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.

氟化物在环境中无处不在。此外，饮用水是人类接触氟化物的主要来源。有趣的是，低浓度的氟化物对骨骼和牙齿的发育有益；然而，长期接触氟化物会对人体健康产生有害影响。此外，临床前研究将氟化物毒性与氧化应激、炎症和细胞凋亡联系起来。另一方面，众所周知，线粒体在活性氧的产生中起着关键作用。相比之下，氟化物对线粒体动力学、生物发生和线粒体自噬等过程的影响鲜为人知。这些过程调节线粒体的大小、含量和分布，它们的净化有助于抵抗活性氧的产生和细胞色素 c 的释放，从而使细胞存活。然而，适应不良反应可能会增强氟化物诱导的毒性。本综述简要介绍了氟化物引起的软组织和硬组织线粒体改变，包括肝脏、生殖器官、心脏、大脑、肺、肾脏、骨骼和牙齿。