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Mutagenicity and clastogenicity of proflavin in L5178Y/TK+/−−3.7.2.C cells

1988; Elsevier BV; Volume: 204; Issue: 2 Linguagem: Inglês

10.1016/0165-1218(88)90106-1

1878-707X

David M. DeMarini, Karen H. Brock, Carolyn L. Doerr, Martha M. Moore,

Cancer-related Molecular Pathways

We evaluated the ability of proflavin to induce specific-locus mutations at the heterozygous thymidine kinase (tk) locus of L5178Y/TK+/−−3.7.2C mouse lymphoma cells, which appears to permit the recovery of mutants due to single-gene and chromosomal mutations. Proflavin was highly mutagenic at the tk locus, producing 724–965 TK mutants/106 survivors (background = 56–85/106; survival = 29–32%). Most of the mutants were small colonies, which suggested that proflavin may induce chromosomal mutations. The potent clastogenicity of proflavin was confirmed by cytogenetic analysis for chromosomal aberrations. At the highest dose analyzed (1.5 μg/ml), proflavin produced 82 aberrations/100 metaphases (background = 2/100). The large-colony TK mutant frequency produced by proflavin (48–109/106 survivors; background = 23/106; survival = 57–61%) was similar to published HPRT mutant frequencies produces by proflavin in L5178Y and CHO cells (50–100/106 survivors; background = 2–50/106; survival = 50–62%). These results lead to the conclusion that proflavin is a potent clastogen and induces a high frequency of small-colony TK mutants; however, it induces a low frequency of HPRT mutants and a low frequency of large-colony TK mutants.