Repeat oral doses of tungsten (W) show retention in kidneys, intestine, and femur as well as translocation of small amounts to neonates. Furthermore, W exposure leads to decreased function of molybdenum (Mo)-containing enzymes in kidneys, liver, and intestine. The chemical disposition of W (administered as sodium tungstate dihydrate in water) in plasma, liver, kidneys, uterus, femur, and intestine of rodents (Sprague-Dawley rats and C57Bl/6N mice) was characterized after repeat exposure by gavage (10 mg kg À1 ) or drinking water (560 mg L À1 ) for 14 consecutive days. Separately, the same species were exposed to drinking water (560 mg L À1 ) during gestation for 9 (mice) or 10 (rats) days. For the rodents exposed during gestation, all the aforementioned tissues were analyzed in addition to the fetus to assess transplacental disposition. Animals were euthanized 24 h after the last day of dosing. At sacrifice, plasma, intestine, liver, kidneys, femur, uterus, and fetus were collected for analysis by inductively coupled plasma mass spectrometry. W was detectable in plasma and all tissues and in fetus of both rats and mice. W accumulation occurred in intestine, kidneys, and femur. The possible sources for enrichment/retention in these tissues include the intestine being the primary route of entry for oral exposures, kidneys being the primary route of elimination (495% excreted through the urine as shown in previous studies), and the ability of W to displace phosphate in bone and be retained in the femur. Enzyme activity of Mo-dependent enzymes xanthine oxidase (XO) and sulfite oxidase (SO) was also evaluated in liver, intestine, and kidneys due to the propensity of W to substitute for Mo. Enzyme activity was reduced in kidneys and intestine, while it was unaltered in liver.