Date of Award

Spring 1989

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Chemistry & Biochemistry

Program/Concentration

Chemistry

Committee Director

Mark S. Elliot

Committee Member

Roy L. Williams

Committee Member

Frank E. Scully, Jr.

Committee Member

Patricia A. Pleban

Call Number for Print

Special Collections LD4331.C45S46

Abstract

Human cultured leukemia cells appear to have a decreased amount of inosine in their tRNA. When cells with inosine deficient tRNA are placed in a hypoxanthine fortified media, they incorporate hypoxanthine into their tRNA by the action of the enzyme tRNA-hypoxanthine ribosyl transferase. This generates the nucleoside inosine in the tRNA. The cultured human leukemia cell lines, CCRF-CEM, HL-60, and HGPRT(-) HL- 60, incorporate hypoxanthine into their tRNA, as determined by tRNA isolation, hydrolysis, and HPLC analysis. Hypoxanthine treatment dramatically inhibited cell growth in conjunction with partial induction of differentiation in the CCRF-CEM, HL-60, and HGPRT ( - ) HL-60 cells cultures. Immunofluorescent analysis of surface differentiation antigens for CCRF-CEM cells established differences that indicated a progression towards a more differentiated phenotype. The HL- 60 and HGPRT(-) HL-60 cells morphologically and functionally differentiated after exposure to hypoxanthine as determined by differential counts and NBT reduction. These results suggest that hypoxanthine induced differentiation of these human cultured leukemia cells is due to the concurrent modification of tRNA with hypoxanthine to form inosine.

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DOI

10.25777/ehkp-3251

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