Abstract
Hydrofluoric acid elicits cell cycle arrest through a mechanism that has long been presumed to be linked with the high affinity of fluoride to metals. However, we have recently found that the acid stress from fluoride exposure is sufficient to elicit many of the hallmark phenotypes of fluoride toxicity. Here we report the systematic screening of genes involved in fluoride resistance and general acid resistance using a genome deletion library in Saccharomyces cerevisiae. We compare these to a variety of acids – 2,4-dinitrophenol, FCCP, hydrochloric acid, and sulfuric acid – none of which has a high metal affinity. Pathways involved in endocytosis, vesicle trafficking, pH maintenance, and vacuolar function are of particular importance to fluoride tolerance. The majority of genes conferring resistance to fluoride stress also enhanced resistance to general acid toxicity. Genes whose expression regulate Golgi-mediated vesicle transport were specific to fluoride resistance, and may be linked with fluoride-metal interactions. These results support the notion that acidity is an important and underappreciated principle underlying the mechanisms of fluoride toxicity.
•• The full article is available in pdf (see attachment) and also online at https://www.frontiersin.org/articles/10.3389/fmicb.2020.01410/full
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Fluoride metabolism
Knowledge of all aspects of fluoride metabolism is essential for comprehending the biological effects of this ion in humans as well as to drive the prevention (and treatment) of fluoride toxicity. Several aspects of fluoride metabolism - including gastric absorption, distribution and renal excretion - are pH-dependent because the coefficient
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Fluoride exposure, dopamine relative gene polymorphism and intelligence: A cross-sectional study in China.
Highlights Urine fluoride was inversely associated with IQ. IQ of children with high-activity MAOA genotype was lower than IQ of those with low-activity or female heterozygote genotype. DAT1 and MAOA gene polymorphism modify the effects of UF on IQ. UF, ANKK1, COMT and MAOA have a high-dimensional interaction on
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[Genetic markers of occupational susceptibility to fluorosis].
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A deep insight into the transcriptome of midgut and fat body reveals the toxic mechanism of fluoride exposure in silkworm.
Highlights 200 mg/L fluoride soaked mulberry leaves exposure inhibits the growth of silkworm larvae. RNA-seq reveals the toxic mechanism of fluoride exposure in silkworm. Fluoride damages oxidative phosphorylation process and disturbs MAPK signaling pathway. The identification of potential transports for fluoride. Fluoride generally exists in the natural environment, and has
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Evaluation of genetic polymorphisms in MMP2, MMP9 and MMP20 in Brazilian children with dental fluorosis.
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