Enzymatic Dehydrochlorination of DDT by Resistant Flies

Sternburg, J. G.; Vinson, Eddie B.; Kearns, C. W.

doi:10.1093/jee/46.3.513

Cited by 43 publications

(11 citation statements)

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“…Analysis of DDT-resistant insects was again fundamental in increasing our understanding of the precise role of GSTs in resistance. Thus, as early as 1953, we knew that there was an insect enzyme with DDT dehydrochlorinase activity, which could convert DDT to the nontoxic DDE (1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene) (Sternburg et al 1953). However, it was not until .30 years later that this activity was shown to be associated with one of the GSTs (Clark and Shamaan 1984).…”

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confidence: 99%

The Molecular Genetics of Insecticide Resistance

2013

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The past 60 years have seen a revolution in our understanding of the molecular genetics of insecticide resistance. While at first the field was split by arguments about the relative importance of mono-vs. polygenic resistance and field-vs. laboratory-based selection, the application of molecular cloning to insecticide targets and to the metabolic enzymes that degrade insecticides before they reach those targets has brought out an exponential growth in our understanding of the mutations involved. Molecular analysis has confirmed the relative importance of single major genes in target-site resistance and has also revealed some interesting surprises about the multi-gene families, such as cytochrome P450s, involved in metabolic resistance. Identification of the mutations involved in resistance has also led to parallel advances in our understanding of the enzymes and receptors involved, often with implications for the role of these receptors in humans. This Review seeks to provide an historical perspective on the impact of molecular biology on our understanding of resistance and to begin to look forward to the likely impact of rapid advances in both sequencing and genome-wide association analysis."Curiouser and curiouser!" cried Alice.Lewis Carroll L ewis Carroll sent Alice down a rabbit hole without the least idea of what was to happen next, but as Alice ventured deeper into Wonderland things became "Curiouser and curiouser!" So indeed have studies on the molecular basis of insecticide resistance. While starting with rather simplistic expectations about the role of single mutations in single genes, resistance has been shown to involve a panoply of multiple mutations in multiple genes, often with independent and complex origins. This review will attempt to place these current findings into context and to examine the extent to which the field has often been historically blindsided by dogma. My arguments will encompass key controversies debated in the field such as the relative importance of mono-vs. polygenic resistance and the implications of resistance-associated mutations for whole-organism fitness in the absence of pesticide. Importantly, we will also examine the role of dogma in shaping the way that resistance research has been pursued over the past 50 years. Key questions addressed are therefore: How many mutations per gene cause resistance? How many mechanisms are there per species (genome)? How many independent genetic origins (mutations) give rise to each mechanism? What new mechanisms are still undiscovered and how might they arise? Monogenic vs. Polygenic ResistanceCrow, DDT, and DrosophilaThe humble fruit fly Drosophila melanogaster has been a key tool in unlocking the molecular basis of insecticide resistance, and early studies by James Crow and others have helped to establish Drosophila as a genetic model for resistance studies. Studies of DDT resistance in Drosophila have also typified arguments surrounding mono-vs. polygenic inheritance of insecticide resistance. In his pioneering review of in...

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confidence: 99%

The Molecular Genetics of Insecticide Resistance

2013

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“…The detoxification of DDT to DDE is the first mechanism of DDT resistance reported in the housefly, and the enzyme responsible for this reaction is DDT-dehydrochlorinase which requires GSH as a cofactor. 6,8) The results of the present study show that DDT resistance in the PK strain is mainly due to the higher activity of DDT dehydrochlorinase with little participation of other factors if any.…”

Section: In Vitro Degradation Of Ddtmentioning

confidence: 58%

The Mechanism of Negative Correlation between DDT and Pyrethroid Resistance Found in a Housefly Strain

Mahmood

Motoyama

1994

J. Pestic. Sci.

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A housefly strain (PR) collected from Pakistan was resistant to p, p'-DDT but supersusceptible to pyrethroids, when compared with a standard susceptible strain (CSMA), demonstrating a negative correlation between DDT and pyrethroid resistance. No significant difference was found between the strains in the rate of cuticular penetration of 14C-DDT, the microsomal degradation of 14C-DDT and the electrophysiological response of the nervous system to DDT. In contrast, the soluble fraction of the PK strain fortified with GSH produced many fold more DDE than that of the CSMA strain, suggesting an increased degradation of DDT by DDT-dehydrochlorinase being responsible for the DDT resistance in the PR strain. With regard to the mechanism of the supersusceptibility of the PK strain to pyrethroids, a comparison of in vivo kinetics of 14C-fenvalerate applied topically implicated a combination of faster penetration and less metabolism of the compound in the PK strain than in the CSMA strain. Based upon the in vitro degradation study, the difference in metabolism was assumed to be due to the cytochrome P450-dependent monooxygenase system in the PK strain, which is less effective in degrading the pyrethroid than in the CSMA strain. The assumption was substantiated by a lower degree of synergism exhibited with piperonyl butoxide in the PK strain as compared to the CSMA strain. Since the negative correlation between DDT and pyrethroid resistance in the PR strain is conferred by independent mechanisms, it is concluded to be of apparent, not intrinsic, nature.

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“…The isolation of S-carboxymethylglutathione and S-carboxymethy1cysteine from lettuce plants treated with fluoroacetate (Ward and Huskisson 1972) suggests that the defluorination mechanism is similar in plant and animal tissues but is distinct from the bacterial system. Sternburg et al (1953) have demonstrated that the DDT resistance of house flies can be related to increased levels of a DDT dehydrochlorinase, while Tahori (1963) has shown that fluoroacetate-resistant house flies are cross resistant to DDT.…”

Section: Discussionmentioning

confidence: 99%

Metabolism and Defluorination of Fluoroacetate in the Brush-Tailed Possum (Trichosurus Vulpecula)

Mead¹,

Oliver²,

King³

1979

Aust. Jnl. Of Bio. Sci.

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The brush-tailed possum (T. vulpecula) from Western Australia was found to be nearly 150 times more resistant to fiuoroacetate intoxication in vivo than the same species from South Australia. Acetone powder preparations from the liver of animals from both populations showed similar abilities to convert fiuoroacetate into fiuorocitrate. Aconitate hydratase activity in liver preparations from both Western Australian and South Australian animals was similarly and competitively inhibited by fiuorocitrate. Both animals were capable of defiuorinating fiuoroacetate at similar rates by a glutathione-dependent enzymic mechanism resulting in the formation of free fiuoride ion and S-carboxymethylcysteine. Glutathione was also capable of partial protection against the toxic effects of fiuoroacetate in vitro by a further unelucidated mechanism.

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Enzymatic Dehydrochlorination of DDT by Resistant Flies

Cited by 43 publications

References 0 publications

The Molecular Genetics of Insecticide Resistance

The Molecular Genetics of Insecticide Resistance

The Mechanism of Negative Correlation between DDT and Pyrethroid Resistance Found in a Housefly Strain

Metabolism and Defluorination of Fluoroacetate in the Brush-Tailed Possum (Trichosurus Vulpecula)

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