The distribution and excretion of mercury were studied in mice and rats given a single injection of HgC12 combined with chelation treatment. BAL-sulph (2,3-dimercaptopropane-l-sulphonate) given intravenously (500 pmol SH/kg) to mice 24 hrs after the mercury injection (2.0 pmol Hg/kg) reduced the kidney Hglevel significantly, while NAPA (N-acetyl-DL-penicillamine) and BAL (2,3-dimercaptopropanol) did not. Severe kidney damage with oliguria was observed in pregnant as well as in non-pregnant rats after injection of 5pmol/kg of HgCL2. The gross pathological changes could be avoided with immediate treatment with BALsulph (500pmol SH/kg), and such treatment protected against the oliguric reaction. Treatment delayed for 24 hrs reduced the renal Hg-levels significantly, but was ineffective in preventing the kidney damage. This indicates that irreversible changes might have occurred in kidneys cells at this time. TheHg-levels in the brain were either unchanged or lowered in animals given BAL-sulph treatment. BAL-sulph is supposed to act by chelation of Hg", particularly in the extracellular space. The complexes formed appears to be rapidly excreted by healthy kidneys. Mercury poisoning with severe renal damage is, however, associated with a block in urinary Hgexcretion. The poisoned animals responded on the BAL-sulph treatment with a substantial raise of faecal mercury excretion.