Manganese intake can vary greatly with food choices, water composition, and
supplement use. Thus, individuals consuming Western diets consume from <1
to >10 mg Mn/d. The levels of manganese intake associated with adverse effe
cts (both deficient and toxic) are debatable. Moreover, many of the symptom
s of manganese deficiency (growth retardation, changes in circulating HDL c
holesterol and glucose levels, reproductive failure) and manganese toxicity
(growth depression, anemia) are nonspecific. The bone deformities observed
in manganese-deficient animals and neurological symptoms of individuals wh
o have inhaled excess manganese are permanent and illustrate the need to id
entify sensitive biomarkers of manganese status that appear before these sy
mptoms. Manganese balance and excretion data are not useful biomarkers of m
anganese exposure but demonstrate that the body is protected against mangan
ese toxicity primarily by low absorption and/or rapid presystemic eliminati
on of manganese by the liver. Serum manganese concentrations in combination
with lymphocyte manganese-dependent superoxide dismutase (MnSOD) activity
and perhaps blood arginase activity, appear to be the best ways to monitor
ingestion of insufficient manganese. Serum manganese concentrations in comb
ination with brain MRI (magnetic resonance imaging) scans, and perhaps a ba
ttery of neurofunctional tests, appear to be the best ways to monitor exces
sive exposure to manganese. (C) 1999 Inter Press, Inc.