The mutagenic interaction between near-ultraviolet (365 nm) radiation and the alkylating agents ethyl methanesulphonate (EMS) and methyl methanesulphonate (MMS) was studied in a repair-competent and an excision-deficient strain of Escherichia coli. Near-UV radiation modified the metabolic response of exposure to these chemicals and either reduced or increased their mutagenic efficiency. Based on these results, an experimental model was formulated to explain the mutagenic interactions that occur between near-UV and various agents that induce prototrophic revertants via error-prone repair of DNA. According to this model, low doses of near-UV provoke conditions for mutation frequency decline (MFD) and lead to a mutagenic antagonism. With increasing near-UV doses, damage to constitutive error-free repair systems increases, favouring the error-prone system and inhibiting the MFD. Under these conditions there will be a progressive decrease in antagonism until at high doses an enhancement of mutation frequency (positive interaction) will occur.