Many studies on bioavailability of toxic metals have made the assumption that observation of toxicity is evidence thatthe metal was taken into the cells (i.e., was "bioavailable"). A second assumption is that results at the high concentrations necessary for toxic effect are applicable to the lower concentrations more commonly found in the environment. These assumptions were specifically tested for mercury (Hg(II)) toxicity (at concentrations of 0.25-50 nM Hg) and uptake (at lower concentrations of 0.005-0.015 nM Hg) in the aquatic bacterium, V. anguillarum. Toxicity was measured as reduction in levels of constitutively expressed bioluminescence in V. anguillarum pRB27. Hg(II) uptake was measured using the Hg(II)-inducible mer-lux operon in V. anguillarum pRB28. In experiments where the predominant Hg species was changed from HgCl2 to Hg(OH)2 or Hg(NH3)2(2+), toxicity results accurately predicted that there would be no effect of the dominant species on Hg(II) uptake at lower HgT concentrations. However, toxicity tests with these same ligands failed to predict that there would be an effect on Hg(II) uptake when conditions were changed from aerobic to anaerobic. Toxicity tests also failed to predict the effect of 5 mM histidine additions on Hg(II) uptake, as histidine addition protected cells completely from Hg toxicity under both aerobic and anaerobic conditions, at concentrations up to 50 nM Hg, but did not prevent Hg(II) uptake. Uptake occurred at low HgT concentrations (0.01 nM) at the same rate when histidine was added under aerobic conditions and was substantially increased under anaerobic conditions. Thus, toxicity assays for Hg under a variety of conditions were not always a reliable predictor of the effects of those conditions on Hg(II) uptake into the cell.