Abstract Exposure of the chick embryo to the nicotinamide analog, 6-aminonicotinamide (6-AN), causes specific changes in chondrogenic cells that result in limb deformity. Autoradiography has further delineated these changes and relates them to altered utilization of molecular precursors of cartilage matrix and DNA. With 35SO 4 to monitor synthesis of glycosaminoglycan, it was shown that, at 6 hr and persisting until 24 hr after treatment, 6-AN inhibited utilization of sulfate by cells in the chondrogenic core while having no detectable effect on cells in the chondrogenic periphery. Similarly, 6-AN suppressed incorporation of [ 3H]thymidine into core cells while having no effect to a slight enhancement effect on chondrogenic and nonchondrogenic cells surrounding the core. These observations support the view that, in response to 6-AN-inhibited NAD(P)-dependent reactions, limb chondrogenic cells (CORE) cease to produce matrix glycosaminoglycan, cease to synthesize DNA, and ultimately succumb. Conversely, presumably as a result of more efficient energy production because they lie closer to a vascular supply of oxygen, cells in the chondrogenic periphery withstand the teratogenic insult and continue proliferating to become the source where subsequent partial repair of the limb occurs.