demecolcine has been researched along with Abnormalities--Drug-Induced* in 3 studies
3 other study(ies) available for demecolcine and Abnormalities--Drug-Induced
Article | Year |
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Bipartite axiation follows incomplete epiboly in zebrafish embryos treated with chemical teratogens.
Medial clefts in the axis of the trunk region are malformations known from many chordates and are mostly referred to as rachischisis anterior. In teleosts, rachischisis was previously ascribed either to secondary rifting of a single uniform axial rudiment, or to the establishment of two (half) axes and body halves physically separate from the very beginning. In order to decide between these conflicting interpretations, we treated zebrafish embryos during blastodisc stages and epiboly with several chemical teratogens causing rachischisis anterior. Treatment with ethanol, Colcemid, hydroxyurea, or cycloheximide was found to delay the proliferation and movements of the deep cells more strongly than the timing of cell differentiation, so that the deep cells embark on organogenesis before having reached their destinations in the uniform germ shield. Treatment with alpha-amanitin, on the other hand, seems primarily to affect the periblast and enveloping layer; the incomplete epiboly observed in these layers appears to restrain deep cell epiboly physically and thus to cause rachischisis. In both instances, the split condition of the embryo's trunk region is clearly due to the ectopic formation of physically separate body halves right from the beginning, a mode we call bipartite axiation. We also describe secondary anomalies specific for individual teratogens, and briefly discuss the possible origins of rachischisis anterior among other chordates including man. Topics: Abnormalities, Drug-Induced; Amanitins; Animals; Cell Differentiation; Cell Division; Cycloheximide; Demecolcine; Ethanol; Fishes; Hydroxyurea; Morphogenesis | 1984 |
Polyploidy and aneuploidy induced by colcemid in Drosophila melanogaster.
Colcemid was fed to Drosophila melanogaster larvae throughout most of the larval period. Surviving individuals were then mated with untreated flies, and their progeny were examined for polyploid flies or flies resulting from X-chromosome nondisjunction. A total of 251 polyploid offspring was recovered from the experimental matings, none from the control. All of the polyploids were evidently triploids, and all but one were obtained from colcemid-fed females: males produced significantly lower frequencies of triploid offspring than females. The highest average frequency of triploid offspring obtained from any treatment group was 18%. Nonrandom distributions of triploid offspring were observed among females raised identically, indicating tht polyploidization occurs mitotically, rather than meiotically, giving rise to clones of tetraploid oogonia. 9 colcemid-fed females produced exclusively triploid offspring. Colcemid also caused a significant increase in X-chromosome nondisjunction in females, though the frequencies of such offspring were at least several-fold lower than the frequencies of triploid offspring. Somatic polyploidy was apparently also indiced since patches of large cells were found on the wings of some flies raised on colcemid-containing food. Various teratological abnormalities were observed among the treated flies, including deformed or missing eyes and partially duplicated thoraxes. Topics: Abnormalities, Drug-Induced; Aneuploidy; Animals; Demecolcine; Drosophila melanogaster; Female; Larva; Male; Mitosis; Polyploidy; Sex Chromosome Aberrations; Teratogens; X Chromosome | 1982 |
[Teratogenic effect of Colcemide on embryogenesis of chick embryos].
Topics: Abnormalities, Drug-Induced; Abnormalities, Multiple; Animals; Chick Embryo; Demecolcine; Embryo, Mammalian; Embryo, Nonmammalian | 1972 |