Morphometry of buccal mucosal cells in fluorosis – A new paradigm

Rao, Subramaniam M; Sherlin, Herald J; Anuja, N; Pratibha, R.; Premkumar, Priya; Chandrasekar, Thiruvengadam

doi:10.1177/0960327111400109

Cited by 11 publications

(5 citation statements)

References 8 publications

(13 reference statements)

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“…Fluoride is thought to inhibit the activity of antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase, and catalase [13]. Moreover, fluoride can alter glutathione levels, often resulting in excessive production of ROS at the mitochondrial level, leading to damage to cellular components [2,32,37].…”

Section: Discussionmentioning

confidence: 99%

Elemental Status and Lipid Peroxidation in the Blood of Children with Endemic Fluorosis

Tkachenko

Kurhaluk

Skaletska

et al. 2020

Biol Trace Elem Res

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The study aimed to assess the levels of trace elements, minerals, and toxic elements as well as lipid peroxidation biomarkers (lipid acyl hydroperoxides, 2-thiobarbituric acid reactive substances (TBARS)) in the blood of children with chronic fluorosis from endemic fluorosis areas (Sosnivka village, Lviv region, western Ukraine). The results were compared with healthy children from Staryi Sambir (Lviv region, western Ukraine), whose drinking water contained permissible levels (< 1 ppm) of fluoride. Thirty-one children from the Sosnivka village in the Lviv region, including 16 females and 15 males aged 7–10 years, with clinically diagnosed fluorosis, were recruited for the study. The children had been exposed to fluoride (> 1.5 ppm) through drinking water for more than 5 years. In the blood, eight macro- and microelements (calcium, zinc, potassium, iron, copper, selenium, manganese, chromium), five additional elements (sulfur, bromine, chlorine, nickel, strontium), and four toxic elements (lead, mercury, cadmium, mercury) were assessed with the X-ray fluorescence method. The results of our study demonstrated a 14-fold decrease in the copper level, a 2.5-fold decrease in the calcium and zinc levels, and a 2-fold decrease in the selenium level in the blood of children with chronic fluorosis compared with the healthy children from the non-fluorosis area. In turn, a 1.7- and 1.4-fold increase in the strontium and lead content, respectively, was noted. The sulfur, chlorine, potassium, calcium, copper, zinc, and selenium levels in the blood samples of children with chronic fluorosis were lower than the reference value. The children had higher blood TBARS levels, while the acyl hydroperoxide levels were non-significantly increased in comparison with healthy children living in the non-fluorosis area. Additionally, the bromine level was correlated positively with the selenium level and acyl hydroperoxides. However, more studies are needed to clarify the relationship between blood mineral status, oxidative stress biomarkers, and chronic fluorosis.

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Section: Discussionmentioning

confidence: 99%

Elemental Status and Lipid Peroxidation in the Blood of Children with Endemic Fluorosis

Tkachenko

Kurhaluk

Skaletska

et al. 2020

Biol Trace Elem Res

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“…Moreover, current literature about the genotoxic potential of fluoride in various cells and/or tissues is contradictory. Studies have shown that fluoride does not induce DNA damage [53–55], whereas other studies have observed fluoride-induced DNA damage in rat and human cells [52,56,57]. The possible mechanisms of fluoride-induced DNA damage are that (1) fluoride directly attacks the free amine groups present in DNA or (2) fluoride acts indirectly through free radicals to create DNA adducts at hydrogen bonds [58].…”

Section: Discussionmentioning

confidence: 99%

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

Suzuki¹,

Bandoski²,

Bartlett³

2015

Free Radical Biology and Medicine

191

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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 (γH2AX), 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 γH2AX 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 γH2AX 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.

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“…Rats exposed to fluoride at 150 mg/L contributed to cell cycle disruption of oral cells as depicted by a lower cell number at G 0 /G 1 as well as mitotic cells (68). In humans, exfoliate cytology in oral mucosa cells of individuals with diagnosed fluorosis pointed out apoptosis process as demonstrated by the increased nuclear size and decreased cell size (69). Toppical application of 1.23% acidulated phosphate fluoride to oral mucosa of rabbits after 1.…”

Section: In Vivo Studiesmentioning

confidence: 98%

Fluoride Induces Apoptosis in Mammalian Cells: In Vitro and In Vivo Studies

Ribeiro

Cardoso

Yujra

et al. 2017

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Apoptosis is genetically programmed cell death, an irreversible process of cell senescence with characteristic features different from other cellular mechanisms of death such as necrosis. In the last years, apoptosis has been extensively studied in the scientific literature, because it has been established that apoptosis plays a crucial role following the time course of chronic degenerative diseases, such as cancer. Thus, several researchers have strugged to detect what chemical agents are able to inter fere with the apoptotic process. Thus, the purpose of this literature review is to assess if fluoride induces apoptosis in mammalian cells using in vivo and in vitro test systems. Certain mammalian cell types such as oral cells, blood and brain were exetensively investigated; the results showed that fluoride is able to induce apoptosis in both intrinsinc and extrinsic pathways. Moreover, other cells types have been poorly investigated such as bone, kidney and reproductive cells with conflicting results so far. Therefore, this area needs further investigation for the safety of human populations exposed to fluoride in a chronic way, as for example in developing countries.

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Morphometry of buccal mucosal cells in fluorosis – A new paradigm

Cited by 11 publications

References 8 publications

Elemental Status and Lipid Peroxidation in the Blood of Children with Endemic Fluorosis

Elemental Status and Lipid Peroxidation in the Blood of Children with Endemic Fluorosis

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

Fluoride Induces Apoptosis in Mammalian Cells: In Vitro and In Vivo Studies

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