Using atomic absorption spectrophotometry, the authots determined zink levels (in correlation with the time-course of copper elimination) in the blood serum and urine of 28 patients with hepatocerebral dystrophy prior to and during the first year of D-penicillamine treatment and in 55 patients who had been on this therapy for a number of years. The zink concentration in the patients' blood serum prior to treatment tended to decline. Such a decrease was also noted in cirrhosis of other etiologies. Thiol therapy resulted in a gradual increase in the urine zink elimination which followed a pattern of the drug dose increment and could be two to three times higher than normal in cases of prolonged treatment. Nevertheless, these patients exhibited no symptoms of zink insufficiency and the zink concentration in the blood serum had been normal for a number of years, which may be explained by an enhanced absorption of zink from the intestines and by its mobilization from the tissue depots. The pathological manifestations observed in six patients with the asthenoneurotic syndrome regressed following zink administration.