MALATHION ANTAGONIZES METABOLISM-BASED CHLORSULFURON RESISTANCE IN LOLIUM-RIGIDUM

Citation
Jt. Christopher et al., MALATHION ANTAGONIZES METABOLISM-BASED CHLORSULFURON RESISTANCE IN LOLIUM-RIGIDUM, Pesticide biochemistry and physiology, 49(3), 1994, pp. 172-182
Citations number
30
Categorie Soggetti
Biology,Physiology,Entomology
ISSN journal
00483575
Volume
49
Issue
3
Year of publication
1994
Pages
172 - 182
Database
ISI
SICI code
0048-3575(1994)49:3<172:MAMCRI>2.0.ZU;2-5
Abstract
A biotype of Lolium rigidum Gaud. (SLR31) is resistant to the sulfonyl urea herbicide chlorsulfuron, despite having a herbicide-sensitive tar get site, acetolactate synthase. This biotype is able to metabolize th e herbicide at a faster rate than a susceptible biotype. Seedlings of this biotype treated with chlorsulfuron in combination with the organo phosphate insecticide malathion exhibited greatly increased mortality and reduced dry weight compared to seedlings treated with chlorsulfuro n alone. The chlorsulfuron LD(50) for resistant biotype SLR31 decrease d 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 sus ceptible 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 bi otype metabolized [phenyl-U-C-14]chlorsulfuron in the culm tissue near est the meristem faster than the susceptible biotype. However, when th e herbicide was given in combination with malathion, metabolism was dr amatically reduced in both biotypes. In seedlings of the resistant bio type given [phenyl-U-C-14]chlorsulfuron alone 83.5 +/- 2.3% of the her bicide 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 s hown to inhibit cytochrome P450-dependant monooxygenase-catalyzed prim isulfuron 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. rig idum may be mediated by a cytochrome P450 isozyme. Other cytochrome P4 50 inhibitors, piperonylbutoxide and tetcyclasis, did not increase chl orsulfuron toxicity for either resistant or susceptible L. rigidum bio types, while 1-aminobenzotriazole caused only a small increase in mort ality and a small reduction in [C-14]chlorsulfuron metabolism in the r esistant biotype. (C) 1994 Academic Press, Inc.