粒体自噬
氟化物
线粒体
氧化应激
活性氧
线粒体生物发生
细胞生物学
毒性
化学
生物发生
神经毒性
氧化磷酸化
细胞凋亡
生物
生物化学
自噬
无机化学
有机化学
基因
作者
Sabino Hazael Avila-Rojas,Omar Emiliano Aparicio‐Trejo,Marco Sánchez-Guerra,Olivier Barbier
标识
DOI:10.1016/j.etap.2022.103916
摘要
Fluoride is ubiquitous in the environment. Furthermore, drinking water represents the main source of exposure to fluoride for humans. Interestingly, low fluoride concentrations have beneficial effects on bone and teeth development; however, chronic fluoride exposure has harmful effects on human health. Besides, preclinical studies associate fluoride toxicity with oxidative stress, inflammation, and apoptosis. On the other hand, it is well-known that mitochondria play a key role in reactive oxygen species production. By contrast, fluoride's effect on processes such as mitochondrial dynamics, biogenesis and mitophagy are little known. These processes modulate the size, content, and distribution of mitochondria and their depuration help to counter the reactive oxygen species production and cytochrome c release, thereby allowing cell survival. However, a maladaptive response could enhance fluoride-induced toxicity. The present review gives a brief account of fluoride-induced mitochondrial alterations on soft and hard tissues, including liver, reproductive organs, heart, brain, lung, kidney, bone, and tooth.
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