The effect of two inhibitors of glycolysis, NaF and iodacetamide on the production of recessive lethal mutations by X-rays in mature Drosophila sperm has been investigated. Pre-treatment with NaF resulted in a consistent and highly significant increase of the mutation frequency. This effect is thought to result from interference with a repair process which makes use of energy produced by glycolysis, and does not arise from an increase of the oxygen tension. When the action of NaF was studied in combination with pre- and post-treatments with N2 and O2, it was observed: (1) that irrespective of pre-treatment with N2 or O2, NaF enhanced the mutation frequency over that in the saline controls; (2) that following irradiation under anoxia, post-treatment with N2 reduced the mutation frequency below that observed with O2 post-treatment, even when the flies had been pre-treated with NaF. These additive effects of NaF pre-treatment and O2 post-treatment have been taken as an indication that, even when glycolysis is inhibited by NaF, some energy is left, which is still available for repair by post-radiation anoxia. This interpretation that the amount of repair in sperm depends on different levels of available energy is supported by the observation that NaF pre-treatment is still effective in increasing the mutation frequency over that in the controls, when N2 was given before, during and after irradiation. Thus repair is maximal with NaCl-N2-R-N2; intermediate with NaF-N2-R2-N2, and minimal with NaF-N2-R-O. Pre-treatment with iodacetamide gave more variable results than that with NaF.