Mercuric Chloride Poisoning Due to Ingestion of a Stool Fixative

Singer, Adam J.; Mofenson, Howard C.; Caraccio, Thomas R.; Ilasi, Joseph

doi:10.3109/15563659409011062

Cited by 11 publications

(7 citation statements)

References 7 publications

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“…Oral ingestion of a stool fixative containing 675 mg of HgCl 2 was rapidly treated with BAL chelation and extensive hydration, and the patient remained without systemic signs of mercury intoxication …”

Section: Mercurymentioning

confidence: 99%

“…270 Oral ingestion of a stool fixative containing 675 mg of HgCl 2 was rapidly treated with BAL chelation and extensive hydration, and the patient remained without systemic signs of mercury intoxication. 271 A 38-year-old male intentionally drank 100 mL of a solution with an unknown concentration of HgCl 2 . He was admitted to the hospital with consistent vomiting and bloody diarrhea.…”

Section: Mercurymentioning

confidence: 99%

See 1 more Smart Citation

Principles and Recent Developments in Chelation Treatment of Metal Intoxication

1999

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Section: Mercurymentioning

confidence: 99%

Section: Mercurymentioning

confidence: 99%

Principles and Recent Developments in Chelation Treatment of Metal Intoxication

1999

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“…Dimercaprol(2,3-dimercaptopropanol or BAL) is a dithi-01 compound that is used as therapeutic agent in the treatment of mercury and other heavy metal poisoning (Kazantzis 1986; Ellenhorn & Barceloux 1988;Kojima et al 1989;Klaassen 1990;Schwartz et of. 1992;Singer et al 1994). Although dimercaprol has the capacity to ameliorate the deleterious effects of mercury intoxication, it shows a low therapeutic index, since the effective therapeutic dose is near the lethal dose (Chisolm, 1970;Andersen 1989;Kojima et al 1989).…”

mentioning

confidence: 99%

Effect of Mercuric Chloride Intoxication and Dimercaprol Treatment on σ‐Aminolevulinate Dehydratase from Brain, Liver and Kidney of Adult Mice

Emanuelli

Rocha

Pereira

et al. 1996

Pharmacology & Toxicology

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Dimercaprol is a compound used in the treatment of mercury intoxication, however with low therapeutic efficacy. It is assumed that dimercaprol acts by reactivating target sulfhydryl-containing proteins. In the present investigation we studied the inhibitory effect of mercuric chloride treatment (3 days with 2.3 or 4.6 mg/kg HgCl2, sc) in mice on cerebral, renal and hepatic delta-aminolevulinate dehydratase (ALA-D) activity, and a possible reversal of the effect of mercury by dimercaprol (0.25 mmol/kg, 24 hr after the last mercury injection). Mercuric chloride did not inhibit cerebral ALA-D at the doses injected. Dimercaprol treatment did not restore the normal enzyme activity of the liver after the 25% inhibition caused by 4.6 mg/kg HgCl2. In the kidney, dimercaprol enhanced the inhibitory effect of 4.6 mg/kg mercuric chloride (from 35% after mercury treatment alone to 65% after mercury plus dimercaprol treatment). Mercury content increased in kidney after exposure to 2.3 or 4.6 mg/kg and the levels attained were higher than in any other organ Mercury accumulated in liver only after exposure to 4.6 mg/kg HgCl2, and dimercaprol further increased mercury deposition. Dimercaprol treatment also increased the levels of mercury in brain of animals exposed to 4.6 mg/kg HgCl2 The enzymes from all sources presented similar sensitivity to the combined effect of HgCl2 and dimercaprol in vitro. In the absence of preincubation, 0-500 muM dimercaprol potentiated the inhibitory effect of HgCl2 on ALA-D activity. In the presence of preincubation, and 100 and 250 muM dimercaprol enhanced ALA-D sensitivity to mercury, whereas 500 muM dimercaprol partially protected the enzyme from mercury inhibition. Dimercaprol (500 muM) inhibited renal and hepatic ALA-D when preincubated with the enzymes. These data suggested that the dimercaprol-Hg complex may have a more toxic effect on ALA-D activity than Hg2+. Furthermore, the present data show that dimercaprol did not acts by reactivating mercury-inhibited sulfhydryl-containing ALA-D, and that indeed it may have an inhibitory effect per se depending on the tissue.

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“…Any benefit from activated charcoal is uncertain and may be outweighed by risks. While having limited binding capacity for metallic compounds in general, there is in vitro evidence for adsorption of mercuric chloride [14], but charcoal could obscure visibility if endoscopy is required [15].…”

Section: Discussionmentioning

confidence: 99%