ABSTRACT
Tannic acid (TA) was tested for genotoxic activity in three different assays (1-3) in Drosophila melanogaster by feeding of larvae or adult flies. TA did not induce sex-linked recessive lethals (1) nor sex-chromosome loss, mosaicism or non-disjunction (2) in male germ cells. In the wing somatic mutation and recombination test (SMART) (3) TA was found to be toxic for larvae of the high bioactivation cross and produced a weak positive response. These results suggest that this compound, when administered orally to larvae or adults of D. melanogaster, is not mutagenic and clastogenic in male germ cells, but weakly genotoxic in somatic cells of the wing imaginal disk.
Subject(s)
Drosophila melanogaster/genetics , Hydrolyzable Tannins/toxicity , Mutagens/toxicity , Animals , Female , Genes, Insect/drug effects , Genes, Lethal , Genes, Recessive , Larva , Male , Mosaicism , Mutagenicity Tests , Nondisjunction, Genetic , Recombination, Genetic , Sex Chromosome AberrationsABSTRACT
To investigate the effects of tannic acid (TA) on ring-X chromosome loss, Drosophila melanogaster females exposed to different TA concentrations were crossed with untreated, methyl methanesulfonate (MMS)- or mitomycin C (MMC)-treated males which carried a ring-X chromosome. Progeny were analyzed for loss of the ring-X. The results of this in vivo study showed that TA had no suppressing effect on chromosome loss occurring spontaneously or after induction by MMS in mature spermatozoa. In contrast, TA caused a significant increase in the frequency of MMC-induced ring-X loss. The increase caused by this co-mutagenic effect reached values of 34, 33 and 40% at TA concentrations of 10, 25 and 50 mM, respectively. These increments may reflect the action of TA on a uvrABC-type enzyme which, by increasing the double-strand breaks (DSBs), somehow interferes with the post-replicational repair responsible for the final DSB correction.
Subject(s)
Chromosome Deletion , Drosophila melanogaster/drug effects , Hydrolyzable Tannins/toxicity , Mutagens/toxicity , X Chromosome/drug effects , Animals , Antimutagenic Agents/pharmacology , Chi-Square Distribution , DNA Repair/drug effects , Drosophila melanogaster/genetics , Drug Synergism , Female , Male , Methyl Methanesulfonate/toxicity , Mitomycin/toxicity , Mutagenicity Tests , Ring Chromosomes , Spermatozoa/drug effectsABSTRACT
Studies were conducted to evaluate the clastogenic activity of drinking water from Porto Alegre and Guaíba (Rio Grande do Sul, Brazil) estuarine waters. Mouse bone marrow was the target organ. C57B1/6 male and female mice received the water samples as their only liquid supply. Bone marrow cells were collected on the 16th day after the beginning of treatment. The analysis of metaphases demonstrated that the water supplies did not increase the structural chromosome aberration frequencies compared to the control groups. Concerning numerical alterations, only one treated female group showed a significant difference (loss of one chromosome) when compared to the control group, but this result is not considered relevant.
Subject(s)
Bone Marrow/drug effects , Chromosome Aberrations , Mutagenesis , Water Pollutants, Chemical/toxicity , Water Supply , Animals , Bone Marrow Cells , Brazil , Chi-Square Distribution , Female , Male , Mice , Mice, Inbred C57BL , Mutagenicity Tests/methodsABSTRACT
In order to investigate the anticlastogenic effect of vanillin on ring-X loss, D. melanogaster females exposed to different vanillin concentrations were crossed with non-treated, MMC- or MMS-treated males. The results obtained with this in vivo investigation showed a significant inhibition of vanillin in the frequencies of spontaneous ring-X loss--59, 56, 38 and 36%--at the different concentrations used. In addition, vanillin treatment caused a significant suppression of MMC-induced ring-X loss. This decrease was observed only in the first 3 days after the interruption of vanillin treatment and at the concentrations of 0.5 and 1% of this flavoring agent. In contrast, vanillin did not show any effect on chromosome loss provoked by MMS. Therefore, the ring-X loss-decreasing effect of vanillin seemed to depend on the quality of DNA lesions and consequently on a specific enzymatic repair process present in the oocytes of D. melanogaster.
Subject(s)
Antimutagenic Agents/pharmacology , Benzaldehydes/pharmacology , Chromosome Deletion , DNA Repair , Animals , Chi-Square Distribution , Drosophila melanogaster/genetics , Female , Male , Mitomycin , Mutagenicity Tests , Oocytes/drug effects , Ring Chromosomes , Spermatozoa/drug effects , X Chromosome/drug effectsABSTRACT
In an investigation of the action of integerrimine on chromosomes, the bone marrow was taken as target organ. Male and female mice of the C57Bl/6 strain received a single acute dose of this pyrrolizidine alkaloid, in 2 concentrations: 18.75 and 37.50 mg/kg. Bone marrow cells were collected 6, 12 and 24 h after treatment. The analysis of metaphasic chromosomes demonstrated that chromosomal damage occurs, correlated with drug concentration. The greatest frequency of chromosomal aberrations was detected 12 h after treatment.
