EconPapers    
Economics at your fingertips  
 

Hepatic and Nephric NRF2 Pathway Up-Regulation, an Early Antioxidant Response, in Acute Arsenic-Exposed Mice

Jinlong Li, Xiaoxu Duan, Dandan Dong, Yang Zhang, Wei Li, Lu Zhao, Huifang Nie, Guifan Sun and Bing Li
Additional contact information
Jinlong Li: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China
Xiaoxu Duan: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China
Dandan Dong: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China
Yang Zhang: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China
Wei Li: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China
Lu Zhao: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China
Huifang Nie: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China
Guifan Sun: Environment and Non-Communicable Diseases Research Center, School of Public Health, China Medical University, Shenyang 110013, China
Bing Li: Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang 110013, China

IJERPH, 2015, vol. 12, issue 10, 1-15

Abstract: Inorganic arsenic (iAs), a proven human carcinogen, damages biological systems through multiple mechanisms, one of them being reactive oxygen species (ROS) production. NRF2 is a redox-sensitive transcription factor that positively regulates the genes of encoding antioxidant and detoxification enzymes to neutralize ROS. Although NRF2 pathway activation by iAs has been reported in various cell types, however, the experimental data in vivo are very limited and not fully elucidated in humans. The present investigation aimed to explore the hepatic and nephric NRF2 pathway upregulation in acute arsenic-exposed mice in vivo . Our results showed 10 mg/kg NaAsO 2 elevated the NRF2 protein and increased the transcription of Nrf2 mRNA, as well as up-regulated NRF2 downstream targets HO-1, GST and GCLC time- and dose-dependently both in the liver and kidney. Acute NaAsO 2 exposure also resulted in obvious imbalance of oxidative redox status represented by the increase of GSH and MDA, and the decrease of T-AOC. The present investigation reveals that hepatic and nephric NRF2 pathway expression is an early antioxidant defensive response upon iAs exposure. A better knowledge about the NRF2 pathway involvment in the cellular response against arsenic could help improve the strategies for reducing the cellular toxicity related to this metalloid.

Keywords: arsenic; ROS; NRF2; liver; kidney (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2015
References: View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.mdpi.com/1660-4601/12/10/12628/pdf (application/pdf)
https://www.mdpi.com/1660-4601/12/10/12628/ (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:gam:jijerp:v:12:y:2015:i:10:p:12628-12642:d:56968

Access Statistics for this article

IJERPH is currently edited by Ms. Jenna Liu

More articles in IJERPH from MDPI
Bibliographic data for series maintained by MDPI Indexing Manager ().

 
Page updated 2025-03-19
Handle: RePEc:gam:jijerp:v:12:y:2015:i:10:p:12628-12642:d:56968