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      Evidence that low concentrations of chlorophyllin (CHLN) increase the genetic damage induced by gamma rays in somatic cells of Drosophila

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      Mutation Research/Genetic Toxicology and Environmental Mutagenesis
      Elsevier BV

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          Abstract

          It was first demonstrated in Salmonella that higher and lower concentrations of chlorophyllin (CHLN) may have effects in opposite directions, higher doses inhibiting and lower doses promoting the mutagenic activity of certain tobacco-related nitrosamines. Previous work of our group demonstrated that CHLN may have both a promoter and an inhibitory effect on mutagenesis in Drosophila. The present paper reviews the evidence obtained in our laboratory using gamma rays as the mutagenic agent, that higher and lower pretreatment concentrations of CHLN are associated with inhibitory and promoting effects, respectively, as in Salmonella. Employing the wing spot test, 48h larvae were pretreated with various concentrations of CHLN from 0 to 69 mM and then treated with 10 Gy gamma rays. With the highest concentration of CHLN, an approximate 54% reduction in mutagenesis was observed. At 35 mM a remnant of this inhibitory effect was found in that a significant decrease was limited to the twin spot category. Evidence of promotion was first seen at 4.3mM CHLN, an effect which persisted for the remaining five lower concentrations, the most pronounced evidence of promotion being found at the four lowest concentrations, 0.03-1.1 mM CHLN. It should be noted that no evidence of genotoxicity was found for CHLN alone, an observation consistent with the several reports in the literature. The results are taken as strong evidence that pretreatment with low concentrations of CHLN promotes DNA damage induced by gamma rays in somatic cells of Drosophila.

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          Author and article information

          Journal
          Mutation Research/Genetic Toxicology and Environmental Mutagenesis
          Mutation Research/Genetic Toxicology and Environmental Mutagenesis
          Elsevier BV
          13835718
          September 2009
          September 2009
          : 679
          : 1-2
          : 84-86
          Article
          10.1016/j.mrgentox.2009.07.004
          19616118
          ecc5d2cb-f012-4c65-a66a-0ad10f72b7f1
          © 2009

          https://www.elsevier.com/tdm/userlicense/1.0/

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