and can possibly be used as anticancer drug. Inhibits cell division Cytochalasin B is used for testing of the genotoxicity of substances. In order to do so, cytokinesis-block micronucleus assay (CBMN assay) with human lymphocytes is applied. This works in vitro. During anaphase of mitosis of meiosis, micronuclei can be detected. These are small nuclei containing one chromosome or part of a chromosome which did not get to one of the cell poles during cell division. The CBMN test is based on the fact that only dividing cells can express micronuclei, which means that only in those cells, chromosome damage can be detected. Because genotoxicity causes abnormalities in cell division, micronuclei can be detected in binucleated cells. Cytokinesis, which is the next stage, is inhibited by cytochalasin B. A key advantage of this method is that it allows simultaneous detection of multiple molecular events leading to chromosome damage and chromosomal instability. The CBMN assay has successfully been applied to normal human lymphocytes, mouse spleen lymphocytes, mouse fibroblasts and Chinese hamster fibroblasts. Inhibits cell movement Cytochalasin B can decrease the number of motile cells when it is added to Yoshida Sarcoma Cells. It can also decrease the motility of the cells and dose-dependently inhibits their growth. Since cytochalasin B unevenly penetrates cells it promotes focal contractions of the broken cortical actin filament network by myosin. This causes superprecipitation which requires active contractions and thus an active energy metabolism. The disorganized cortical contractions disrupt the assembly of pseudopodia which are involved in cell movement. Induces nuclear extrusion Nuclear extrusion induced by cytochalasin B begins with the movement of the nucleus to the plasma membrane, followed by bulge formation in the membrane. The nucleus then moves to the outside of the membrane, but stays connected to the cell by a thread-like cytoplasmic bridge. If the cells are kept in cytochalasin B containing medium for several hours, the process becomes irreversible. Extrusion could be assisted by the CB-induced weakening of the plasma membrane. Inhibits glucose transport It has been shown that cytochalasin B binds covalently to mammalian glucose transporter proteins when irradiated with UV light. It bound tighter to AraE and GalP than their usual substrates. Cytochalasin B has been shown to inhibit GLUT1, 2, 3 and 4. Binding to GLUT1 occurs at the inside as cytochalasin B acts as it acts as a competitive inhibitor of glucose exit. Additional evidence comes from photolabeling