Cytochalasins are mycotoxins that have the ability to bind to actin filaments and block polymerization and the elongation of actin. As a result, they can change cellular morphology, inhibit cellular processes such as cell division, and cause cells to undergo apoptosis. Cytochalasins also have the ability to permeate cell membranes, prevent cellular translocation, cause cells to enucleate, and affect other aspects of biological processes unrelated to actin polymerization. Cytochalasin B is an alkaloid isolated from the fungus Helminthosporium dermatioideum, as well as hormiscium species and rhoma species. (2, 4, 5, 8)
Oral, dermal, inhalation, and parenteral (contaminated drugs). (6)
Mechanism of Toxicity
Cytochalasins are known to bind to the barbed, fast growing plus ends of microfilaments, which then blocks both the assembly and disassembly of individual actin monomers from the bound end. Once bound, cytochalasin essentially caps the end of the new actin filament. One cytochalasin will bind to one actin filament. By blocking the polymerization and elongation of actin, cytochalasins can change cellular morphology, inhibit cellular processes such as cell division, and cause cells to undergo apoptosis. Cytochalasin B also inhibits glucose transport and platelet aggregation. It blocks adenosine-induced apoptotic body formation without affecting activation of endogenous ADP-ribosylation in leukemia HL-60 cells. (4, 5, 8, 9)
No indication of carcinogenicity to humans (not listed by IARC).
Uses/Sources
Cytochalasin B is isolated from a fungus, Helminthosporium dermatioideum, as well as hormiscium species and rhoma species. (2)
Minimum Risk Level
Not Available
Health Effects
Major biological effects of cytochalasins include inhibition of the division of cytoplasm, reversible inhibition of cell movement, induction of nuclear extrusion, inhibition of such processes as phagocytosis, platelet aggregation and clot retraction, glucose transport, thyroid secretion, and release of growth
hormone. Some cytochalasins have been shown to have developmental effects. Cytochalasin B also causes gradual but marked decline in intracellular levels of putrescine and spermidine. (3, 11)
Symptoms
Not Available
Treatment
Consider activated charcoal after gastrointestinal absportion. Nitroprusside is recommended to reverse peripheral ischemia secondary to vasoconstriction and for the treatment of hypertension. Anticoagulant therapy with intravenous heparin is also recommended. (1)
