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Environ Toxicol Pharmacol. 2014 Jul;38(1):332-40. doi: 10.1016/j.etap.2014.06.008. Epub 2014 Jun 27.

The effects and underlying mechanism of excessive iodide on excessive fluoride-induced thyroid cytotoxicity.

Author information

1
Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong District, Tianjin 300011, PR China; School of Public Health, Tianjin Medical University, 22 Qi Xiang Tai Road, Heping District, Tianjin 300070, PR China. Electronic address: liuhongliang@cdctj.gov.cn.
2
Tianjin Centers for Disease Control and Prevention, 6 Huayue Road, Hedong District, Tianjin 300011, PR China.
3
School of Public Health, Tianjin Medical University, 22 Qi Xiang Tai Road, Heping District, Tianjin 300070, PR China.
4
Department of Environmental Health and MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China.
5
Department of Environmental Health and MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Hubei, Wuhan 430030, PR China. Electronic address: wangaiguo@mails.tjmu.edu.cn.

Abstract

In many regions, excessive fluoride and excessive iodide coexist in groundwater, which may lead to biphasic hazards to human thyroid. To explore fluoride-induced thyroid cytotoxicity and the mechanism underlying the effects of excessive iodide on fluoride-induced cytotoxicity, a thyroid cell line (Nthy-ori 3-1) was exposed to excessive fluoride and/or excessive iodide. Cell viability, lactate dehydrogenase (LDH) leakage, reactive oxygen species (ROS) formation, apoptosis, and the expression levels of inositol-requiring enzyme 1 (IRE1) pathway-related molecules were detected. Fluoride and/or iodide decreased cell viability and increased LDH leakage and apoptosis. ROS, the expression levels of glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the combination of the two elements. Collectively, excessive fluoride and excessive iodide have detrimental influences on human thyroid cells. Furthermore, an antagonistic interaction between fluoride and excessive iodide exists, and cytotoxicity may be related to IRE1 pathway-induced apoptosis.

KEYWORDS:

Apoptosis; Cytotoxicity; Fluoride; IRE1; Iodide; Thyroid

PMID:
25104093
DOI:
10.1016/j.etap.2014.06.008
[Indexed for MEDLINE]

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