The present study was undertaken in order to observe the excretion of I-containing compounds in the urine after oral administration of radioiodide in therapeutic amounts for treatment of thyrotoxicosis. In the literature it is generally agreed that a large portion of iodine excreted in the urine is inorganic iodide. Since the amount of organic radioiodine compounds excreted in the urine is much lower than inorganic iodide, identifi cation of those compounds is difficult. In order to study these minor components, inorganic iodide in the urine collected at 8 hours' intervals for 24 hours was removed as much as possible by passing through an Amberlite IR 120 column. The affluent was concentrated under N2 atmosphere in order to avoid spontaneous transformation to iodide. High voltage paper electrophoresis and radioautography of the concentrated extracts.were carried out as described in the previous papers.1) '2) '3) '4) ' Each band was identified by RJ values (ratio of mobility of 131I components/mobility of inorganic iodide) measured from the radioautograms. The paper strips were cut into appropriate sections for counting radioactivity in a well-type scintillation counter. Radioactivity in each section was expressed as percentage of total 131I compounds. The black bands corresponding to the 131I-compounds developed by HVPE-radioautography of those extracts were classified into 9 fractions in respect to their RJ values. By referring to the RJ values of known Icontaining compounds under similar conditions, the bands 1, 5, 6, 7 and 8' were assigned to I-, monoiodo-tyrosine (MIT), diiodo-tyrosine (DIT), triiodo-thyronine (T3) and diiodo-thyronine (T2). To confirm these identities, the extracts of each section were chromato-graphed by two different solvents. A correlation was found between the percentage of each 131I compound and BMR of the patients with diverse states of thyroidal function. Fig. 12 shows that the percentage of DIT in the urine increases with accelation of BMR. However, percentage values of T3, T2 and MIT decrease when BMR increases as illustrated in Fig. 11, 13 and 14. DIT may arise by metabolism of thyroxine (T4) as shown by Albert5) and Rall6) , and hence T4 is present in circulation, DIT may appear in the urine. It is known that the quantity of T4 in circulating blood of the patients with thyrotoxicosis is increased. In addition, the fractional turnover of T4 is abnormally high in the experimental thyrotoxicosis as reported by Ingbar et al7) . From these facts the present results can be explained in this maner that the percentage of DIT of urine after 131I-therapy for thyrotoxicosis increases when BMR is elevated. Urinary T3 could be derived from free T3 in circulation as reported by Inada8) who also found that the fractional turnover of T3 was considerably high and that a major proportion of the iodine excreted in the urine was in the form of inorganic iodide in the patients with hyperthyroidism. The present results are consistent with Inada's report. The origin of the urinary T2 and MIT remains to be solved in the future.