Abstract

The distribution and excretion of mercury were studied in mice and rats given a single injection of HgCl2 combined with chelation treatment. BAL-sulph (2,3-dimercaptopropane-1-sulphonate) given intravenously (500 mumol SH/kg) to mice 24 hrs after the mercury injection (2.0 mumol Hg/kg) reduced the kidney Hg-level 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 5 mumol/kg of HgCl2. The gross pathological changes could be avoided with immediate treatment with BAL-sulph (500 mumol SH/kg), and such treatment protect 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. The Hg-levels in the brain were either unchanged or lowered in animals given BAL-sulph treatment. BAL-sulph is supposed to act by chelation 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 Hg-excretion. The poisoned animals responded on the BAL-sulph treatment with a substantial raise of faecal mercury excretion.

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