Formation of viable cell fragments by treatment with colchicine (original) (raw)

Experimental evolution of cell populations of chinese hamster treated with colchicine. induction of high degree of ploidy and a phase-specific lethal effect

International Journal of Cancer, 1972

M soon after pulses of H3TdR. If, after being treated with colchicine, the cultures are replaced in a normal medium, there is no resumption of proliferation and the cells follow a progressive polyploidization as 4 result of repeated C-mitoses. If, instead, the cultures are trypsinized or detached mechanically, and then plated again, or if the culture medium is changed periodically, the cultures resume their division processes. This phenomenon has been interpreted as resulting from the progressive dilution of intracellular as well as free colchicine according to Borisy and Taylor (1967a, b). The resumption of proliferation is not immediate but progressive. The later the cultures resume their proliferation the higher the degree ofploidy. In these cultures, characterized by high ploidy, there is an increase of the percentage of multipolar mitoses and of the number of poles. It is impossible to maintain in the same cultures a high degree of ploidy, which decreases progressively as a result of the multipolar mitoses. All the cells become polyploid, without regard to the phase of the cycle in which they are at the time of treatment. But the cells that were in G I , M and G , can complete at the most two cycles, going into mitosis with:a decreasing frequency; after 70 h they disappear rapidly from the population. This pattern is identical in the cultures that resume proliferation as well as in the other ones. The cells found in late-S and above all in G , at the time of treatment may endoreduplicate and appear as endoreduplicated mitoses 22-24 h after treatment with a 10-15% relative frequency. Some assumptions have been made in order to explain the phase-specific response in regard to the lethal effect as well as to endoreduplication. We have related these results to the moment at which colchicine enters the cells.

MORPHOLOGICAL AND KINETIC ASPECTS OF MITOTIC ARREST BY RECOVERY FROM COLCEMID AND

The Journal of cell biology, 1966

The cffcct of Colccmid on the in vivo systcm of regenerating rat liver and on the in vitro system of HeLa cell cultures was studied to determine some of the morphological and kinetic aspects of mctaphase blockage and recovery. The results indicated that under certain conditions the blocking cffccts of the drug were rcvcrscd; a functional bipolar spindle reorganized, and normal division resulted. Individual HeLa cells were followed by time-lapse cincmicrography prior to, during, and after Colcemid treatment. There was no apparent effect on cells in intcrphase. Cells cntcrcd mitosis at a normal rate and passed through prophase. A spindle was formcd in most cells, albeit deformed, stunted, or shrunken. Within a certain range of drug concentrations, the spindlc lengths showcd characteristic unimodal distributions. After a 2-hr exposure to the drug followed by 1 hr in fresh medium, spindle lengths were restored to normal. Cells arrcstcd in metaphasc for periods as long as 5 hr were capable of reconstituting a normal functional spindle. Cells blocked for periods longcr than 5 to 6 hr failed to rccover.

Morphological and Kinetic Aspects of Mitotic Arrest by and Recovery From Colcemid

The Journal of Cell Biology, 1966

The cffcct of Colccmid on the in vivo systcm of regenerating rat liver and on the in vitro system of HeLa cell cultures was studied to determine some of the morphological and kinetic aspects of mctaphase blockage and recovery. The results indicated that under certain conditions the blocking cffccts of the drug were rcvcrscd; a functional bipolar spindle reorganized, and normal division resulted. Individual HeLa cells were followed by time-lapse cincmicrography prior to, during, and after Colcemid treatment. There was no apparent effect on cells in intcrphase. Cells cntcrcd mitosis at a normal rate and passed through prophase. A spindle was formcd in most cells, albeit deformed, stunted, or shrunken. Within a certain range of drug concentrations, the spindlc lengths showcd characteristic unimodal distributions. After a 2-hr exposure to the drug followed by 1 hr in fresh medium, spindle lengths were restored to normal. Cells arrcstcd in metaphasc for periods as long as 5 hr were capable of reconstituting a normal functional spindle. Cells blocked for periods longcr than 5 to 6 hr failed to rccover.

Comparative analysis of colchicine induced micronuclei in different cell types in vitro

Mutation research, 1996

In the present study we analyzed the induction of micronuclei (MN) by colchicine, at different treatment times, in four histogenetically different cell cultures: human skin fibroblasts (HSF), bovine skin fibroblasts (BSF), bovine bladder fibroblasts (BBF) and human skin epithelial cells (HK), developed and characterized in our laboratory. The frequencies of dead cells, nuclear budding and mitotic index were also evaluated. The HSF and BSF cell lines showed similar frequencies of micronucleated cells (4.7% and 4.9%, respectively) at 96 h of treatment time. The BBF cell line showed the lowest frequency of micronucleated cells (2.6%) and HK did not show any MN. The studied cell lines differed in their responses to colchicine. The data revealed the relevance of utilization of other end-points as growth curves, dead cells, mitotic index and other nuclear alterations for accurate analysis of the effect of agents that disturb cell cycle or are cytotoxic.

Effect of cytochalasin B on the induction of chromosome missegregation by colchicine at low doses in human lymphocytes

Mutat Res Fundam Mol Mech Mut, 1997

The aim of the present work was to investigate the possible interference of cytochalasin B (cyt B) with low concentration treatment with colchicine in the induction of chromosome/chromatid loss and micronuclei in human lymphocytes mitotically activated in vitro. Thus, cells from a single female donor were treated with colchicine (10 or 25 nM, from 24 h after PHA addition to fixation at 66 h) either in the presence or absence of cyt B.