| 包装 | 价格(元) |
| 1mg | 询价 |
| 5mg | 询价 |
| 10mg | 询价 |
| 50mg | 询价 |
Colcemid is a cytoskeletal inhibitor that induces mitotic arrest in the G2/M phase or meiotic arrest in the vesicle rupture (GVBD) phase in mammalian cells or oocytes, respectively.
Cell lines | Syrian hamster embryo cells |
Preparation Method | Treatment of Syrian hamster embryo cells in culture with 0.01-0.1 µg/ml of colcemid for 48 h resulted in morphological and neoplastic transformation of the cells. |
Reaction Conditions | 0.01-0.1 µg/ml of colcemid for 48 h |
Applications | Cell transformation was observed with doses which were non-cytotoxic and did not cause mitotic inhibition of the cells. Higher dose of colcemid (greater than 0.1 µg/ml) resulted in mitotic inhibition of the cells and a significant loss of colony forming ability, but no increase in the frequency of morphological transformation.A 14-fold increase in the number of aneuploid cells with a near diploid chromosome complement was found in cultures treated with 0.1 µg/ml colcemid and both chromosome loss and gain were induced. |
Animal models | Tumor bearing mice |
Preparation Method | Mice were injected intravenously with Colcemid |
Dosage form | 5.82 µg/hr for 4h |
Applications | A mitotic linear accumulation was obtained by continuous colcemid infusion at 5.82 µg/hr. Low dose colcemid infusion (0.582 and 1.455 µg/hr) for 14 hours did not accumulated mitotic cells, but doses more than 5.82 µg/hr of colcemid blocked it completely, accumulating 25.5% of cells after a 20 hours infusion. |
| 产品描述 | Colcemid is a cytoskeletal inhibitor that induces mitotic arrest in the G2/M phase or meiotic arrest in the vesicle rupture (GVBD) phase in mammalian cells or oocytes, respectively[1][2].Colchicine interferes with microtubule polymerization by tightly binding to tubulin dimers and prevents spindle microtubule formation by depolymerization[7]. Cell transformation was observed with doses which were non-cytotoxic and did not cause mitotic inhibition of the cells. Higher dose of colcemid (greater than 0.1 μg/ml) resulted in mitotic inhibition of the cells and a significant loss of colony forming ability, but no increase in the frequency of morphological transformation.A 14-fold increase in the number of aneuploid cells with a near diploid chromosome complement was found in cultures treated with 0.1 μg/ml colcemid and both chromosome loss and gain were induced[4]. Colcemid was more cytotoxic to cells in G2 + M than to G1 + S phase cells, and it slowed the progression of G1 cells to S. These effects of colcemid were much greater in aneuploid B16 melanoma cells than in pseudodiploid Chinese hamster ovary (CHO) cells[5]. Colcemid promotes UVC-induced apoptosis in Chinese hamster ovary cells (CHO.K1).Although colcemid did not affect the excision of UV-induced DNA damages such as photoproducts or cyclobutane pyrimidine dimers, colcemid accumulated the DNA breaks when it was added to cells following UV-irradiation[3]. A mitotic linear accumulation was obtained by continuous colcemid infusion at 5.82 μg/hr. Low dose colcemid infusion (0.582 and 1.455 μg/hr) for 14 hours did not accumulated mitotic cells, but doses more than 5.82 μg/hr of colcemid blocked it completely, accumulating 25.5% of cells after a 20 hours infusion[6]. References: |
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