Abstract

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    The US National Toxicology Program has shown equivocal evidence of carcinogenic activity of sodium fluoride (NaF) in male F344/N rats based on the occurrence of five osteosarcomas in treated animals. In the study the osteosarcomas developed mainly in the rat vertebrae. To provide a possible mechanistic basis for the observed

  • Analysis of chromosomal abnormalities at anaphase-telophase induced by sodium fluoride in vitro

    Don Chinese-hamster cells were treated with 25, 50, or 75 micrograms/milliliter (microg/ml) of sodium-fluoride (7681494) to determine the chromosomal effects of fluoride exposure on these cells. Cultures were assayed at 12, 24, and 36 hours after initiation of treatment. Chromosomal aberrations were recorded for all the concentrations used. Maximum effect

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    On the basis of observations that endemic fluorosis occurs more often in malnourished populations, a series of studies tested the hypothesis that deficient dietary intake of calcium, protein or energy affects fluoride metabolism so that the margin of safe fluoride exposure may be reduced. The objective of the investigation was

  • Genetic effects of hydrogen fluoride on Drosophila Melanogaster

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  • Genotoxic effect and rat hepatocyte death occurred after oxidative stress induction and antioxidant gene downregulation caused by long term fluoride exposure

    Studies focusing on possible genotoxic effects of excess fluoride are contradictory and inconclusive. Currently, studies have reported a probable link to oxidative stress, DNA damage and apoptosis induced by fluoride in rat hepatocytes. We developed an in vivostudy administering three doses of fluoride by gavage given to rats for 60 day.

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