QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ackerman, C. J. Search for Related Content PubMed PubMed Citation Articles by Ackerman, C. J.

Reversal of Sulfaguanidine Toxicity in the Rat¹

Department of Biochemistry and Nutrition, Virginia Polytechnic Institute, Blacksburg

Growth was inhibited when weanling rats were fed complete diets containing 1% sulfaguanidine. Addition of all known vitamins, including biotin, folacin and vitamin B₁₂ failed to stimulate growth. Whole dry egg, whole milk powder, calf, beef and pork liver, pork shoulder, round steak, distillers, solubles at a dietary level of 10% also failed to stimulate growth. Dried rat, cow or chicken feces, at a level of 5%, were also without effect. Meat meal, of indeterminate composition, at a level of 5% of the diet stimulated growth of rats which had ceased to grow due to the ingestion of sulfaguanidine.

When meat meal (5%) was incorporated into the sulfaguanidine-containing diet of weanling rats, growth was as good or better than was observed in similar animals fed diets containing no sulfaguanidine or meat meal.

The growth-promoting factor of meat meal was stable to dry heat and refluxing with 6N HCl for 24 hours, but was destroyed or inactivated by refluxing with NH₄OH or NaOH. Activity of meat meal was retained in the acid-insoluble residue after refluxing with 5N HCl for 13 hours. Comparison of the stability of meat meal with thyroid powder indicates that the active principle in meat meal was not thyroxine.

Manuscript received 11 April 1957.