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.
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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
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Exocyclic DNA adducts in sheep with skeletal fluorosis resident in the proximity to the Portoscuso-Portovesme industrial estate on Sardinia Island, Italy
The mechanisms by which fluoride produces its toxic effects are still not clear. Therefore, we conducted a cross-sectional study to evaluate the fluoride-induced toxicity on randomly selected sheep with skeletal fluorosis resident near the large non-ferrous metallurgy Portoscuso-Portovesme industrial estate and the Carbonia and Gonnessa towns (control district) in respect
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Influence of methionine upon the concentration of malondialdehyde in the tissues and blood of rats exposed to sodium fluoride
The aim of the study has been to determine the influence upon the kidney, liver, and the blood prooxidative system, exercised by administration of methionine (Met), under conditions of oxidative stress induced by sodium fluoride (NaF).The experiment was carried out on Wistar FL rats (adult females) that, for 35 days,
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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N-acetylcysteine protects against fluoride-induced oxidative damage in primary rat hepatocytes
Fluoride induces the overproduction of free radicals, which might in turn affect various biochemical parameters. Therefore, the aim of this study was to elucidate the role of N-acetylcysteine (NAC) in decreasing fluoride-induced oxidative stress. The fluoride intoxicated (0.002; 0.082; 0.164mmol/l) rat hepatocytes was pre-treated (60min) and simultaneously treated with NAC
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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
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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
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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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