Zhang Yi, Wu Jialong, Jiang Lai, Lu Chenkang, Huang Zhengwei, Liu Bin
Department of Endodontics and Operative Dentistry, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
College of Stomatology, Shanghai Jiao Tong University, Shanghai, China.
Front Physiol. 2021 Dec 7;12:773055. doi: 10.3389/fphys.2021.773055. eCollection 2021.
As a strong oxidant, fluorine can induce oxidative stress resulting in cellular damage. Ferroptosis is an iron-dependent type of cell death caused by unrestricted lipid peroxidation (LPO) and subsequent plasma membrane rupture. This article indicated a relationship between fluorosis and ferroptosis. Evidence of the depletion of glutathione (GSH) and increased oxidized GSH can be found in a variety of organisms in high fluorine environments. Studies have shown that high fluoride levels can reduce the antioxidant capacity of antioxidant enzymes, while increasing the contents of reactive oxygen species (ROS) and malondialdehyde (MDA), resulting in oxidative stress and fluoride-induced oxidative stress, which are related to iron metabolism disorders. Excessive fluorine causes insufficient GSH, glutathione peroxidase (GSH-Px) inhibition, and oxidative stress, resulting in ferroptosis, which may play an important role in the occurrence and development of fluorosis.
作为一种强氧化剂,氟可诱导氧化应激,导致细胞损伤。铁死亡是一种由不受限制的脂质过氧化(LPO)和随后的质膜破裂引起的铁依赖性细胞死亡类型。本文表明了氟中毒与铁死亡之间的关系。在高氟环境中的多种生物体中都能发现谷胱甘肽(GSH)耗竭和氧化型GSH增加的证据。研究表明,高氟水平会降低抗氧化酶的抗氧化能力,同时增加活性氧(ROS)和丙二醛(MDA)的含量,导致氧化应激和氟诱导的氧化应激,这与铁代谢紊乱有关。过量的氟会导致GSH不足、谷胱甘肽过氧化物酶(GSH-Px)受到抑制以及氧化应激,从而导致铁死亡,这可能在氟中毒的发生和发展中起重要作用。
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