The metabolic pathway for and metabolites of
selenium (Se) administered intravenously to rats in the form of
selenate at a dose of 0.3 mg Se kg-1
body weight were studied by speciating Se in the bloodstream, liver and urine by HPLC-inductively coupled
argon plasma mass spectrometry.
Selenate was not taken up by red blood cells (RBCs) and disappeared from the bloodstream much faster than
selenite, without any change in its chemical form before it disappeared from the plasma.
Selenium excreted into the urine after the administration of
selenate showed different patterns from those of
selenite in both amounts and chemical forms. With the
selenate group, the concentration 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 excreted 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.
Selenate was reduced in vitro on incubation in either a liver homogenate or supernatant fraction, although much more slowly than in the whole body.
Selenate was not reduced by
glutathione or
dithiothreitol. The results suggest that in contrast to
selenite, which is taken up by and reduced in RBCs, and then transferred to the liver, approximately 20% of the
selenate administered 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
selenoproteins or excreted into the urine after being methylated.