RESUMO
The induction of sex chromosomes meiotic nondisjunction (ND) by hydroquinone (HQ) given orally was investigated in Drosophila melanogaster 2-7, 8-22, 24, 48, 72 and 96 h-old females. ND was assessed by a system where exceptional females (XXY) and only 1/4 of the expected regular progeny are viable. Oocytes were treated at different stages of development. 4% HQ tested only in 72 h-old females induced ND in oocytes sampled in brood I (mostly mature oocytes at metaphase I). 6% HQ increased ND in brood I of 8-22 h-old females, while other broods, (including cells treated at early prophase) were also affected in older flies, the highest significance being attained in the 48 h-old series. Newly hatched females (2-7 h-old) were refractory to the treatment, though oocytes sampled in the first three subcultures are comparable to cells showing enhancement of ND in series run with older females. Toxicity of 2, 4 and 6% HQ increased with concentration and females' age: (a) 2% was not toxic; (b) 4% was toxic only to 72 h-old females; (c) 6% was increasingly toxic to females 24, 48 and 72 h-old. The results indicate that age plays a significant role on both chromosomal segregation and toxicity and suggest that in Drosophila HQ is metabolized to its reactive species. The lack of toxic and aneugenic effect in very young females could reflect a more efficient detoxification due to the known high specific activity of glutathione-S-transferase (GST) after eclosion. The decline in GST activity around day 2 of adult life coincides with the high effect of HQ in 48 h-old females.
Assuntos
Hidroquinonas/toxicidade , Meiose/efeitos dos fármacos , Mutagênicos/toxicidade , Animais , Aberrações Cromossômicas , Drosophila melanogaster , Feminino , Glutationa Transferase/metabolismo , Inativação Metabólica , Oócitos/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Cromossomos Sexuais/efeitos dos fármacosRESUMO
Two arsenic compounds, sodium arsenite (NaAsO2) and sodium arsenate (Na2HAsO4), were tested for their possible genotoxicity in germinal and somatic cells of Drosophila melanogaster. For germinal cells, the sex-linked recessive lethal test (SLRLT) and the sex chromosome loss test (SCLT) were used. In both tests, a brood scheme of 2-3-3 days was employed. Two routes of administration were used for the SLRLT: adult male injection (0.38, 0.77 mM for sodium arsenite; and 0.54, 1.08 mM for sodium arsenate) and larval feeding (0.008, 0.01, 0.02 mM for sodium arsenite; and 0.01, 0.02 mM for sodium arsenate). For the SCLT the compounds were injected into males. Controls were treated with a solution of 5% sucrose which was employed as solvent. The somatic mutation and recombination test (SMART) was run in the w+/w eye assay as well as in the mwh +/+ flr3 wing test, employing the standard and insecticide-resistant strains. In both tests, third instar larvae were treated for 6 hr with sodium arsenite (0.38, 0.77, 1.15 mM), and sodium arsenate (0.54, 1.34, 2.69 mM). In the SLRLT, both compounds were positive, but they were negative in the SCLT. The genotoxicity of both compounds was localized mainly in somatic cells, in agreement with reports on the carcinogenic potential of arsenical compounds. Sodium arsenite was an order of magnitude more toxic and mutagenic than sodium arsenate. This study confirms the reliability of the Drosophila in vivo system to test the genotoxicity of environmental compounds.