Mercury binding to bile components and the correlation between the amount of mercury bound in the bile fraction 2 and the rate of mercury biliary excretion were studied in female rats exposed to intravenously injected HgCl2 after pretreatment with a series of 14 chemical agents. After pretreatment with the tested agent, 203Hg was detectable both in the bile fraction 1 and 2. Distribution pattern of 203Hg between the two fractions appeared to be linked with the chemical structure of the formed mercury complex. Pretreatment with these agents did not inhibit the formation of the bile fraction 3. By their influence on the 203Hg distribution between the bile fractions 1 and 2, the tested agents can be roughly divided into 3 groups: the content of 203Hg in the bile fraction 2 is about 10--20% and does not change significantly within the first 24 hours after 203 HgCl2 injection (cysteine, penicillamine, disodium ethylenediaminotetraacetate -- Na2EDTA, sodium diethyldithiocarbamate, sodium alanindithiocarbamate, acrylonitrile); the the 203Hg content in the bile fraction 2 increases (thiophenolacetate); the content of 203Hg in fraction 2 is initially several times higher than that in the bile fraction 1, but then decreases during the first 24 hours (2,3-dimercaptopropanol -- BAL, sodium 2,3-dimercaptopropanesulphonate, spironolactone, Thiomestron). The rate of mercury biliary excretion (Rb) was found to be closely correlated with the relative amount of mercury present in the bile fraction 2 (a2), if a2 > 30%, both in vivo (Rb = 1.077 a2 + 0.758) and invitro (Rb = 1.067 a2 + 0.519) experiments. Practically identical values of the constant accompanying a2 in the two equations seem to indicate that one of the decisive factors influencing the rate of mercury biliary excretion in rats is rather the mercury affinity for the bile fraction 2 components than the agent-induced mercury transport mechanisms. For a2 < 30% the correlation is non-linear and the excretion is rather inhibited than enhanced.