A marked inhibition of the incorporation of S35-sulfate by normal calf costal cartilage was produced by potassium ascorbate in the presence of catalytic amounts of cupric ions. The effect of the various components of the ascorbic acid oxidizing system (potassium ascorbate, cupric ions, cuprous ions, hydrogen peroxide, dehydroascorbie acid) was investigated. The results of experiments in which hydrogen peroxide, catalase, or sodium azide were used singly or in combination suggest that the inhibition produced by the aseorbic acid oxidizing system is due, to a considerable extent, to the production of hydrogen peroxide. Dehydroaseorbie acid was also found to inhibit the incorporation of S35-sul/ate by cartilage slices. However, the gradual fall in pH which resulted from the addition of dehydroaseorbic acid could account to a large extent for the inhibitory effect observed because the incorporation of S35-sulfate by cartilage slices decreases sharply as the pH is lowered. The incorporation of SSS-sulfate by cartilage slices is inhibited also by increasing the concentration of phosphate.The state of ascorbic acid deficiency is associated with a defect in the production of intracellular ground substance. The component of ground substance primarily affected, and the mechanisms involved, have not, as yet, been clearly elucidated. A decrease in the incorporation, of S35-sulfate into granulation tissue (1-3), cartilage (4), and a number of other tissues (5) has been observed in scorbutic guinea pigs. Earlier work (6, 7) has established that most of the S36-sulfate retained by an animal beyond 24 hours is found in sulfated mucopolysaccharides. Bostr6m and M~.nsson (8) have studied the incorporation of S36-sulfate into the chondroitin sulfate of costal cartilage slices prepared from normal calves and have indicated a number of factors which influence this reaction. The influence of ascorbic acid on the incorporation of SSS-sulfate by slices of costal cartilage from normal calves is considered in the present communication.* Arthritis and Rheumatism Foundation Fellow.