NDLI: Fluoride induces oxidative damage and SIRT1/autophagy through ROS-mediated JNK signaling.

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Fluoride induces oxidative damage and SIRT1/autophagy through ROS-mediated JNK signaling.

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Fluoride induces oxidative damage and SIRT1/autophagy through ROS-mediated JNK signaling.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Suzuki, Maiko Bandoski, Cheryl Bartlett, John D.
Description	Country affiliation: Morocco Author Affiliation: Suzuki M ( Department of Mineralized Tissue Biology, The Forsyth Institute & Harvard School of Dental Medicine, 245 First Street, Cambridge, MA.); Bandoski C ( Department of Mineralized Tissue Biology, The Forsyth Institute & Harvard School of Dental Medicine, 245 First Street, Cambridge, MA.); Bartlett JD ( Department of Mineralized Tissue Biology, The Forsyth Institute & Harvard School of Dental Medicine, 245 First Street, Cambridge, MA. Electronic address: jbartlett@forsyth.org.)
Abstract	Fluoride is an effective caries prophylactic, but at high doses can also be an environmental health hazard. Acute or chronic exposure to high fluoride doses can result in dental enamel and skeletal and soft tissue fluorosis. Dental fluorosis is manifested as mottled, discolored, porous enamel that is susceptible to dental caries. Fluoride induces cell stress, including endoplasmic reticulum stress and oxidative stress, which leads to impairment of ameloblasts responsible for dental enamel formation. Recently we reported that fluoride activates SIRT1 and autophagy as an adaptive response to protect cells from stress. However, it still remains unclear how SIRT1/autophagy is regulated in dental fluorosis. In this study, we demonstrate that fluoride exposure generates reactive oxygen species (ROS) and the resulting oxidative damage is counteracted by SIRT1/autophagy induction through c-Jun N-terminal kinase (JNK) signaling in ameloblasts. In the mouse-ameloblast-derived cell line LS8, fluoride induced ROS, mitochondrial damage including cytochrome-c release, up-regulation of UCP2, attenuation of ATP synthesis, and H2AX phosphorylation (Î³H2AX), which is a marker of DNA damage. We evaluated the effects of the ROS inhibitor N-acetylcysteine (NAC) and the JNK inhibitor SP600125 on fluoride-induced SIRT1/autophagy activation. NAC decreased fluoride-induced ROS generation and attenuated JNK and c-Jun phosphorylation. NAC decreased SIRT1 phosphorylation and formation of the autophagy marker LC3II, which resulted in an increase in the apoptosis mediators Î³H2AX and cleaved/activated caspase-3. SP600125 attenuated fluoride-induced SIRT1 phosphorylation, indicating that fluoride activates SIRT1/autophagy via the ROS-mediated JNK pathway. In enamel organs from rats or mice treated with 50, 100, or 125 ppm fluoride for 6 weeks, cytochrome-c release and the DNA damage markers 8-oxoguanine, p-ATM, and Î³H2AX were increased compared to those in controls (0 ppm fluoride). These results suggest that fluoride-induced ROS generation causes mitochondrial damage and DNA damage, which may lead to impairment of ameloblast function. To counteract this impairment, SIRT1/autophagy is induced via JNK signaling to protect cells/ameloblasts from fluoride-induced oxidative damage that may cause dental fluorosis.
File Format	HTM / HTML
ISSN	08915849
Volume Number	89
e-ISSN	18734596
Journal	Free Radical Biology and Medicine
Language	English
Publisher	Elsevier
Publisher Date	2015-12-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Free radicals biology Autophagy Fluorides Pharmacology Jnk Mitogen-activated Protein Kinases Metabolism Oxidative Stress Drug Effects Phosphates Reactive Oxygen Species Sirtuin 1 Animals Apoptosis Blotting, Western Cell Proliferation Cells, Cultured Dna Damage Fluorescent Antibody Technique Immunoenzyme Techniques Genetics Male Mice Mice, Inbred C57bl Mitochondria Pathology Phosphorylation Rna, Messenger Rats Rats, Sprague-dawley Real-time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Journal Article Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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