RESUMO
Experiments on Wistar rats studied the state of the posterity born as a result of mating of intact females with males, who were injected with the antitumor drug platidiam one month before mating (once, intravenously, maximal tolerance dose). The pre- and postimplantation death rate did not grow in female rats mated with test males. However, the fetuses showed visceral anomalies and delayed development of skeleton. A decrease in the muscle tone, as well as ability for the training and extrapolation behavior, were observed in some newborn rat pups.
Assuntos
Antineoplásicos/toxicidade , Cisplatino/toxicidade , Efeitos Tardios da Exposição Pré-Natal , Anormalidades Induzidas por Medicamentos/epidemiologia , Animais , Animais Recém-Nascidos , Feminino , Morte Fetal/induzido quimicamente , Feto/efeitos dos fármacos , Masculino , Gravidez , Ratos , Ratos Wistar , Estatísticas não Paramétricas , Fatores de TempoRESUMO
The experiments performed on Wistar rats showed morphological damages of the rat testis over a one-month period after platidiam administration (4 mg/kg, one-time intravenous injection), namely a decrease in the index of spermatogenesis, in the number of normal spermatogonia, Leydig cells, and testis tubes at the 12th stage of meiosis and an increase in the number of testis tubes squamous epithelium. In the remote period (3 and 6 month after platidiam administration) the recovery of morphological and functional state of the rat testis was observed.
Assuntos
Antineoplásicos/farmacologia , Cisplatino/farmacologia , Testículo/efeitos dos fármacos , Animais , Células Intersticiais do Testículo/efeitos dos fármacos , Células Intersticiais do Testículo/patologia , Masculino , Ratos , Ratos Wistar , Contagem de Espermatozoides/efeitos dos fármacos , Espermatogênese/efeitos dos fármacos , Espermatogônias/efeitos dos fármacos , Espermatogônias/patologia , Estatísticas não Paramétricas , Testículo/patologia , Fatores de TempoRESUMO
The effects of nuclear gene mutations cdc28-srm and srm1 on the maintenance of various recombinant facultative genetic structures (FGSs) in Saccharomyces cerevisiae were studied. These structures are ARS1 TRP1 mini-coils, noncentromeric circular plasmids containing various ARS elements, and extended linear yeast artificial chromosomes (YAC). These mutations led to an increase in the mitotic stability of some of the FGS tested and the disturbed maintenance of the others. Mutation srm1 imposed a stabilizing effect on the maintenance of various recombinant FGSs with ARS chromosomal elements. Mutation cdc28-srm destabilized the maintenance of only those recombinant FGS that shared full or detectable homology with sequences of the nuclear genome of the yeast cell.
Assuntos
Genes Fúngicos , Recombinação Genética , Saccharomyces cerevisiae/genética , Cromossomos Artificiais de Levedura , Mitose/genética , Mutação , Conformação de Ácido Nucleico , Plasmídeos , Homologia de Sequência do Ácido NucleicoRESUMO
With the postmeiotic progeny of triploids used as initial material, n + 1 disomics at chromosomes II, III, VII, VIII, and X were isolated. Disomy at the chromosomes listed (as well as for chromosomes IV and XIV, as demonstrated previously) is associated with decreased spontaneous rho- mitochondrial mutability. This suggests that a disturbance of the chromosome balance itself as such can lead to considerable changes in the spontaneous variability of the mitochondrial genome. From crosses between n + 1 disomics at chromosome IV and for each of the remaining above-mentioned six chromosomes, double n + 2 disomics were isolated, carrying nonchromologous pairs of extra chromosomes. Analysis of mitotic stability of the chromosome IV and spontaneous rho- mutability in double disomics shows that the effect of disomy on spontaneous rho- mutability most probably cannot be explained by direct competition between different genetic structures maintained in Saccharomyces cerevisiae cells. Disturbance of the chromosome balance in disomy is accompanied by essential qualitative changes in processes mediating the maintenance of genetic structures in yeast cells.
Assuntos
Aberrações Cromossômicas , DNA Mitocondrial/genética , Genes Fúngicos , Família Multigênica , Mutagênese/fisiologia , Saccharomyces cerevisiae/genética , Variação Genética , Mitose/genéticaRESUMO
The cdc28-srm mutation in Saccharomyces cerevisiae decreases spontaneous and induced mitochondrial rho- mutability and the mitotic stability of native chromosomes and recombinant circular minichromosomes. The effects of cdc28-srm on the genetic stability of cells support the hypothesis that links cell cycle regulation in yeast to changes in chromatin organization dependent on the start gene CDC28 (Hayles and Nurse, 1986).
Assuntos
Ciclo Celular/fisiologia , Genes Fúngicos , Saccharomyces cerevisiae/genética , Ciclo Celular/genética , Cromatina/fisiologia , Cruzamentos Genéticos , Meios de Cultura , Genótipo , Mitose , Mutação , Plasmídeos , Saccharomyces cerevisiae/crescimento & desenvolvimentoRESUMO
The srm5 mutation diminishes the spontaneous rho- mutation rate by an order of magnitude. Frequency of rho- mutations is 500 times lower in homozygous cultures, as compared with those of normal SRM+/SRM+ diploids. The rate of spontaneous loss of extra chromosome IV is about 25 times higher in srm5 disomes, as compared with SRM+ ones. Haploid srm1 srm5 transformants loose recombinant circular minichromosomes spontaneously about 4 times more frequently than srm1SRM5 cells. The data presented suggest that general control of mitotic stability of different (mitochondrial and nuclear, nuclear as well as recombinant) genetic structures operates in Sacch. cerevisiae. Autonomously replicating sequences (ARS elements) seem to be involved in this mechanism.
Assuntos
DNA Fúngico/genética , DNA Mitocondrial/genética , Genes Fúngicos , Mutação , Recombinação Genética , Saccharomyces cerevisiae/genética , Genótipo , PloidiasRESUMO
In the yeast Saccharomyces cerevisiae the disomy for chromosome XIV resembles the previously described disomy for chromosome IV in that it leads to a significant decrease in spontaneous rho- mutability. The nuclear srm1 mutation, reducing spontaneous rho- mutability, diminishes significantly the mitotic disome stability. So, the mechanisms of spontaneous rho- mutagenesis and mitotic disome stability seem to compete for the function affected by the srm1 mutation.
