Re: cutlers alleged ala literature

here is a couple

Abstract

Experimental neurotoxicity in rat models was induced by an intramuscular injection of mercuric chloride.View the MathML source-α-lipoic acid was administered as an antidote in three protocols of experimental design. Two protocols of short-term exposure of mercury was designed, one with prophylactic therapy and the other with curative therapy of lipoic acid. The third protocol was with prophylactic therapy of lipoic acid on long-term exposure of mercury. Enhanced lipid peroxidation, depleted non-enzymic and perturbed enzymic antioxidant status were observed in cerebral cortex, cerebellum and sciatic nerves of the toxic groups. The ameliorating effect of lipoic acid and its therapeutic efficacy during various modes of therapy, on the antioxidant status was established in the nervous tissues.
Keywords

mercuric chloride,View the MathML source-α-lipoic acid, lipid peroxidation, enzymic and non-enzymic antioxidants

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The effect of dl-α-lipoic acid on heavy-metal intoxication in mice and dogs

R.R. Grunert

From the Stine Laboratory, E. I. du Pont de Nemours and Co., Newark, Delaware, USA

Received 2 July 1959. Available online 30 November 2004.

Abstract

From a study of acute heavy-metal toxicity it has been found that dl-α-lipoic acid (a) is effective for the prevention and reversal of arsenic intoxication in mice and dogs; (b) effectively prevents mercury intoxication in mice provided a sufficiently large excess is used; (c) prevents gold intoxication in mice only under very specific conditions; and (d) fails to protect mice against a lethal dose of lead.

3-(6-Carboxyhexyl)-1,3-dithiolane was as effective as dl-α-lipoic acid in preventing arsenic intoxication in mice.

Copyright © 1960 Published by Elsevier Inc.

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The role of thiols, dithiols, nutritional factors and interacting ligands in the toxicology of mercury

James P.K. RooneyCorresponding author

Abstract

Mercury has been a known as a toxic substance for centuries. Whilst the clinical features of acute mercury poisoning have been well described, chronic low dose exposure to mercury remains poorly characterised and its potential role in various chronic disease states remains controversial. Low molecular weight thiols, i.e. sulfhydryl containing molecules such as cysteine, are emerging as important factors in the transport and distribution of mercury throughout the body due to the phenomenon of “Molecular Mimicry” and its role in the molecular transport of mercury. Chelation agents such as the dithiols sodium 2,3-dimercaptopropanesulfate (DMPS) and meso-2,3-dimercaptosuccinic acid (DMSA) are the treatments of choice for mercury toxicity. Alpha-lipoic acid (ALA), a disulfide, and its metabolite dihydrolipoic acid (DHLA), a dithiol, have also been shown to have chelation properties when used in an appropriate manner. Whilst N-acetyl-cysteine (NAC) and glutathione (GSH) have been recommended in the treatment of mercury toxicity in the past, an examination of available evidence suggests these agents may in fact be counterproductive. Zinc and selenium have also been shown to exert protective effects against mercury toxicity, most likely mediated by induction of the metal binding proteins metallothionein and selenoprotein-P. Evidence suggests however that the co-administration of selenium and dithiol chelation agents during treatment may also be counter-productive. Finally, the issue of diagnostic testing for chronic, historical or low dose mercury poisoning is considered including an analysis of the influence of ligand interactions and nutritional factors upon the accuracy of “chelation challenge” tests.