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Mercury metabolism

Paracelsus The bitter attacks by Theophrastus Bom-bastus of Hohenheim, known as Paracelsus (1493-1541), against the doctrines of Galenos and Avicenna heralded the end of the first epoch of liver research (ca. 2000 BC - ca. 1500 AD). Paracelsus also initiated the era of iatric chemistry. He regarded the liver as the site of chemical and material transformations, particularly the processing of nutrient and metabolic mercurial ... [Pg.9]

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). [Pg.109]

Mercury (II) oxide, 3-4 Mercury-in-glass thermometers, 7-8 Mercury thermometers, 2 Metabolic energy, 218 Metal A substance having characteristic... [Pg.691]

Mendeleev, Dimitri, 104,107 Mendelevium, oxidation number, 414 Mercuric perchlorate, 237 Mercurous perchlorate, 237 Mercury, oxidation numbers, 414 Mercury (planet), data on, 444 Metabolism, oxidative, 429 Metallic alloys, 309 bond, 303 elements. 303 radius, 380 substances, 81 Metals alkali, 94... [Pg.462]

Choi S-C, TT Chase, R Bartha (1994) Metabolic pathways leading to mercury methylation in Desulfovibrio desulfuricans LS. Appl Environ Microbiol 60 4072-4077. [Pg.177]

Jackson TA. 1998. Mercury in aquatic ecosystems. In Langston WJ, Bebiarmo MJ, editors. Metal metabolism in aquatic environments. London, UK Chapman Hall, p. 77-158. [Pg.117]

Doi R. 1991. Individual difference of methyhnercury metabolism in animals and its significance in methylmercury toxicity. In Suzuki T, Imura N, Clarkson TW, editors. Advances in mercury toxicology. New York (NY) Plenum Press. [Pg.172]

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. [Pg.178]

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). [Pg.425]

In mammals, as in yeast, several different metallothionein isoforms are known, each with a particular tissue distribution (Vasak and Hasler, 2000). Their synthesis is regulated at the level of transcription not only by copper (as well as the other divalent metal ions cadmium, mercury and zinc) but also by hormones, notably steroid hormones, that affect cellular differentiation. Intracellular copper accumulates in metallothionein in copper overload diseases, such as Wilson s disease, forming two distinct molecular forms one with 12 Cu(I) equivalents bound, in which all 20 thiolate ligands of the protein participate in metal binding the other with eight Cu(I)/ metallothionein a molecules, with between 12-14 cysteines involved in Cu(I) coordination (Pountney et ah, 1994). Although the role of specific metallothionein isoforms in zinc homeostasis and apoptosis is established, its primary function in copper metabolism remains enigmatic (Vasak and Hasler, 2000). [Pg.329]

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]. [Pg.150]

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. [Pg.229]


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See also in sourсe #XX -- [ Pg.165 ]

See also in sourсe #XX -- [ Pg.482 , Pg.487 ]




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