Metabolism of mercurials

There appears to be adequate information on the metabolism of mercury, and there are no special metabolites or metabolic pathways that are unique to children and require further evaluation. 

Rothstein A, Hayes AL. 1960. The metabolism of mercury in the rat studied by isotope techniques. J Pharmacol Exp Ther 130 166-176. 

Reynolds WA, Pitkin RM (1975) Transplacental passage of methylmercury and its uptake by primate fetal tissues. Proc.- Soc. Exp. Biol. Med. 148 523 Rossi LC, Clemente GF, Santaroni G (1976) Mercury and selenium distribution in a defined area and in its population. Arch. Environ. Health 31 160 Rothstein A, Hayes AD (1960) The metabolism of mercury in the rat studied by isotope technique. J. Pharmacol. Exp. Ther. 130 166 Rowland I, Davies M, Grasso P (1977) Biosynthesis of methylmercury compounds by the intestinal flora of the rat. Arch. Environ. Health 32 24 Skerfving S, (1972) "Normal" concentrations of mercury in human tissue and urine. In Friberg L, Vostal J (eds) CRC Press, Cleveland, Ohio (Mercury in the Environment, p. 109)... 

The biochemical basis for the toxicity of mercury and mercury compounds results from its ability to form covalent bonds readily with sulfur. Prior to reaction with sulfur, however, the mercury must be metabolized to the divalent cation. When the sulfur is in the form of a sulfhydryl (— SH) group, divalent mercury replaces the hydrogen atom to form mercaptides, X—Hg— SR and Hg(SR)2, where X is an electronegative radical and R is protein (36). Sulfhydryl compounds are called mercaptans because of their ability to capture mercury. Even in low concentrations divalent mercury is capable of inactivating sulfhydryl enzymes and thus causes interference with cellular metaboHsm and function (31—34). Mercury also combines with other ligands of physiological importance such as phosphoryl, carboxyl, amide, and amine groups. It is unclear whether these latter interactions contribute to its toxicity (31,36). 

Hoffman DJ, Heinz GH. 1998. Effects of mercury and selenium on glutathione metabolism and oxidative stress in mallard ducks. Environ Toxicol Chem 17 161-166. 

Now consider a psychiatric patient who presents with a pH of 7.50, a PaC02 of 20 mm Hg (2.7 kFh), an HC03 of 16 mEq/L (mmol/L), a sodium concentration of 140 mEq/L (mmol/L), and a chloride level of 103 mEq/L (mmol/L). Because this person is alkalemic, the low PaC02 is the primary disturbance and represents respiratory alkalosis. If this disturbance is a chronic respiratory alkalosis with metabolic compensation, the expected AHC03 is 0.4 x APaC02 (in millimeters of mercury) or 0.4 x 20, which is 8 mEq/L (mmol/L). As such, the predicted HC03 concentration should be 24 mEq/L (mmol/L) [normal] - 8 mEq/L (mmol/L) [expected compensation] or 16 mEq/L (16 mmol/L). 

Penicillamine is reported to be more than 80% bound to plasma protein. The compound is metabolized in the liver. N-acetylpenicillamine is more effective than penicillamine in protecting against the toxic effect of mercury, presumably because it is even more resistant to metabolism [7,2]. 

Raj, A.I.M. and P.S. Hameed. 1991. Effect of copper, cadmium and mercury on metabolism of the freshwater mussel Lamellidens marginalis (Lamarck). Jour. Environ. Biol. 12 131-135. 

Sublethal effects of mercury on birds, administered by a variety of routes, included adverse effects on growth, development, reproduction, blood and tissue chemistry, metabolism, and behavior. Histopathology and bioaccumulation were also noted. 

Hoffman, D.J., H.M. Ohlendorf, C.M. Mam, and G.W. Pendleton. 1998. Association of mercury and selenium with altered glutathione metabolism and oxidative stress in diving ducks from the San Francisco Bay region, USA. Environ. Toxicol. Chem. 17 167-172. 

The rate of uptake from blood and by different organs varies widely, and so does the rate of elimination from different organs. Inorganic mercury is characterized by a markedly non-uniform distribution in the body. Compartmentali-zation of mercury within different parts of the organ or in subcellular structures, the binding of mercury to various chemical compounds within the cell, and the metabolic transformation of mercury, complicate the evaluation of distribution. 

Molds and other plant diseases are controlled by fungicides, which act to affect the growth or metabolism of fungal pests. Many different fungicides exist, including sulfur, aryl- and alkyl-mercurial compounds, Aw-dithiocarbamates, and chlorinated phenols. 

Unknown important responses are destructive in many systems chemical plant explosions caused by impurity built up in reactors Minimata disease, the result of microorganisms metabolizing inorganic mercury and passing it up the food chain the dust bowl of the 1930 s - all are examples of important system responses that were initially unknown and unsuspected [Adams (1991)]. 

Exposure is also affected by absorption. Even though we may come into contact with an agent, if little is taken up into the body (or absorbed), there is little effect. For example, the metallic mercury from a broken thermometer, if swallowed, is very poorly absorbed by the gut and will be excreted in the feces. However, if this same amount of mercury were allowed to evaporate and be inhaled, there would be very serious health consequences. This example shows that metabolism and excretion modify absorption. What is not absorbed (and even some of what is absorbed) may be excreted from the body by various routes, including the urine, feces, and sweat or through exhalation. Excretion reduces the effect because it lowers the amount of toxicant in the body, thus reducing exposure to sensitive organs. 

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