A brief review on experimental fluorosis

Perumal, Ekambaram; Paul, Vanaja; Govindarajan, Vimal; Panneerselvam, Lakshmikanthan

doi:10.1016/j.toxlet.2013.09.005

Cited by 161 publications

(74 citation statements)

References 150 publications

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“…Chronic fluoride intoxication has been reported to cause toxicity to the liver (Gazzano et al, 2010;Perumal et al, 2013). In the present study, daily exposure to 100 mg/L NaF for 5 weeks was found to cause liver toxicity, as evidenced by strong increases in AST and ALT levels, and hepatocyte degeneration.…”

Section: Discussionsupporting

confidence: 46%

“…A substantial body of evidence has confirmed that chronic fluorosis produces harmful effects on teeth and bones, as well as on other organs including the heart, liver, and kidneys (Gazzano et al, 2010;Perumal et al, 2013). Hepatotoxicity is of particular concern to the public as the liver is the main organ responsible for the metabolism of fluoride ingested through the gastrointestinal tract.…”

Section: Introductionmentioning

confidence: 99%

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Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract

Niu

He²,

et al. 2018

J. Toxicol. Sci.

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-Emerging evidence has demonstrated that iron overload plays an important role in oxidative stress in the liver. This study aimed to explore whether fluoride-induced hepatic oxidative stress is associated with iron overload and whether grape seed proanthocyanidin extract (GSPE) alleviates oxidative stress by reducing iron overload. Forty Kunming male mice were randomly divided into 4 groups and treated for 5 weeks with distilled water (control), sodium fluoride (NaF) (100 mg/L), GSPE (400 mg/kg bw), or NaF (100 mg/L) + GSPE (400 mg/kg bw). Mice exposed to NaF showed typical poisoning changes of morphology, increased aspartate aminotransferase and alanine aminotransferase activities in the liver. NaF treatment also increased MDA accumulation, decreased GSH-Px, SOD and T-AOC levels in liver, indicative of oxidative stress. Intriguingly, all these detrimental effects were alleviated by GSPE. Further study revealed that NaF induced disorders of iron metabolism, as manifested by elevated iron level with increased hepcidin but decreased ferroportin expression, which contributed to hepatic oxidative stress. Importantly, the iron dysregulation induced by NaF could be normalized by GSPE. Collectively, these data provide a novel insight into mechanisms underlying fluorosis and highlight the potential of GSPE as a naturally occurring prophylactic treatment for fluoride-induced hepatotoxicity associated with iron overload.

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Section: Discussionsupporting

confidence: 46%

Section: Introductionmentioning

confidence: 99%

Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract

Niu

He²,

et al. 2018

J. Toxicol. Sci.

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“…On the other hand, low doses of fluoride could contribute to prevent dental and bony diseases, achieved by modifying water fluoridation programs (1.0 mg/L) and processing ingredients in toothpastes and gels [10]. In recent reports, accumulated toxic factors of NaF and SO 2 in environment could induce morphological and genetic alterations in respiratory, reproductive, immune, and cardiovascular systems [11][12][13][14][15], widely existing in bone and tooth of animals and humanity [16]. Furthermore, cautions must be exercised when evaluating toxic effects.…”

Section: Introductionmentioning

confidence: 99%

Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Gao

Liang

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: We investigated the combined toxic effect of sodium fluoride (NaF) and sulfur dioxide (SO₂) on kidney morphological changes and DNA damage in male Wistar rats. Methods: In this study we selected totally 96 male Wistar rats (12-week-old) then randomly group-housed them into four cages, treated with deionized water, NaF, SO₂ and co-treatment of NaF and SO₂ respectively. Morphological changes of kidney were detected by hematoxylin and eosin (H&E) staining at 2, 4, 6 and 8 weeks. Correspondingly, tailing ratio and comet length were measured by BAB Bs Comet Assay System, including DNA damage special unit were calculated to evaluate the grades of kidney DNA damage at the same time. Results: Treated groups showed a body weight decrease when compared to control group. However, no significant difference in the relative weight of kidney was found in all four groups. It is noteworthy that at 2, 4, 6 and 8 weeks after exposure, the morphological alteration of renal tubules were observed in all treated groups, especially in group-IV. Also, at 4 and 6 weeks, notable DNA damage was found in all treated groups, as assessed by significantly increasing trend of comet length tailing ratio. Conclusion: The study manifests that presence of NaF and SO₂ will not only induce renal tissue lesions but also impact DNA integrity. In addition, this combined exposure exhibits a synergistic effect, characterizing a dose-dependence and time correlation. These findings may provide novel insights regarding perturbations of DNA damage and its functions as a potential new mechanism, by which cautious interpretation of NaF and SO₂ co-exposure evolved in both animals and human beings is necessary.

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“…In the US alone, it has been estimated that ~85% of adults have 44 experienced enhanced tooth decay owing to F -deficiency (Perumal et al, 2013;Su et 45 al., 2013). However, the therapeutic range is very narrow and in excess can disrupt 46 thyroid metabolism, impair brain function, cause bone deformities, and in severe 47 cases result in paralysis and cancer (Harrison, 2005;Meenakshi and Maheshwari, 48 2006; Viswanathan et al, 2009).…”

mentioning

confidence: 99%

Novel DGT method with tri-metal oxide adsorbent for in situ spatiotemporal flux measurement of fluoride in waters and sediments

et al. 2016

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This is an open access article published under a Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits distribution and reproduction for non-commercial purposes, provided the author and source are cited. General rightsCopyright for the publications made accessible via the Queen's University Belfast Research Portal is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights.Take down policy The Research Portal is Queen's institutional repository that provides access to Queen's research output. Every effort has been made to ensure that content in the Research Portal does not infringe any person's rights, or applicable UK laws. If you discover content in the Research Portal that you believe breaches copyright or violates any law, please contact openaccess@qub.ac.uk.

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A brief review on experimental fluorosis

Cited by 161 publications

References 150 publications

Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract

Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract

Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Novel DGT method with tri-metal oxide adsorbent for in situ spatiotemporal flux measurement of fluoride in waters and sediments

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