Mercuric toxicity

The toxic effects of mercury and mercury compounds as well as their medicinal properties have been known for many centuries. In the first century AD, Pliny indicated the use of mercuric sulfide (cinnabar or vermilion) in medicine and in cosmetics. This compound was probably known to the Greeks in the time of Aristotle (13). 

Galen, a physician whose views outUved him by about a thousand years, died about 200 AD. He beUeved that mercurials were toxic, and did not use any mercury compound therapeutically. However, as a result of Arabian influence, the therapeutic uses of mercury were slowly recognized by Western Europe. In the thirteenth century mercury ointments were prescribed for treating chronic diseases of the skin. Mercury and its compounds, such as mercurous chloride, mercuric oxide, mercuric chloride, and mercuric sulfide, were used widely from the fifteenth to the nineteenth centuries, and to some extent in the twentieth century. During the first half of the twentieth century, the primary therapeutic uses of mercury included bactericidal preparations, such as mercuric chloride, mercuric oxycyanide, and mercuric oxide and diuretics, such as aryl HgX (Novasural) and mercurated ahyl derivatives (14). 

Dimethylsilicone rubbers show a high compression set which can be reduced to some extent by additives such as mercurous oxide and cadmium oxide. These materials are undesirable, however, because of their toxicity. Substantially reduced compression set values may be obtained by using a polymer containing... 

Fire Hazards - Flash Point Not flammable Flammable Limits in Air (%) Not flammable Fire Extinguishing Agents Not pertinent Fire Extinguishing Agents Not To Be Used Not pertinent Special Hazards (f Combustion Products Heat of fire may cause material to form fumes of mercuric chloride, which are toxic Behavior in Fire Not pertinent Ignition Temperature Not pertinent Electrical Hazard Not pertinent Burning Rate Not pertinent. 

Mercuric Nitrate (Mercury Nitrate, Mercury Pemitrate). Hg(NO3)2 0, mw 342.61, OB to HgO and N2 +26.4% wh deliq powd or colorl crysts, mp 79°, bp dec, d 4.39g/cc. Sol in w and nitric acid, insol in ale. Prepd by action of hot nitric acid on ale. Highly toxic and a dangerous fire risk in contact with organic materials, It has been used for the nitration of aromatic organic compds and in the prepn of MF... 

Mercurous Nitrate (Mercury Protonitrate). HgN03.H20, mw 280.64, OB to HgO N2 +17.1%, mp 70° dec, bp explds, d 4.78g/cc. Short prismatic crysts effloresces and becomes anhydrous in dry air sensitive to light. Sol in small quantities of warm w (hydrolyzes in larger quantities), w acidified with nitric acid. Prepd by action of cold dil nitric acid upon an excess of Hg with slight warming. Highly toxic may explode if shocked or heated. There is no US Specification for Mercurous Nitrate Refs 1) Merck (1968), 6,62-L 2) CondChem-... 

Mercuric chloride, other mercury-containing antibacterials and silver will inhibit enzymes in the membrane, and for that matter in the cytoplasm, which contain thiol, -SH, groups. A similar achon is shown by 2-bromo-2-nitropropan-l,3-diol (bronopol) and iso-thiazolones. Under appropriate condihons the toxic action on cell thiol groups may be reversed by addition of an extrinsic thiol compound, for example cysteine or thioglycollic aeid (see also Chapters 12 and 23). 

Slimicide and biocide toxic pollutants containing pentachlorophenol are used at mills in the pulp, paper, and paperboard industry. Initially, pentachlorophenol was used as a replacement for heavy metal salts, particularly mercuric types. Trichlorophenols are also used because of their availability as a byproduct from the manufacture of certain herbicides. Formulations containing organo-bromides and organo-sulfur compounds are also being used. Substitution of alternative slimicide and biocide formulations can lead to the virtual elimination of pentachlorophenol and trichlorophenol from these sources. 

El-Begearmi, M.M., H.E. Ganther, and M.L. Sunde. 1980. Toxicity of mercuric chloride in Japanese quail as affected by methods of incorporation into the diet. Poult. Sci. 59 2216-2220. 

Handy, R.D. and W.S. Penrice. 1993. The influence of high oral doses of mercuric chloride on organ toxicant concentrations and histopathology in rainbow trout, Oncorhynchus mykiss. Comp. Biochem. Physiol. 106C 717-724. 

Heisinger, J.F., C.D. Hansen, and J.H. Kim. 1979. Effect of selenium dioxide on the accumulation and acute toxicity of mercuric chloride in goldfish. Arch. Environ. Contam. Toxicol. 8 279-283. 

Koizumi, T. and Y. Yamane. 1984. Protective effect of molybdenum on the acute toxicity of mercuric chloride. III. Chem. Pharm. Bull. 32 2316-2324. 

Oxidation of cyclic and acyclic hydroxylamines with yellow mercuric oxide appears to proceed with high regioselectivity (109-115). Regioselectivity is determined by the electronic nature of the substituents (116). The oxidative regioselectivity of Mn02 is comparable to that of HgO, but due to its lower toxicity, it has been proposed to use Mn02 rather than HgO (Table 2.2) (117). 

With respect to Cr a distinction should be made between Cr(III), which is the common oxidation state in the soils, being rather immobile and so toxic, and Cr(VI), which is very mobile and very toxic. With respect to Hg, the situation is even more complex, due to the occurrence of mercuric mercury (Hg2+), mercurous mercury (Hg2+), elemental mercury (Hg°) and organic mercury species, such as methyl mercury, (CH3)2Hg (see Section 18.5). Furthermore, volatilization of elemental mercury and organic mercury species is common. A description of these... 

Methylation of divalent inorganic mercury salt has been shown in vivo in rat intestine [61] and in vitro in human intestine [62], yet it is seldom followed by toxic effects. MeHg has been found in hen tissues [63 ] and probably in rat brain [64] after ingestion of divalent mercuric salts. 

The inhibition of amino-acid transport has been regarded as the main toxic effect of mercury compounds [82], The biochemical mechanism underlying the inhibition is unclear. In unfertilized sea-urchin eggs an interaction with the amino-acid carrier was found, whereas in fertilized eggs inhibition of amino-acid transport was indirect and might result from an elevation of the Na + content of the egg caused by the inhibition of the Na+ pump [83]. The action on the diffusional process could be mediated by an effect on membrane phospholipids or on membrane proteins, or by interaction with Ca2+ which stabilizes membrane structure. Mercuric chloride in skate liver cells inhibited amino acid transport, decreased Na + /K + -ATPase (adenosinetriphosphatase) activity, impaired volume regulatory mechanisms and increased the permeability of the plasma membrane to potassium [84]. It has been suggested that... 

Oral or parenteral administration of mercuric chloride promotes lipid peroxidation [127-129], possibly via a reduction of glutathione peroxidase activity. However, several studies argue against lipid peroxidation being responsible, at least for the early hours of cell toxicity of mercury [130-133]. 

Selenium lessens the toxicity of divalent mercury in animals, the protection being less at continuous mercury exposure. Selenium has been found to affect the distribution of mercuric mercury in mice [134], rats [135], rabbits [136, 137] and pigs [ 138]. Mercury forms a mercury-selenium protein complex with selenium with little biological activity [139]. Mercury is thus retained longer in the blood, liver and spleen and as a consequence lessens accumulation in the kidney. In fish, selenium pretreatment probably retarded mercury uptake rather than promoting mercury excretion [140]. 

Information concerning the effects of selenium in man is lacking and it is doubtful whether administration of selenium in man has any effect on the toxicity of mercuric mercury. However, mercury and selenium were found in the cellular lysozomes in renal tubular cells in two patients with inorganic mercury poisoning [143]. 

In this work on compounds containing the C—F link, it was obviously desirable to prepare 2-fluoroethanol, both for toxicity tests on the compound itself, and as a starting material for the production of other fluorine compounds. Swarts1 was unable to obtain 2-fluoroethanol by the action of silver fluoride or mercuric fluoride on either ethylene chlorohydrin or ethylene bromohydrin. He obtained acetaldehyde in each case. He ultimately obtained fluoroethanol in very poor yield by the indirect method of hydrolysing fluoroacetin (from bromoacetin and mercuric fluoride) for 80 hr. with dilute mineral acid. 

Adams, P.M., Hanlon, R.T., and Forsythe, J.W. Toxic exposure to ethylene dibromide and mercuric chloride effects on laboratory-reared octopuses, Neurotoxicol. TeratoL, 19(6) 519-523, 1988. 

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