A population of Lolium rigidum Gaud. displays resistance to the herbicide chlorotoluron endowed by enhanced metabolism of this herbicide. The level of resistance in intact plants of this population is light dependent. Resistance is about 4-fold at 110 mu mol photons m(-2). s(-1), but increases to 11-fold at 600 mu mol photons m(-2). s(-1). For seedlings grown in the dark, the rate of chlorotoluron metabolism is identical between biotypes; however, seedlings of the resistant biotype grown in the light display enhanced chlorotoluron metabolism compared to the susceptible biotype. Specifically, light with blue wavelengths induces chlorotoluron metabolism in the resistant biotype. An analysis of the metabolites produced indicates that two routes of chlorotoluron metabolism occur in L. rigidum. These are characterised by initial reactions leading to ring-methyl hydroxylation or N-demethylation of the herbicide. The ring-methyl hydroxylation pathway is increased greatly in light-grown resistant seedlings compared to susceptible seedlings, whereas the N-demethylation pathway is only slightly increased. The differential induction of these two pathways in resistant L. rigidum by light suggests that enhanced activity of two different enzymes may be involved in chlorotoluron resistance.