Vincristine induces somatic segregation, via mitotic crossing-over, in diploid cells of Aspergillus nidulans

Chiuchetta, Simone Jurema Ruggeri; Castro-Prado, Marialba Avezum Alves de

doi:10.4067/s0716-97602002000100006

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“…The proportion prototrophic/auxotrophic segregants would be 4+/4− if CLX did not induce mitotic crossing‐over and would be 4+/2− if recombinogenesis occurred (Figure 2). Thus, HI values equal to or over to 2.0 indicate that CLX induced recombinogenesis (Pires and Zucchi, 1994; Chiuchetta and Castro‐Prado, 2002a). HI was determined for each nutritional marker after the phenotypic analyses of the haploid mitotic segregants.…”

Section: Methodsmentioning

confidence: 99%

Chlorhexidine digluconate induces mitotic recombination in diploid cells of Aspergillus nidulans

Souza-Júnior¹,

Castro-Prado²

2005

Oral Diseases

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Section: Methodsmentioning

confidence: 99%

Chlorhexidine digluconate induces mitotic recombination in diploid cells of Aspergillus nidulans

Souza-Júnior¹,

Castro-Prado²

2005

Oral Diseases

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“…1). The homozygotization index (HI), or the ratio between prototrophic and auxotrophic segregants, equal to or over 2.0 (4+/2-), reveals the recombinagenic effect of the compound under analysis (Pires & Zucchi 1994, Chiuchetta & Castro-Prado 2002, Busso & Castro-Prado 2004. …”

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Benznidazole-induced genotoxicity in diploid cells of Aspergillus nidulans

Kaneshima

Castro-Prado

2005

Mem. Inst. Oswaldo Cruz

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Genotoxic effects of benznidazole were studied by the induction of homozygosis of genes previously present in heterozygous. UT448//A757 diploid strain was used in the benznidazole's recombinagenesis test. Although toxic effects on growth of colonies were not observed, 75 and 100 µM benznidazole induced an increasing of mitotic recombination events in diploid strain. Results were related to the induction of chromosomal breaks by the antiparasitic drug.Key words: benznidazole -somatic recombination -genotoxicity -homozigotization index Chagas disease, caused by Trypanosoma cruzi, is one of the most serious parasitic diseases of Latin America, where some 16 -18 million people are infected by the T. cruzi (WHO 1991). Although in Brazil the disease is under strict control, there are still about 4 million people infected by the parasite (Dias 1998). Benznidazole is used in the treatment of Chagas disease in the acute phase, at the start of the chronic phase, in congenital cases and accidental infection (Fragata Filho et al. 1997). Several adverse effects have been described in patients undergoing treatment with the anti-parasitic drug (Cançado 1997, Fragata Filho et al. 1997.The mutagenic action of the benznidazol has been studied in streptomycin-resistant Klebsiella pneumoniae strain and in Salmonella typhimurium TA100 strain. Mutagenic effect of the drug has also been observed in TA100 strain in the presence and in the absence of the microsomal hepatic fraction of mice, using 50 to 1000 µM concentrations (Voogd et al. 1975, Nagel & Nepomnaschy 1983.The mutagenic activity of benznidazole has also been determined in the simplified version of Ames test with sensitive (TA100 and TA102) and less sensitive (TA98 and TA97) S. typhimurium strains (Melo & Ferreira 1990) in the same plate. The drug's mutagenic effect was accounted to the interaction of reactive metabolites of benznidazole with the DNA and with nuclear proteins (Gorla et al. 1986, Zahoor et al. 1987, Ferreira et al. 1988).Benznidazole's genotoxicity has been studied in peritoneal macrophages of mice treated with benznidazole (Lacava & Luna 1994). These authors reported the clastogenic effect of the drug owing to increase in the frequency of chromatid breaks and to the formation of acrocentric chromosomes. Moya and Trombotto (1988) In spite of these contradictory results, the clastogenic effect of benznidazole (Lacava & Luna 1994) suggest its participation in the carcinogenic process due to the occurrence of mitotic crossing-over that induces the loss of heterozygosity of tumor suppressor genes (Zimmermann 1971, Weinberg 1991, Beumer et al. 1998. The evaluation of the recombinagenic potential of benznidazol in heterozygous cells of Aspergillus nidulans will be provided. Information on the participation of the anti-parasitic drug in the carcinogenesis process will be thus ensued. MATERIALS AND METHODSStrains and culture media -A. nidulans strains used are described in Table I. Minimum medium (MM) was Czape-Dox with 1% (w/v) glucose. Complete medium (CM) has pre...

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Parasexuality in asexual development mutants of Aspergillus nidulans

Becker

Castro-Prado

2006

Biol. Res.

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The parasexual cycle with parameiosis has been characterized previously by the occurrence of genetic recombination and haploidization inside heterokaryotic hyphae prior to conidial formation. The aim of current research was to characterize, through genetic and cytological analyses, an asexual development mutant strain of A. nidulans and to use it to obtain parameiotic segregants. Analyses showed the medusa phenotype of the B84 strain, whose mutant allele was mapped in the chromosome I. The heterokaryons B84(med)//G422(med+) and B84(med)//G839(brl) were formed in liquid MM+2% CM and inoculated in the appropriate selective media. Two mitotic segregant groups were obtained: aneuploids and haploid stable recombinants. Mitotic segregants, wild-types, and developmental mutants, which did not produce new visible mitotic sectors in the presence of Benomyl and which showed normal meiotic behavior during the sexual cycle, were classified as parameiotics.

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Vincristine induces somatic segregation, via mitotic crossing-over, in diploid cells of Aspergillus nidulans

Cited by 3 publications

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Chlorhexidine digluconate induces mitotic recombination in diploid cells of Aspergillus nidulans

Chlorhexidine digluconate induces mitotic recombination in diploid cells of Aspergillus nidulans

Benznidazole-induced genotoxicity in diploid cells of Aspergillus nidulans

Parasexuality in asexual development mutants of Aspergillus nidulans

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