control. Selenite exposure was associated with a significant increase of caspase-3 activities suggesting the induction of apoptosis. Selenite exposure at high levels ( >= 10 mu M) and longer exposure times ( >= 20 h) induces mitochondria] membrane potential damage (Delta Psi(m)), DNA damage and elevated production of ROS which could be associated with cell death. (C) 2012 Elsevier Inc. All rights reserved.
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