Abstract
Fluoride is ubiquitous in the environment. Furthermore, drinking water represents the main source of exposure to fluoride for humans. Interestingly, low fluoride concentrations have beneficial effects on bone and teeth development; however, chronic fluoride exposure has harmful effects on human health. Besides, preclinical studies associate fluoride toxicity with oxidative stress, inflammation, and apoptosis. On the other hand, it is well-known that mitochondria play a key role in reactive oxygen species production. By contrast, fluoride’s effect on processes such as mitochondrial dynamics, biogenesis and mitophagy are little known. These processes modulate the size, content, and distribution of mitochondria and their depuration help to counter the reactive oxygen species production and cytochrome c release, thereby allowing cell survival. However, a maladaptive response could enhance fluoride-induced toxicity. The present review gives a brief account of fluoride-induced mitochondrial alterations on soft and hard tissues, including liver, reproductive organs, heart, brain, lung, kidney, bone, and tooth.
Keywords
*Original abstract online at https://www.sciencedirect.com/science/article/pii/S1382668922001090?via%3Dihub
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Fluoride in Drinking Water: A Scientific Review of EPA’s Standards.
Excerpts: Summary Under the Safe Drinking Water Act, the U.S. Environmental Protection Agency (EPA) is required to establish exposure standards for contaminants in public drinking-water systems that might cause any adverse effects on human health. These standards include the maximum contaminant level goal (MCLG), the maximum contaminant level (MCL), and the secondary
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Necessity to Pay Attention to the Effects of Low Fluoride on Human Health: an Overview of Skeletal and Non-skeletal Damages in Epidemiologic Investigations and Laboratory Studies.
Due to the implementation of water improvement and fluoride reduction plans supported by central and local governments in recent years, areas with high fluoride exposure are being gradually decreased. Therefore, it is of practical importance to study the effect of low fluoride on human health. Epidemiologic investigations and in vivo
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The effects of the inhalation of hydrogen fluoride. I. The response following exposure to high concentrations.
The effects of inhalation exposure to hydrogen-fluoride (7664-39-3) (HF) were examined in New-Zealand-white-rabbits and guinea-pigs. Animals were exposed to HF in enclosed chambers at concentrations ranging from 8 to 0.024 milligrams per liter (mg/l) for 5 minutes to 41 hours. Mortality rates were recorded, general physical conditions were monitored, and
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Effect of fluoride on enzymes from serum, liver, kidney, skeletal and heart muscles of mice.
White mice maintained on water containing 100 ppm NaF showed changes in the enzyme level in serum, liver, kidney, heart and skeletal muscles. Enzymes studies were alkaline phosphatase (ALP), acid phosphatase (AcP), glutamate-oxalacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), lactic dehydrogenase (LDH), isocitric dehydrogenase (ICDH) and cholinesterase (CE). AcP was markedly
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Systematic impacts of fluoride exposure on the metabolomics of rats.
Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,
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