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  Vol. 125 No. 1, January 1990 TABLE OF CONTENTS
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  PAPERS READ BEFORE THE NINTH ANNUAL MEETING OF THE SURGICAL INFECTION SOCIETY, DENVER, COLO, APRIL 13 TO APRIL 14, 1989-PAR T II
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Dietary Nucleotides Reverse Malnutrition and Starvation-Induced Immunosuppression

Roland P. Pizzini, BS; Saroj Kumar, MS; Anil D. Kulkarni, PhD; Fredrick B. Rudolph, PhD; Charles T. Van Buren, MD

Arch Surg. 1990;125(1):86-90.


Abstract

• The requirement of dietary nucleotide sources for maximal helper T-cell function has been demonstrated. The effect of dietary nucleotide restriction was tested during two forms of nutritional stress: starvation and protein malnutrition. In the starvation model, mice were fed chow diet, nucleotide free or nucleotide free supplemented with 0.25% yeast RNA, for at least 4 weeks. The animals were then starved for 5 days, at which time they were killed and mitogen assays were performed using spleen cells. Animals previously maintained on the nucleotide-free diet supplemented with RNA showed a significant increase in spontaneous concanavalin A and phytohemagglutinin-stimulated blastogenesis. Protein malnutrition was induced by feeding Balb/c mice a protein-free diet for 7 to 10 days. These mice then received either the protein-free diet, the nucleotide-free diet, or the nucleotide-free diet supplemented with 0.25% yeast RNA. Popliteal lymph node assays were then performed. The chow diet, nucleotide-free diet, and nucleotide-free diet supplemented with 0.25% yeast RNA led to a restoration of body weight, but only the chow and supplemented diets restored significant popliteal lymph node immune reactivity. These studies using starvation and protein-malnutrition models clearly indicate the nutritional role of nucleotides in the maintenance and restoration of the immune response.

(Arch Surg. 1990;125:86-90)



Author Affiliations

From the Department of Surgery, Division of Immunology and Organ Transplantation, The University of Texas Medical School, Houston (Mr Pizzini, Ms Kumar, and Drs Kulkarni and Van Buren) and the Department of Biochemistry, Rice University, Houston (Dr Rudolph).


Footnotes

Accepted for publication August 28, 1989.

Read before the Ninth Annual Meeting of the Surgical Infection Society, Denver, Colo, April 14, 1989.

Reprint requests to the Department of Surgery, Division of Immunology and Organ Transplantation, The University of Texas Medical School, Houston, TX 77030 (Dr Kulkarni).



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