Effect of Colchicine and cytochalasin B on ooplasmic segregation of ascidian eggs

1974 ◽  
Vol 175 (3) ◽  
pp. 243-248 ◽  
Author(s):  
M. Zalokar
Author(s):  
Awtar Krishan ◽  
Nestor Bohonos

Cytochalasin B, a mould metabolite from Helminthosporium dermatioideum has been shown to interfere with specific cell activities such as cytoplasmic cleavage and cell movement. Cells undergoing nuclear division in the presence of cytochalasin B are unable to complete the separation of the resulting daughter cells. In time-lapse studies, the daughter cells coalesce after an initial unsuccessful attempt at separation and form large multinucleate polyploid cells. The present report describes the fine structure of the large polyploid cells induced in Earle's L-cell monolayer cultures by exposure to cytochalasin B (lγ/ml) for 92 hours.In the present material we have seen as many as 7 nuclei in these polyploid cells. Treatment with cytochalasin B for longer periods of time (6 to 7 days, with one medium change on the 3rd day) did not increase the number of nuclei beyond the 7 nuclei stage. Figure 1 shows a large polyploid cell with four nuclei. These nuclei are indistinguishable in their fine structure from those of the cells from control cultures but often show unusually large numbers of cytoplasmic invaginations and extensions of the nuclear surface (Figure 2).


Nanomaterials ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1929
Author(s):  
Tereza Cervena ◽  
Andrea Rossnerova ◽  
Tana Zavodna ◽  
Jitka Sikorova ◽  
Kristyna Vrbova ◽  
...  

The evaluation of the frequency of micronuclei (MN) is a broadly utilised approach in in vitro toxicity testing. Nevertheless, the specific properties of nanomaterials (NMs) give rise to concerns regarding the optimal methodological variants of the MN assay. In bronchial epithelial cells (BEAS-2B), we tested the genotoxicity of five types of NMs (TiO2: NM101, NM103; SiO2: NM200; Ag: NM300K, NM302) using four variants of MN protocols, differing in the time of exposure and the application of cytochalasin-B combined with the simultaneous and delayed co-treatment with NMs. Using transmission electron microscopy, we evaluated the impact of cytochalasin-B on the transport of NMs into the cells. To assess the behaviour of NMs in a culture media for individual testing conditions, we used dynamic light scattering measurement. The presence of NMs in the cells, their intracellular aggregation and dispersion properties were comparable when tests with or without cytochalasin-B were performed. The genotoxic potential of various TiO2 and Ag particles differed (NM101 < NM103 and NM302 < NM300K, respectively). The application of cytochalasin-B tended to increase the percentage of aberrant cells. In conclusion, the comparison of the testing strategies revealed that the level of DNA damage induced by NMs is affected by the selected methodological approach. This fact should be considered in the interpretation of the results of genotoxicity tests.


1974 ◽  
Vol 249 (18) ◽  
pp. 5778-5783
Author(s):  
Shin Lin ◽  
James A. Spudich

1994 ◽  
Vol 76 (4) ◽  
pp. 1657-1663 ◽  
Author(s):  
H. H. Simms ◽  
R. D′Amico

Expression of the receptor CD11b/CD18 on the polymorphonuclear leukocyte (PMN) surface is important for several aspects of PMN function during endotoxemia. The mechanisms underlying regulation of CD11b/CD18 expression during hypoxemia and endotoxemia, however, are less clear. We investigated the effects of exposure of whole blood PMNs to lipopolysaccharide (LPS) during hypoxemia. During hypoxemia (10–30% O2 saturation), LPS reduced CD11b/CD18 expression. Both kinetic assays and experiments with microfilament stabilizers (phalloidin, cytochalasin B) demonstrated that this was most likely due to receptor shedding. Incubation of whole blood PMNs with an anti-CD14 monoclonal antibody (MEM18) largely prevented the LPS-induced reduction of CD11b/CD18 expression. Decreased CD11b/CD18 expression reduced PMN functional capability, as the binding of its ligand (erythrocytes opsonized with the 3rd component of complement Cbi) and intracellular H2O2 production were reduced. After exposure to LPS, N-formyl-methionyl-leucyl-phenylalanine could rapidly induce new CD11b/CD18 receptors to the cell surface, and this was not inhibited by actinomycin D or cycloheximide. After reoxygenation (> 90% O2 saturation), CD11b/CD18 expression was restored, and this was abrogated by exposure to cytochalasin B. Lipid A was able to reproduce the effects of LPS during hypoxemia and hypoxemia-reoxygenation but required a 10-fold greater concentration to do so. These results demonstrate that during hypoxemia an important pathophysiological property of LPS is to reduce CD11b/CD18 expression. This results in diminished PMN functional capability, which would contribute to the pathogenicity of LPS during acute infectious states.


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