Abstract
Selenium causes “alkali disease” or “blind staggers” in livestock in the Dakotas, Kansas, Montana, Wyoming, and other Western States where the soil and vegetation are high in selenium content. Therefore the toxic properties of selenium and its compounds are of great importance in these areas.
As far as we know, there is no reliable agent which is of value in preventing or curing the symptoms of selenium poisoning, though protective action of arsenic has been demonstrated by Moxon et al. 1
Peters, Stocken, and Thompson 2 described the effectiveness of BAL in counteracting the effects of arsenical poisoning. The protective action of this compound in arsenical poisoning was believed to be due to the release of SH groups by BAL which could compete with the tissue SH groups for the arsenic, and act as a detoxifying agent. The nature of the reaction between arsenic and BAL made it seem probable that BAL would react similarly with other metals, and Gilman, Allen, and Philips 3 have reported its effectiveness as an antidote for bichloride of mercury and cadmium poisoning, and Braun, Lusky, and Calvery 4 showed similar results against poisoning by antimony, bismuth, chromium and nickel. However, they demonstrated that lead and selenium were made more toxic by BAL.
Our experiments performed using BAL as an antagonist against selenium poisoning confirmed the results already described 4 However, we have found no explanation in the literature of the apparent synergism between BAL and selenium, hence our work has been directed along this line.
Experimental. Healthy white rats 6 to 8 weeks old, 120 and 150 g of weight were used. Selenium was administered by intraperitoneal injections in the form of a freshly prepared aqueous solution of sodium selenite (SS).
Get full access to this article
View all access options for this article.