Journal
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 25, Issue 34, Pages 33926-33935Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s11356-018-3406-z
Keywords
Fluoride; Apoptosis; Mitochondrion; ER stress; Death receptor; Pathway
Categories
Funding
- program for Changjiang scholars and innovative research team in university [IRT 0848]
- Shuangzhi Project of Sichuan Agricultural University [03572437, 03571800]
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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.
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