Many organisms can easily dispose of toxic inorganic arsenic species throug
h gradual methylation of the element and further urinary excretion. In orde
r to clarify the urinary excretion of arsenobetaine observed in a human cas
e of intoxication by arsine, the capacity of highly methylated arsenical sy
nthesis has been investigated in rats acutely exposed during 1 h to increas
ing concentrations of the same gas [4 to 80 mg AsH3/m(3)]. Urinary metaboli
tes of arsenic were determined with good agreement in two (Belgian and Ital
ian) laboratories using two different analytical procedures. The sum of ino
rganic, mono- and dimethylated metabolites of arsenic in urine was shown to
be related to the intensity of exposure to arsine; A biphasic relationship
was observed: 1 h exposure to > 60 mg AsH3/m(3) led to metabolite excretio
n which is roughly 10 times higher than for exposure levels below that limi
t, suggesting the saturation of a binding site reserve and the availability
for metabolism of a greater proportion of the As absorbed above this thres
hold. Arsenobetaine production: if any, could only be detected when its pre
sence in food was excluded; in addition, amounts appeared negligible and co
uld be disregarded as a common arsenic metabolite in rats.