Increased clastogenicity and decreased inhibition of DNA synthesis by neocarzinostatin and tallysomycin in ataxia telangiectasia lymphoid cells.
Cytogenetic damage in cells cultured from normal individuals and patients with ataxia telangiectasia (A-T) and xeroderma pigmentosum (XP) was induced by the chemotherapeutic antibiotics neocarzinostatin (NCS), tallysomycin (TLM) and bleomycin (BLM). Chromosomal breakage was specifically elevated in A-T cells when compared to the other genotypes tested. Similar results were not observed with the clastogens mitomycin C (MMC) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) as all cells responded similarly. All 5 chemical agents caused a marked suppression of de novo DNA synthesis in normal and XP long-term lymphoid cell lines while the A-T cells seemed resistant to this effect of NCS, TLM and BLM.
D000903:Antibiotics, Antineoplastic / Q000494:pharmacology*; D001260:Ataxia Telangiectasia / Q000235:genetics*; D001761:Bleomycin / Q000494:pharmacology* / Q000031:analogs & derivatives; D002478:Cells, Cultured; D002869:Chromosome Aberrations; D004247:DNA / Q000096:biosynthesis; D004260:DNA Repair; D006801:Humans; D009154:Mutation / Q000187:drug effects*; D009353:Zinostatin / Q000494:pharmacology*
D000903:Antibiotics, Antineoplastic; D001761:Bleomycin; D004247:DNA; D009353:Zinostatin; C016126:talisomycin