D-ribose inhibits DNA repair synthesis in human lymphocytes.
D-ribose is cytotoxic for quiescent human lymphocytes and severely inhibits their PHA-induced proliferation at concentrations (25-50 mM) at which other simple sugars are ineffective. In order to explain these effects, DNA repair synthesis was evaluated in PHA-stimulated human lymphocytes treated with hydroxyurea and irradiated. D-ribose, in contrast to other reducing sugars, did not induce repair synthesis and therefore did not apparently damage DNA in a direct way, although it markedly inhibited gamma ray-induced repair. Taking into account that lymphocytes must rejoin physiologically-formed DNA strand breaks in order to enter the cell cycle, we suggest that D-ribose exerts its cytotoxic activity by interfering with metabolic pathways critical for the repair of DNA breaks.
D001089:Arabinose / Q000494:pharmacology; D004260:DNA Repair / Q000187:drug effects* / Q000528:radiation effects; D005720:Gamma Rays; D006801:Humans; D006918:Hydroxyurea / Q000494:pharmacology; D007700:Kinetics; D008213:Lymphocyte Activation / Q000187:drug effects; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D010835:Phytohemagglutinins; D012266:Ribose / Q000494:pharmacology*; D013936:Thymidine / Q000097:blood
D010835:Phytohemagglutinins; D012266:Ribose; D001089:Arabinose; D013936:Thymidine; D006918:Hydroxyurea