期刊
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
卷 2017, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2017/9251303
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资金
- NIH grants from the National Center for Research Resources [5P20RR02194007]
- National Institute of General Medical Sciences [8P20GM103549-07]
- National Institute of Environmental Health Sciences [R56ES022665, R21ES026752]
- Training Program in Environmental Toxicology [T32ES007079-26A2]
- Internal Lied Basic Science Grant Program of the KUMC Research Institute
- NIH Clinical and Translational Award [UL1TR000001]
- Biomedical Research Training Program (BRTP) from the University of Kansas Medical Center
Arsenite is a known carcinogen and its exposure has been implicated in a variety of noncarcinogenic health concerns. Increased oxidative stress is thought to be the primary cause of arsenite toxicity and the toxic effect is thought to be linear with detrimental effects reported at all concentrations of arsenite. But the paradigm of linear dose response in arsenite toxicity is shifting. In the present study we demonstrate that arsenite effects on mitochondrial respiration in primary hepatocytes follow a nonlinear dose response. In vitro exposure of primary hepatocytes to an environmentally relevant, moderate level of arsenite results in increased oxidant production that appears to arise from changes in the expression and activity of respiratory Complex I of the mitochondrial proton circuit. In primary hepatocytes the excess oxidant production appears to elicit adaptive responses that promote resistance to oxidative stress and a propensity to increased proliferation. Taken together, these results suggest a nonlinear dose-response characteristic of arsenite with low-dose arsenite promoting adaptive responses in a process known as mitohormesis, with transient increase in ROS levels acting as transducers of arsenite-induced mitohormesis.
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