Cytochalasin B

Cytochalasin B, a mold metabolite, has been shown to inhibit cytokinesis and motility (3), morphogenie development (18), endocytosis (5), and the transport of sugars (8-10, 12). I t has also been demonstrated that this drug inhibits the stimuatcd elaboration of extracellular substances from glands-the release of thyroxine from the thyroid gland after stimulation by thyroid-stimulating hormone (TSH) (19), and the release of o~-amylase from the parotid gland after stimulation by epinephrine (1). To date, the effects of cytochalasin B on other aspects of hormone-mediated responses have not been reported. Therefore, studies were initiated to study the effects of the drug on another hormonemodified system--the induction of tyrosine aminotransferase (E.C. 2.6.1.5) by insulin, cortisol, or N6-2CO-dibutyryl adenosine-31-5r-cyclic monophosphate. These studies were carried out with Reuber hepatoma (H-35) cells grown in culture.