| Literature DB >> 30338467 |
Qin Wei1, Huidan Deng1, Hengmin Cui2,3,4, Jing Fang1,5, Zhicai Zuo1,5, Junliang Deng1,5, Yinglun Li1,5, Xun Wang1,5, Ling Zhao1,5.
Abstract
Fluorine or fluoride can have toxic effects on bone tissue and soft tissue at high concentrations. These negative effects include but not limited to cytotoxicity, immunotoxicity, blood toxicity, and oxidative damage. Apoptosis plays an important role in fluoride-induced toxicity of kidney, liver, spleen, thymus, bursa of Fabricius, cecal tonsil, and cultured cells. Here, apoptosis activated by high level of fluoride has been systematically reviewed, focusing on three pathways: mitochondrion-mediated, endoplasmic reticulum (ER) stress-mediated, and death receptor-mediated pathways. However, very limited reports are focused on the death receptor-mediated apoptosis pathways in the fluoride-induced apoptosis. Therefore, understanding and discovery of more pathways and molecular mechanisms of fluoride-induced apoptosis may contribute to designing measures for preventing fluoride toxicity.Entities:
Keywords: Apoptosis; Death receptor; ER stress; Fluoride; Mitochondrion; Pathway
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Year: 2018 PMID: 30338467 DOI: 10.1007/s11356-018-3406-z
Source DB: PubMed Journal: Environ Sci Pollut Res Int ISSN: 0944-1344 Impact factor: 4.223