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Description
Cytochalasin D (22144-77-0) is a potent inhibitor of actin polymerization which also causes the disruption of actin filaments. More potent that cytochalasin B (10-fold) and does not inhibit monosaccharide transport across cell membranes. Disruption of actin microfilaments leads to activation of p53. Cell permeable
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Chemical Properties
Powder
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Uses
Cytochalasin D acts as an anti-hypertensive drug acting on human intestinal epithelial caco-2 cells. Also has activity in HMG-CoA reductase inhibitors used in the lowering of cholesterol. Actin inhib
itor, actin polymerization inhibitor affecting cell movement, growth, phagocytosis and even secretion.
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Uses
A cell cycle arresting compound used in actin polymerization studies and cytological research
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Uses
Cytochalasin D is the most studied of the cytochalasins. Like most of the members of this mycotoxin class, cytochalasin D exhibits potent inhibition of actin filament function leading to cell death by apoptosis. This led to early investigation of the metabolite as an antitumour agent. Cytochalasin D has become one of the standard cellular probes for investigating the role of actin in cell biology.
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Definition
ChEBI: An organic heterotricyclic compound that is a mycotoxin produced by Helminthosporium and other moulds which is cell permeable and a potent inhibitor of actin polymerisation and DNA synthesis.
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General Description
Needles or fluffy white powder.
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Reactivity Profile
CYTOCHALASIN D may be sensitive to exposure to heat. CYTOCHALASIN D can react with strong oxidizing agents, strong acids and strong bases. .
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Fire Hazard
Flash point data for CYTOCHALASIN D are not available; however, CYTOCHALASIN D is probably combustible.
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Biological Activity
Potent disruptor of actin filament function. Alters tight junction permeability. Unlike cytochalasin B, does not inhibit monosaccharide transport across the plasma membrane.
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Biochem/physiol Actions
Cell permeable fungal toxin; potent inhibitor of actin polymerization. Disrupts actin microfilaments and activates the p53-dependent pathways causing arrest of the cell cycle at the G1-S transition. Inhibits smooth muscle contraction. Inhibits insulin-stimulated, but not basal, transport of glucose.
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Safety Profile
Poison by ingestion,
subcutaneous, and intraperitoneal routes. An
experimental teratogen. Experimental
reproductive effects. Human mutation data
reported. When heated to decomposition it
emits toxic fumes of NOx.
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References
1)) Goddetteand et al. (1986), Actin polymerization. The mechanism of action of cytochalasin D; J. Biol. Chem., 261 15974
2) Rubtsova et al. (1998), Disruption of actin microfilaments by cytochalasin D leads to activation of p53; FEBS Lett., 430 353
