Primate lenses are unique in that they convert tryptophan (trp) into 3-hydroxykynurenine glucoside (30HKG). This is the major short-wave absorbing pigment present in human lenses and it may play a role in protecting the eye from UV-induced photodamage. A study has been performed on aspects of this metabolic pathway in human lenses. A significant rate of synthesis could be observed in a 24-hr period using intact lenses to which radiolabelled tryptophan had been added. Label was found in kynurenine (Kyn), 3-hydroxykynurenine (30HKyn) and 30HKG, although always to the greatest extent in the latter metabolite. Considerable variation in the proportion of label incorporated into 30HKG was observed. Older lenses tended to accumulate a greater percentage into the glucoside; the data indicating a generally greater flux through the trp catabolic pathway in lenses above 60 years of age. Pulse-chase experiments on lens pairs suggested that there may be a significant loss or metabolism of 30HKG. Biosynthesis of 30HKG was found to take place in the lens epithelial cells. A linear rate of 30HKG efflux from organ cultured lenses was observed indicating that one pathway for removal of this compound involves diffusion through the lens capsule. That this pathway also occurs in vivo was confirmed by analysing samples of human vitreous humour. Based on efflux rates from cultured lenses (1.07 x 10(-3) +/- 0.293 x 10(-3) mumol hr-1, n = 5), half-life values for 30HKG in the lens ranging between 7 and 40 hr were calculated.(ABSTRACT TRUNCATED AT 250 WORDS)