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 of permeability of lipid bilayer membranes
to hydrogen fluoride (HF) is 1 million times higher than that . This means that
fluoride readily crosses cell membranes as HF, in response to a pH gradient
between adjacent body fluid compartments. After ingestion, plasma of F– fluoride
levels increase rapidly due to the rapid absorption from the stomach, an event
that is pH-dependent and distinguishes fluoride from other halogens and most
other substances. The majority of fluoride not absorbed from the stomach will
be absorbed from the small intestine. In this case, absorption is not pH-dependent.
Fluoride not absorbed will be excreted in feces. Peak plasma fluoride
concentrations are reached within 20–60 min following ingestion. The levels
start declining thereafter due to two main reasons: uptake in calcified tissues
and excretion in urine. Plasma fluoride levels are not homeostatically
regulated and vary according to the levels of intake, deposition in hard
tissues and excretion of fluoride. Many factors can modify the metabolism and
effects of fluoride in the organism, such as chronic and acute acid-base disturbances,
hematocrit, altitude, physical activity, circadian rhythm and hormones, nutritional
status, diet, and genetic predisposition. These will be discussed in detail in
this review.
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