MALATHION ANTAGONIZES METABOLISM-BASED CHLORSULFURON RESISTANCE IN LOLIUM-RIGIDUM

JT Christopher, C Preston, Stephen Powles

    Research output: Contribution to journalArticle

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    Abstract

    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.
    Original languageEnglish
    Pages (from-to)172-182
    JournalPesticide Biochemistry and Physiology
    Volume49
    DOIs
    Publication statusPublished - 1994

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    chlorsulfuron
    Malathion
    Lolium rigidum
    Lolium
    malathion
    biotypes
    Herbicides
    metabolism
    herbicides
    Seedlings
    cytochrome P-450
    Cytochrome P-450 Enzyme System
    seedlings
    microsomes
    Microsomes
    lethal dose 50
    Zea mays
    Acetolactate Synthase
    primisulfuron
    toxicity

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    @article{de6631ea76084d7badc4c8a9e58b03e6,
    title = "MALATHION ANTAGONIZES METABOLISM-BASED CHLORSULFURON RESISTANCE IN LOLIUM-RIGIDUM",
    abstract = "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.",
    author = "JT Christopher and C Preston and Stephen Powles",
    year = "1994",
    doi = "10.1006/pest.1994.1045",
    language = "English",
    volume = "49",
    pages = "172--182",
    journal = "Pesticide Biochemistry and Physiology",
    issn = "0048-3575",
    publisher = "Academic Press",

    }

    MALATHION ANTAGONIZES METABOLISM-BASED CHLORSULFURON RESISTANCE IN LOLIUM-RIGIDUM. / Christopher, JT; Preston, C; Powles, Stephen.

    In: Pesticide Biochemistry and Physiology, Vol. 49, 1994, p. 172-182.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - MALATHION ANTAGONIZES METABOLISM-BASED CHLORSULFURON RESISTANCE IN LOLIUM-RIGIDUM

    AU - Christopher, JT

    AU - Preston, C

    AU - Powles, Stephen

    PY - 1994

    Y1 - 1994

    N2 - 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.

    AB - 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.

    U2 - 10.1006/pest.1994.1045

    DO - 10.1006/pest.1994.1045

    M3 - Article

    VL - 49

    SP - 172

    EP - 182

    JO - Pesticide Biochemistry and Physiology

    JF - Pesticide Biochemistry and Physiology

    SN - 0048-3575

    ER -