A biotype of Lolium rigidum Gaud. (SLR31) is resistant to the sulfonylurea herbicide chlorsulfuron, despite having a herbicide-sensitive target site, acetolactate synthase. This biotype is able to metabolize the herbicide at a faster rate than a susceptible biotype. Seedlings of this biotype treated with chlorsulfuron in combination with the organophosphate insecticide malathion exhibited greatly increased mortality and reduced dry weight compared to seedlings treated with chlorsulfuron alone. The chlorsulfuron LD(50) for resistant biotype SLR31 decreased form 293.5 g ai ha(-1) in the absence of malathion to 84.6 g ai ha(-1) in the presence of 1000 g ai ha(-1) malathion. The LD(50) for a susceptible biotype was also reduced from 7.6 g ai ha(-1) in the absence of malathion to 0.9 g ai ha(-1). Excised seedlings of the resistant biotype metabolized [phenyl-U-C-14]chlorsulfuron in the culm tissue nearest the meristem faster than the susceptible biotype. However, when the herbicide was given in combination with malathion, metabolism was dramatically reduced in both biotypes. In seedlings of the resistant biotype given [phenyl-U-C-14]chlorsulfuron alone 83.5 +/- 2.3% of the herbicide taken into the culms tissue was metabolized after 9 hr. However, when the herbicide was given in combination with 70 mu M malathion, only 13.0 +/- 2.2% [phenyl-U-C-14]chlorsulfuron was metabolized after 9 hr. Thus, malathion increases chlorsulfuron toxicity for L. rigidum by inhibiting herbicide metabolism. As malathion has previously been shown to inhibit cytochrome P450-dependant monooxygenase-catalyzed primisulfuron metabolism by Zea mays microsomes, this result supports the hypothesis that chlorsulfuron metabolism by Zea mays microsomes, this result supports the hypothesis that chlorsulfuron metabolism in L. rigidum may be mediated by a cytochrome P450 isozyme. Other cytochrome P450 inhibitors, piperonylbutoxide and tetcyclasis, did not increase chlorsulfuron toxicity for either resistant or susceptible L. rigidum biotypes, while 1-aminobenzotriazole caused only a small increase in mortality and a small reduction in [C-14]chlorsulfuron metabolism in the resistant biotype. (C) 1994 Academic Press, Inc.