PSEUDOURIDINE has occurred in all hitherto analysed biological systems as a component of soluble ribonucleic acid. Other types of ribonucleic acid do not contain bound pseudouridine. Free pseudouridine is not utilized for the synthesis of ribonucleic acid, and, so far, no phospho-kinases have been found which catalyse pseudouridine phosphorylation1. Hence, pseudouridine liberated during the degradation of soluble ribonucleic acid is no longer metabolically active and leaves the organism by means of urinary excretion. The urinary pseudouridine-level depends on the physiological state of the organism. In some disease states there occurs a steep rise in the urinary excretion of pseudouridine. Considerably enhanced amounts of pseudouridine excreted were found in patients with leukaemia, gout and psoriasis2–4. All this seems to indicate that increased excretion of pseudouridine may be expected in such cases where increased tissue degradation occurs. Though the type of the degradation of the lower components of nucleic acids differs in individual animal species, we presume that, as a rule, pseudouridine is the end-product of the degradation of pseudouridylic acid bound in soluble ribonucleic acid. We presume, therefore, that urinary pseudouridine may be used as a suitable indicator for the degradation of tissue soluble ribonucleic acids. The urinary excretion of the rest of nucleic acid catabolites gives a general picture of the degradation of either a complex of nucleic acids (uric acid5) or of deoxyribonucleic acids (for example, deoxycytidine in rats6).