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Increased clastogenicity and decreased inhibition of DNA synthesis by neocarzinostatin and tallysomycin in ataxia telangiectasia lymphoid cells
Affiliation:1. Department of Chemical Engineering and Metallurgy, University of Sonora, Blvd. Rosales y Luis Encinas, Hermosillo, Sonora CP 83000, Mexico;2. National Center of Research and Technological Development, CENIDET-TecNM-SEP, Prol. Av. Palmira S/N. Col. Palmira, Cuernavaca, Morelos CP 62490, Mexico;3. Department of Ophthalmology, Wake Forest School of Medicine Winston-Salem, NC USA;4. Department of Anesthesia, Division of Critical Care Medicine, Harvard Medical School Boston, MA USA
Abstract: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.
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