Decreased DNA repair synthesis and defective colony-forming ability of ataxia telangiectasia fibroblast cell strains treated with N-methyl-N'-nitro-N-nitrosoguanidine.
DNA repair synthesis and posttreatment colony-forming ability were measured in six human fibroblast cell strains derived from patients with the autosomal recessive disorder, ataxia telangiectasia (AT), and five cell strains from normal individuals. All 11 cell strains showed approximately equal levels of DNA repair synthesis after methyl methanesulfonate and ultraviolet light treatments assayed by the benzoylated naphthoylated diethylaminoethyl-cellulose method. Four AT cell strains exhibited 27 to 41% of the repair shown by normal cell strains after treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Two AT cell strains had normal levels of repair synthesis after MNNG treatment. All the AT strains tested had normal survival after treatment with methyl methanesulfonate and ultraviolet light as assayed by posttreatment colony-forming ability. The six AT cell strains exhibited diminished survival after MNNG treatment. The inhibition of [3H]thymidine uptake as a function of MNNG concentration was similar for all the normal and AT cell strains tested.
D000477:Alkylating Agents / Q000627:therapeutic use; D001260:Ataxia Telangiectasia / Q000188:drug therapy / Q000378:metabolism* / Q000532:radiotherapy; D002455:Cell Division / Q000187:drug effects*; D002999:Clone Cells / Q000187:drug effects*; D004260:DNA Repair / Q000187:drug effects* / Q000528:radiation effects; D004273:DNA, Neoplasm / Q000096:biosynthesis; D006801:Humans; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology*; D014466:Ultraviolet Rays
D000477:Alkylating Agents; D004273:DNA, Neoplasm; D008769:Methylnitronitrosoguanidine