Colchicine exposed to ultraviolet light is photoisomerized to form the lumicolchicines. Other studies have shown that light-altered colchicine has reduced biologic activity in plants and lower animals. The effects of colchicine and lumicolchicine on arresting mitosis in metaphase were studied in human lymphocytes in tissue culture. Lumicolchicine was ineffective and not different from controls, even in concentrations of 1 x loa M. The possible clinical relevance of these data are discussed.Colchicine and certain related alkaloids are highly light-sensitive. When colchicine in solution is exposed to sunlight for prolonged periods of time or to ultraviolet light for shorter times, three products, a-, /3-, and y-lumicolchicine, are isolated in varying quantities, depending upon the experimental conditions (1). These photoisomers can be differentiated from the parent compound and each other by such physical properties as solubility in alcohol, melting point and ultraviolet spectra. One feature they share is the absence of the 350 m p absorption band associated with the troponoid system of colchicine (2). Their structural formulae (Fig 1) have been established recently with some certainty; 8-and y-lumicolchicine a r e stereoisomers (3) and a-lumicolchicine is a dimer of /34umicolchicine (2).Previous work from this laboratory (4) has shown that when a dilute nonaqueous solution of '4c-or unlabeled colchicine was exposed to ultraviolet light for 1 to 7 days and purified by thin-layer and paper chromatography, a single new radioactive peak or untraviolet absorbing spot was quantitatively formed. T h e new substance, which migrated faster than colchicine in all chromatographic systems tested, is undoubtedly one or more of the lumicolchicines as evidenced by the disappearance of the 350 mfi absorption band.Colchicine is clinically beneficial in the treatment of acute gout. It has, in addition, a number of biologic actions, even in small concentration. Colchicine specifically binds to proteins in the cellular organoids termed microtubules (5). Such binding results in disruption of the microtubular structure into its subunits, leading to mitotic arrest in metaphase (6). The purpose of this paper is to report on the effect of