• For elemental and inorganic Hg, the half-life in blood is 1-2 months. The whole-body half-life is slightly longer, but that does not take into account Hg in the brain, which is cleared very slowly. Excretion occurs primarily via urine and feces and, to a small extent, saliva, bile, sweat, and lungs.

  • DMPS and DMSA can be used to increase Hg excretion. Dimercaprol (BAL), used in the past for chelation, is contraindicated because it redistributes Hg to the brain.

  • MeHg readily crosses the blood-brain barrier. The rapid uptake of MeHg in the brain has been proposed to be due to lipid solubility, but evidence in rats suggests that the transport is due to the formation of MeHg-cysteine complexes.

  • MeHg accumulates in the brain where it is slowly converted to inorganic Hg. Whether CNS damage is due to MeHg per se, to its biotransformation to inorganic Hg, or to both is still controversial. The mechanisms and cellular site for the biotransformation in humans are not well understood. Both free-radical and enzymatic biotransformation has been proposed.

  • The critical organ for MeHg toxicity is the brain. Both adult and fetal brains are vulnerable. For elemental Hg, the critical organs are the brain and kidney. Both MeHg and elemental Hg are converted to mercuric Hg in the brain, where it is trapped. The biological mechanisms for removing mercuric Hg from the brain are limited. The critical organ for mercuric Hg toxicity is the kidney, where it accumulates.

  • There is emerging evidence that the cardiovascular and immune systems might be major sites of MeHg toxicity (see Chapter 5).

  • The high affinity of MeHg and mercuric Hg for sulfhydryl groups is believed to be a major mechanism that underlies their toxicity. If those sulfhydryl groups are in the active center of critical enzymes, severe inhibition of essential biochemical pathways occurs.

  • The toxicology of the three species of Hg — elemental Hg, mercuric Hg and MeHg — are intertwined, because MeHg and elemental Hg are transformed to inorganic Hg in the brain. Risk-assessment models for MeHg in humans are complicated because of inadequate data regarding the cumulative neurotoxic effects of MeHg per se and its biotransformation product mercuric Hg, which has a very long half-live in the brain.

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