Abstract
The effects of sodium fluoride (NaF) exposure on the induction of oxidative stress and alteration of gene expressions were studied in the liver of female zebrafish (Danio rerio). Zebrafish, exposed to 15 ppm NaF for 30 and 90 days, exhibited liver histopathology including hyperplassia, cytoplasmic degeneration and nuclear fragmentation. Antioxidant enzyme (GST, CAT, SOD) activities in the liver altered significantly; the mRNA levels for the genes encoding antioxidant proteins, such as Gst, Cat, Cu/ZnSod, MnSod as well as Gpx were significantly upregulated at 30 days NaF-treatment along with the stress marker gene Hsp70 and phase I detoxyfying gene Cyp1A1. Moreover, the transcriptional pattern of Ucp2, related to mitochondrial reactive oxygen species (ROS) production, upregulated significantly at 90 days NaF-treatment. ROS generation was evidensed by fluoroscence microscopy. The results of this study will help to understand the mechanism of oxidative stress induced by NaF in fish.
*Abstract online at https://link.springer.com/article/10.1007%2Fs00128-014-1271-0
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Challenges of fluoride pollution in environment: Mechanisms and pathological significance of toxicity – A review.
Highlights Fluoride exposure induces mitochondrial function dysfunction. Fluoride exposure mediates organs injury involved in apoptosis and autophagy. Fluoride exposure induces inflammatory reaction. Fluoride exposure results changes in intestinal microbial abundance. Fluoride is an important trace element in the living body. A suitable amount of fluoride has a beneficial effect on
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Self-recovery study of fluoride-induced ferroptosis in the liver of zebrafish (Danio rerio).
Highlights Self-recovery relieved F-induced ferroptosis in zebrafish. Self-recovery reduced the histopathological damage and oxidative stress. Self-recovery reversed levels of FTH and SLC7A11, Fe2+ metabolism and GSH synthesis. Lipid peroxidation, Fe2+ metabolism related to self-recovery alleviating F toxicity. Ferroptosis plays a key role in fluorosis in aquatic organisms, but whether it
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Effect of long term fluoride exposure on lipid composition in rat liver
Chronic fluorosis can severely damage many systems of human body, but its pathogenesis is unclear. Normal composition and structure of cellular membrane lipids are a basic factor to maintain cell function. In this investigation, cellular membrane lipids of the liver were analysed after a long term fluoride treatment for rats
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Chronic exposure to environmentally relevant concentration of fluoride alters Ogg1 and Rad51 expressions in mice: Involvement of epigenetic regulation.
Highlights Almost 200 million people all over the world are facing dreadful effects of fluoride. Mice were treated orally with environmentally relevant concentration of fluoride for 8 months. Fluoride treatment resulted into histopathology, oxidative stress response and transcriptional alterations of Ogg1 and Rad51. DNA fragmentations and apoptosis induction was
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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
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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Fluoride & Oxidative Stress
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