Abstract
Toxic effects of the pyrethroid pesticide deltamethrin and water-borne fluoride, alone and in combination, on free radical mediated parameters are reported in rats. Twenty-four healthy adult Wistar rats of both sexes were divided into 4 groups with 6 rats in each group. Group I receiving no treatment served as the control. Group II and group III were orally administered deltamethrin (1/100 of LD50) and 20-ppm fluoride in their drinking water, respectively, for 28 days. An additional group IV was co-administered deltamethrin and fluoride at the same dosages as groups II and III. Enhanced oxidative stress was observed as shown by significantly increased lipid peroxidation and alterations in antioxidant parameters, especially in the fluoride- deltamethrin co-exposed group IV.
NOTE FROM FAN: Deltamethrin is a brominated pyrethroid insecticide. The specific foods that this pesticide is approved for in the U.S. are here.
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Effect of deltamethrin and fluoride co-exposure on the brain antioxidant status and cholinesterase activity in Wistar rats
The study evaluated the effect of commercial preparation of deltamethrin, Butox®, and fluoride (F-) co-exposure on the brain antioxidant status and cholinesterase activity in rats. Group A was untreated. Group B was gavaged Butox®, providing deltamethrin at the dose rate of 1.28 mg per kg body weight per day. Group
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Co-exposure to non-toxic levels of cadmium and fluoride induces hepatotoxicity in rats via triggering mitochondrial oxidative damage, apoptosis, and NF-kB pathways.
Fluoride (F) and cadmium (Cd) are two common water pollutants. There is low information about their co-exposure in low doses. So, in this study, we evaluated the combination effects of non-toxic doses of F and Cd and the possible mechanism of their combined interaction. Male rats were exposed to non-toxic
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Effects of chronic fluorosis on the brain.
Highlights Reviewing the mechanism of brain injury caused by chronic fluorosis is of great significance for protecting residents in fluorosis endemic areas. Abstract This article reviews the effects of chronic fluorosis on the brain and possible mechanisms. We used PubMed, Medline and Cochraine databases to collect data on fluorosis, brain injury,
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WITHDRAWN: Co-exposure effects of arsenic and fluoride on intelligence and oxidative stress in school-aged children: a cohort study.
This article has been withdrawn at the request of the editor. The Publisher apologizes for any inconvenience this may cause. as of November 6, 2020 Highlights Pioneer biomonitoring study on rural children to address As and F- co-exposure. High dental Fluorosis found in relation to urinary As and F- levels in
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Co-exposure to arsenic and fluoride to explore the interactive effect on oxidative stress and autophagy in myocardial tissue and cell
Highlights Arsenic and fluoride change mitochondrial ultrastructure in myocardium. Arsenic and fluoride induce myocardial oxidative stress and autophagy. There is interactive effect of arsenic and fluoride on myocardial injury. Co-contamination of arsenic and fluoride is widely distributed in groundwater. However, little is known about the interactively influence of arsenic and fluoride,
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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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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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