Abstract

Sodium fluoride (NaF), one of the most frequently used fluoride compound is composed of Na+ and F-. Apart from its use in water fluoridation, NaF also acts as a major component for different dental products like toothpastes, gels and mouth rinses etc. The present study was carried out to explore the toxic impact of chronic NaF exposure on a non-target organism, Drosophila melanogaster. The larvae exposed to different concentrations of NaF through food showed a significant increase in HSP70 expression both qualitatively and quantitatively. The altered tail length and tail intensity in Comet assay validate the increased DNA damage in treated larvae. The activity of AChE, oxidative stress marker enzymes, phase I and phase II detoxifying enzymes were found to be significantly inhibited in the treated larvae when compared to control though there was no evidence of dose dependent change in each case. The alterations in the mentioned parameters can be due to increased body Fluoride ion (F-) concentration since the analysis with ion electrode analyzer revealed that F- concentration increased significantly with NaF treatment. Hence, the results suggest that D. melanogaster manifest prominent toxic response when subjected to chronic exposure to sub-lethal NaF concentrations.

• Related Studies :

  • DNA damage, apoptosis and cell cycle changes induced by fluoride in rat oral mucosal cells and hepatocytes

    AIM:  To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes. METHODS:  Ten male SD rats weighing 80-120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in

  • Co-exposure to arsenic and fluoride on oxidative stress, glutathione linked enzymes, biogenic amines and DNA damage in mouse brain.

    We studied the effects of combined exposure to arsenic and fluoride on (i) brain biogenic amines, oxidative stress and its correlation with glutathione and linked enzymes; (ii) alterations in the structural integrity of DNA; and (iii) brain and blood arsenic and fluoride levels. Efficacy of alpha-tocopherol in reducing these changes

  • Ameliorative effects of N-acetylcysteine on fluoride-induced oxidative stress and DNA damage in male rats' testis

    This study was to elucidate DNA damage in rats treated with sodium fluoride (NaF) by performing 8-Hydroxy-2-deoxyguanosine (8-OHdG) immunohistochemical staining assays on seminiferous tubules of rats' testis, and also to evaluate the protective effects of N-acetylcysteine (NAC) on spermatogenesis. Male Sprague Dawley (SD) rats were exposed to a single dose

  • Genotoxic effect and rat hepatocyte death occurred after oxidative stress induction and antioxidant gene downregulation caused by long term fluoride exposure

    Studies focusing on possible genotoxic effects of excess fluoride are contradictory and inconclusive. Currently, studies have reported a probable link to oxidative stress, DNA damage and apoptosis induced by fluoride in rat hepatocytes. We developed an in vivostudy administering three doses of fluoride by gavage given to rats for 60 day.

  • Epigallocatechin gallate effectively ameliorates fluoride-induced oxidative stress and DNA damage in the liver of rats

    RETRACTION MADE IN MARCH 2020: The Editors-in-Chief of the Canadian Journal of Physiology and Pharmacology were alerted to cases of image manipulation in the article entitled “Epigallocatechin gallate effectively ameliorates fluoride-induced oxidative stress and DNA damage in the liver of rats” (see http://dx.doi.org/10.1139/cjpp-2012-0347). Thus, the Editors-in-Chief have retracted the paper from

• Related FAN Content :

  • Fluoride & Oxidative Stress

    A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure

  • Fluoride/Osteosarcoma Link Is Biologically Plausible

    The "biological plausiblility" of a fluoride-osteosarcoma link is widely acknowledged in the scientific literature. The biological plausibility centers around three facts: 1) Bone is the principal site of fluoride accumulation, particularly during the growth spurts of childhood; 2) Fluoride is a mutagen when present at sufficient concentrations, and 3) Fluoride can stimulate the proliferation of osteoblasts (bone-forming cells).

  • Fluoride's Mutagenicity: The "Oral Health Research Institute's" Studies

    Although many in vitro and in vivo studies have detected mutagenic effects from fluoride exposure, the Oral Health Research Institute at Indiana University's School of Dentistry has repeatedly failed to find any such effect in multiple studies on the subject.

  • Fluoride content in tea and its relationship with tea quality.

    J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected

  • Fluoride's Mutagenicity: In vitro Studies

    According to the National Toxicology Program, "the preponderance of evidence" from laboratory "in vitro" studies indicate that fluoride is a mutagenic compound. Many substances which are mutagens, are also carcinogens (i.e. they can cause cancer). As is typical for in vitro studies, the concentrations of fluoride that have generally been tested