Lead acetate (116 mg/kg/day), arsenic (11 or 13.8 mg/kg/day as sodium
arsenite), a lead-arsenic mixture or vehicle were administered to adul
t mice through gastric intubation during 14 days. Then, the regional c
ontent of norepinephrine (NE), dopamine (DA), serotonin (5-HT), 3,4 di
hydroxyphenyl-acetic acid (DOPAC), 5-hydroxyindole-3-acetic acid (5-HI
AA), arsenic, and lead were quantified. Compared with the accumulation
after single element exposures, the mixture elicited a higher accumul
ation of lead and a lower arsenic accumulation in the brain. Compared
to controls, lead induced only an augmentation of DOPAC (200%) in the
hypothalamus. By contrast, the mixture provoked increases of DOPAC in
the hypothalamus (250%), DA and 5-HIAA in the striatum (67 and 187%, r
espectively) and NE decreased in the hypothalamus (45%). Although thes
e alterations were similar to those produced by arsenic alone; the mix
ture provoked a 38% decrease of NE in the hippocampus and increases of
5-HT in midbrain and frontal cortex (100 and 90%, respectively) over
control values, alterations that were not elicited by either metal alo
ne. These results demonstrate an interaction arsenic/lead on the centr
al monaminergic systems of the adult mouse. (C) 1997 Elsevier Science
Inc.