Jt. Christopher et al., MALATHION ANTAGONIZES METABOLISM-BASED CHLORSULFURON RESISTANCE IN LOLIUM-RIGIDUM, Pesticide biochemistry and physiology, 49(3), 1994, pp. 172-182
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.