In order to clarify the pathogenesis of steroid cataracts as one of the side effects of the administration of dexamethasone phosphate (DX), investigations were conducted into the in vitro effects of FAD and DX on the macromolecular phosphate compounds separated from the lens supernatant using Sephadex G-50. Phosphate turnover in the macromolecular phosphate compounds was reduced by DX, but the loss was partially prevented by the addition of FAD. These macromolecular phosphate compounds were identified as nucleic acids, mostly RNA and a small amount of protein. An experiment was devised using the incorporation of tritiated uridine and thymidine into the macromolecular phosphate compounds. The incorporation of uridine-3H into RNA and thymidine-3H into DNA was inhibited by the addition of DX, but this loss of turnover rate was partially prevented in RNA by the simultaneous administration of FAD; no change was found in the DNA fraction treated with FAD. There probably is a close relationship between FAD and the turnover of macromolecular phosphate compounds in the lens, and FAD, as a new physiological role, probably has an ability to reactivate the depressed turnover of RNA resulting from a DX administration. The possible role of nucleic acid turnover on the pathogenesis of steroid cataracts was discussed with relationship to adrenal dysfunction leading to a phosphorylation insufficiency caused by DX.