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 Boctor, A. M. Articles by Harper, A. E. Search for Related Content PubMed PubMed Citation Articles by Boctor, A. M. Articles by Harper, A. E.

Tyrosine Toxicity in the Rat: Effect of high intake of p-hydroxyphenylpyruvic acid and of force-feeding high tyrosine diet¹

Department of Biochemistry, University of Wisconsin, Madison, Wisconsin and Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts

Rats fed a low protein diet containing 5% of tyrosine develop external pathological lesions within a few days. The objective of the experiments described below was to determine whether this syndrome could be produced by feeding p-hydroxyphenylpyruvic acid or was altered by maintaining the food intake of rats fed a high tyrosine diet through force-feeding. When p-hydroxyphenylpyruvic acid was substituted for tyrosine, signs of toxicity did not develop within 2 weeks. Plasma tyrosine concentration and liver tyrosine transaminase activity were greatly elevated in rats fed the high tyrosine or the high p-hydroxyphenylpyruvic acid diet. The activity of p-hydroxyphenylpyruvate hydroxylase was not elevated in rats fed a high tyrosine diet; however, this enzyme appeared to be preferentially retained in the livers of rats fed p-hydroxyphenylpyruvic acid while liver weight was decreasing. Rats force-fed the high tyrosine diet showed only a transitory improvement in weight gain and 2 of 7 died within 8 days, which indicates that low food intake is an effect and not a cause of tyrosine toxicity. The results make it unlikely that intermediates of the main pathway of tyrosine degradation are responsible for the development of the signs of tyrosine toxicity.

² Present address: Department of Pharmacology, New York University Medical Center, New York.

Manuscript received 7 March 1968.