Fluoride induced oxidative stress, immune system and apoptosis in animals: a review

Arup Giri, V. Bharti, Kunzes Angmo, Sahil Kalia, B. Kumar
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引用次数: 8

Abstract

Halfway through the twentieth century, fluoride piqued the interest of toxicologists due to its deleterious effects due to high concentrations in animals as well as in human populations suffering from several types of disorders and in in-vivo experimental models. Until the 1990s, the toxicity of fluoride was largely ignored due to its “good reputation” for preventing caries via topical application and in dental toothpaste. However, in the last decade, interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. In recent years, several investigations demonstrated that fluoride can induce oxidative stress and modulate intracellular redox homoeostasis; lipid peroxidation and protein carbonyl content, as well as alter gene expression and cause apoptosis. Genes modulated by fluoride include those related to the stress response, metabolic enzymes, the cell cycle, cell–cell communications and signal transduction. The primary purpose of this review is to examine recent findings on the effects of fluoride on oxidative stress, immune system and apoptosis in the animal as well as in human system.
氟诱导动物氧化应激、免疫系统和细胞凋亡的研究进展
20世纪中期,氟化物引起了毒理学家的兴趣,因为在动物和患有几种疾病的人群以及体内实验模型中,氟化物的浓度很高,会产生有害影响。直到20世纪90年代,氟化物的毒性在很大程度上被忽视了,因为它可以通过局部应用和牙膏来预防龋齿。然而,在过去的十年中,由于意识到这种元素即使在低剂量下也会与细胞系统相互作用,对其不良影响的兴趣重新浮出水面。近年来,一些研究表明,氟化物可诱导氧化应激并调节细胞内氧化还原稳态;脂质过氧化和蛋白质羰基含量,以及改变基因表达和引起细胞凋亡。受氟化物调节的基因包括与应激反应、代谢酶、细胞周期、细胞间通讯和信号转导有关的基因。本文综述了近年来氟对动物及人体氧化应激、免疫系统和细胞凋亡影响的研究进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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