Mercury compounds, redistribution

The redistribution reaction in lead compounds is straightforward and there are no appreciable side reactions. It is normally carried out commercially in the liquid phase at substantially room temperature. However, a catalyst is required to effect the reaction with lead compounds. A number of catalysts have been patented, but the exact procedure as practiced commercially has never been revealed. Among the effective catalysts are activated alumina and other activated metal oxides, triethyllead chloride, triethyllead iodide, phosphorus trichloride, arsenic trichloride, bismuth trichloride, iron(III)chloride, zirconium(IV)-chloride, tin(IV)chloride, zinc chloride, zinc fluoride, mercury(II)chloride, boron trifluoride, aluminum chloride, aluminum bromide, dimethyl-aluminum chloride, and platinum(IV)chloride 43,70-72,79,80,97,117, 131,31s) A separate catalyst compound is not required for the exchange between R.jPb and R3PbX compounds however, this type of uncatalyzed exchange is rather slow. Again, the products are practically a random mixture. 

Recently, redistribution reactions between phenyllead compounds have been used to prepare triphenyllead chloride from tetraphenyllead and diphenyllead dichloride 202>, and, using mercury acetate in acetic acid as a catalyst, phenyllead triacetate from diphenyllead diacetate and lead tetraacetate, and diphenyllead diacetate from tetraphenyllead and lead tetraacetate 325>. The mercury acetate catalyst is notable in that it does not catalyze the redistribution of alkyllead compounds. 

The data indicate that zinc-induced metallothionein binds mercury in the renal cortex and shifts the distribution of mercury from its site of toxicity at the epithelial cells of the proximal tubules. Thus, the renal content of mercury is increased, yet less is available to cause toxicity. In contrast, the renal toxicity of mercuric chloride is exacerbated in zinc-deficient animals (Fukino et al. 1992). In the zinc-deficient state, less mercury accumulates in the kidneys, but the toxicity is greater. The mechanism of the protection appears to involve more than simply a redistribution of renal mercury, because in the absence of mercury exposure, zinc deficiency increases renal oxidative stress (increased lipid peroxidation, decreased reduced ascorbate). When mercury exposure occurs, the oxidative stress is compounded (increased lipid peroxidation and decreased glutathione and glutathione peroxidase). Thus, zinc appears to affect the biochemical protective mechanisms in the kidneys as well. 

Information for other organometallic compounds is scarce. The corresponding methyl and ethyl derivatives of mercury, tin, and silicon were shown to undergo redistribution to yield random equilibrium mixtures of all possible metal alkyls. Rapid intermolecular exchange of the methyl groups in mixtures of trimethylaluminum-dimethylcadmium and dimethylzinc-dimethylcadmium was also demonstrated by NMR. The redistribution of mercury derivatives was found to be much slower. Further data are also available for thallium. - The four-center intermediate 154 was suggested to explain the observations [Eq. (6.149)] ... 

Methylmercury compounds undergo extensive enterohepatic recirculation therefore, introduction of a nonabsorbable mercury-binding substance into the intestinal tract should facilitate their removal from the body. A polythiol resin has been used for this purpose in humans and appears to be effective. The resin has certain advantages over penicillamine. It does not cause redistribution of mercury in the body with a subsequent increase in the concentration of mercury in blood, and it has fewer adverse effects than do sulfhydryl agents that are absorbed. Clinical experience with various treatments for methylmercury poisoning in Iraq indicates that penicillamine, N-acetylpenicillamine, and an oral nonabsorbable thiol resin all can reduce blood concentrations of mercury however, clinical improvement was not clearly related to reduction of the body burden of methylmercury. 

---