The metabolic pathway for and metabolites of selenium (Se) administered int
ravenously to rats in the form of selenate at a dose of 0.3 mg Se kg(-1) bo
dy weight were studied by speciating Se in the bloodstream, liver and urine
by HPLC-inductively coupled argon plasma mass spectrometry. Selenate was n
ot taken up by red blood cells (RBCs) and disappeared from the bloodstream
much faster than selenite, without any change in its chemical form before i
t disappeared from the plasma. Selenium excreted into the urine after the a
dministration of selenate showed different patterns from those of selenite
in both amounts and chemical forms. With the selenate group, the concentrat
ion of Se in urine was highest at 0-6 h and the chemical species of Se was
selenate at 0-6 h; thereafter a monomethylselenol-related Se compound (MMSe
*) and trimethylselenonium ions (TMSe) appeared, selenate not being excrete
d after 6 h. On the other hand, in the selenite group, the concentration of
Se peaked at 6-12 h, and the chemical species of Se were MMSe* and TMSe. S
elenate was reduced in vitro on incubation in either a liver homogenate or
supernatant fraction, although much more slowly than in the whole body. Sel
enate was not reduced by glutathione or dithiothreitol. The results suggest
that in contrast to selenite, which is taken up by and reduced in RBCs, an
d then transferred to the liver, approximately 20% of the selenate administ
ered to rats was excreted into the urine without any change in its chemical
form with the present dose, and the major portion of selenate was taken up
by the liver, reduced and then utilized for the synthesis of selenoprotein
s or excreted into the urine after being methylated.