Metabolic Resistance to Acetolactate Synthase Inhibiting Herbicide Tribenuron-Methyl in Descurainia sophia L. Mediated by Cytochrome P450 Enzymes

2018 ◽  
Vol 66 (17) ◽  
pp. 4319-4327 ◽  
Author(s):  
Qian Yang ◽  
Jinyao Li ◽  
Jing Shen ◽  
Yufang Xu ◽  
Hongjie Liu ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Acetolactate Synthase ◽  
Cytochrome P450 Enzymes ◽  
Metabolic Resistance ◽  
Descurainia Sophia ◽  
Tribenuron Methyl

scholarly journals Potential Metabolic Resistance Mechanisms to Ivermectin in Anopheles Gambiae: A Synergist Bioassay Study

2020 ◽  
Author(s):  
Patricia Nicolas ◽  
Caroline Kiuru ◽  
Martin Wagah ◽  
Martha Muturi ◽  
Urs Duthaler ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Anopheles Gambiae ◽  
Control Strategies ◽  
Resistance Mechanisms ◽  
World Health ◽  
Malaria Vectors ◽  
Malaria Vector Control ◽  
Cytochrome P450 Enzymes ◽  
Metabolic Resistance ◽  
Active Efflux

Abstract Background Despite remarkable success obtained with current malaria vector control strategies in the last 15 years, additional innovative measures will be needed to achieve the ambitious goals set for 2030 by the World Health Organization (WHO). New tools will need to address insecticide resistance and residual transmission as key challenges. Endectocides such as ivermectin are drugs that kill mosquitoes which feed on treated subjects. Mass administration of ivermectin can effectively target outdoor and early biting vectors, complementing the still effective conventional tools. Although this approach has garnered attention, development of ivermectin resistance is a potential pitfall. Herein, we evaluate the potential role of xenobiotic pumps and cytochrome P450 enzymes in protecting mosquitoes against ivermectin by active efflux and metabolic detoxification, respectively. Methods We determined the lethal-concentration 50 for ivermectin in colonized Anopheles gambiae, then we used chemical inhibitors and inducers of xenobiotic pumps and cytochrome P450 enzymes in combination with ivermectin to probe the mechanism of ivermectin detoxification. Results Dual inhibition of xenobiotic pumps and cytochromes have a synergistic effect with ivermectin, greatly increasing mosquito mortality. Inhibition of xenobiotic pumps alone had no effect on ivermectin-induced mortality. Induction of xenobiotic pumps and cytochromes may confer partial protection from ivermectin.Conclusion there is a clear pathway for development of ivermectin resistance in malaria vectors. Detoxification mechanisms mediated by cytochrome P450 enzymes are more important than xenobiotic pumps in protecting mosquitoes against ivermectin.

scholarly journals Effects of a novel combination of two mutated acetolactate synthase (ALS) isozymes on resistance to ALS-inhibiting herbicides in Flixweed (Descurainia Sophia)

Weed Science ◽  
2021 ◽  
pp. 1-36
Author(s):  
Yufang Xu ◽  
Lina Xu ◽  
Jing Shen ◽  
Xuefeng Li ◽  
Mingqi Zheng
Keyword(s):  
Resistance Management ◽  
Acetolactate Synthase ◽  
Expression Level ◽  
Cross Resistance ◽  
Resistance Mutations ◽  
Relative Expression ◽  
Chemical Structures ◽  
Descurainia Sophia ◽  
Relative Expression Level ◽  
Tribenuron Methyl

Abstract Flixweed [Descurainia sophia (L.) Webb ex Prantl] is a notorious broadleaf weed that is widely distributed in winter wheat growing areas of China, and has evolved resistance to tribenuron-methyl mainly due to target-site resistance (TSR) mutations in acetolactate synthase (ALS). In the current research, two ALS genes were identified in tribenuron-methyl-susceptible (TS) or -resistant (TR) D. sophia. Resistance mutations of Asp-376-Glu and Pro-197-Ala were identified on ALS1 and ALS2 isozymes in TR D. sophia, respectively. The TR D. sophia evolved 10836.3-fold resistance to tribenuron-methyl and displayed cross-resistance to multiple ALS-inhibiting herbicides with different chemical structures. Dose response experiments and ALS activity assay indicated that two mutated ALS isozymes contributed differentially in resistance to tribenuron-methyl, flucetosulfuron and pyribenzoxim. In addition, the relative expression level of ALS1 gene was 2.2- and 1.6-fold higher than ALS2 genes in TR D. sophia on the 1st and 7th days after tribenuron-methyl treatment (DAT), respectively. In contrast, the relative expression level of ALS1 and ALS2 in TS D. sophia is similar. This is the first research that explored different roles of ALS isozymes in resistance to ALS-inhibiting herbicides, which might provide a new perspective for the weed resistance management.

scholarly journals Assessing cross-resistance within the pyrethroids in terms of their interactions with key cytochrome P450 enzymes and resistance in vector populations

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
C. L. Moyes ◽  
R. S. Lees ◽  
C. Yunta ◽  
K. J. Walker ◽  
K. Hemmings ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Binding Affinity ◽  
Malaria Vector ◽  
Pyrethroid Resistance ◽  
Resistance Mechanisms ◽  
Cross Resistance ◽  
Type I ◽  
Cytochrome P450 Enzymes ◽  
Metabolic Resistance ◽  
The Common

Abstract Background It is important to understand whether the potential impact of pyrethroid resistance on malaria control can be mitigated by switching between different pyrethroids or whether cross-resistance within this insecticide class precludes this approach. Methods Here we assess the relationships among pyrethroids in terms of their binding affinity to, and depletion by, key cytochrome P450 enzymes (hereafter P450s) that are known to confer metabolic pyrethroid resistance in Anopheles gambiae (s.l.) and An. funestus, in order to identify which pyrethroids may diverge from the others in their vulnerability to resistance. We then investigate whether these same pyrethroids also diverge from the others in terms of resistance in vector populations. Results We found that the type I and II pyrethroids permethrin and deltamethrin, respectively, are closely related in terms of binding affinity to key P450s, depletion by P450s and resistance within vector populations. Bifenthrin, which lacks the common structural moiety of most pyrethroids, diverged from the other pyrethroids tested in terms of both binding affinity to key P450s and depletion by P450s, but resistance to bifenthrin has rarely been tested in vector populations and was not analysed here. Etofenprox, which also lacks the common structural moiety of most pyrethroids, diverged from the more commonly deployed pyrethroids in terms of binding affinity to key P450s and resistance in vector populations, but did not diverge from these pyrethroids in terms of depletion by the P450s. The analysis of depletion by the P450s indicated that etofenprox may be more vulnerable to metabolic resistance mechanisms in vector populations. In addition, greater resistance to etofenprox was found across Aedes aegypti populations, but greater resistance to this compound was not found in any of the malaria vector species analysed. The results for pyrethroid depletion by anopheline P450s in the laboratory were largely not repeated in the findings for resistance in malaria vector populations. Conclusion Importantly, the prevalence of resistance to the pyrethroids α-cypermethrin, cyfluthrin, deltamethrin, λ-cyhalothrin and permethrin was correlated across malaria vector populations, and switching between these compounds as a tool to mitigate against pyrethroid resistance is not advised without strong evidence supporting a true difference in resistance.

scholarly journals Neonicotinoid’s resistance monitoring, diagnostic mechanisms and cytochrome P450 expression in green peach aphid [Myzus persicae (Sulzer) (Hemiptera: Aphididae)]

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261090
Author(s):  
Muhammad Umair Sial ◽  
Khalid Mehmood ◽  
Shafqat Saeed ◽  
Mureed Husain ◽  
Khawaja Ghulam Rasool ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Myzus Persicae ◽  
Green Peach Aphid ◽  
Single Point ◽  
Single Point Mutation ◽  
Transcriptional Level ◽  
Cytochrome P450 Enzymes ◽  
Metabolic Resistance ◽  
Resistance Level ◽  
P450 Gene

Green peach aphid [Myzus persicae (Sulzer) (Hemiptera: Aphididae)] is a significant pest with a known history of insecticide resistance. Neonicotinoids could manage this pest; however, their frequent use led to the evolution of resistance in field populations of M. persicae. Toxicity data for neonicotinoid insecticides synergized with pipernyl butoxide (PBO) in a field population (FP) were collected and compared to a laboratory susceptible clone (SC) of aphids. The enhanced expression of metabolic resistance-related cytochrome P450 gene CYP6CY3 and an arginine-threonine substitution were detected in FP, causing a single point mutation (R81T) at β1 subunit of nicotinic acetylcholine receptor (nAChR) within D loop. High level of resistance to imidacloprid was developed in FP with 101-fold resistance ratio and moderate resistance level (10.9-fold) to acetamiprid. The results of PBO synergized bioassay suggested that cytochrome P450 enzymes were involved in the resistance to neonicotinoids. The mRNA transcriptional level of CYP6CY3 gene was significantly higher (3.74 fold) in FP compared to SC. The R81T mutation associated with neonicotinoid resistance had 26% resistant allele frequency in FP. Both P450 enzymes and R81T mutation of nAChR were found in field-evolved neonicotinoid resistance. It is concluded that field-evolved resistance in green peach aphid could be managed by using appropriate synergists such as PBO.

scholarly journals Potential metabolic resistance mechanisms to ivermectin in Anopheles gambiae: a synergist bioassay study

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Patricia Nicolas ◽  
Caroline Kiuru ◽  
Martin G. Wagah ◽  
Martha Muturi ◽  
Urs Duthaler ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Anopheles Gambiae ◽  
Control Strategies ◽  
Resistance Mechanisms ◽  
World Health ◽  
Malaria Vectors ◽  
Malaria Vector Control ◽  
Cytochrome P450 Enzymes ◽  
Metabolic Resistance ◽  
Active Efflux

Abstract Background Despite remarkable success obtained with current malaria vector control strategies in the last 15 years, additional innovative measures will be needed to achieve the ambitious goals for malaria control set for 2030 by the World Health Organization (WHO). New tools will need to address insecticide resistance and residual transmission as key challenges. Endectocides such as ivermectin are drugs that kill mosquitoes which feed on treated subjects. Mass administration of ivermectin can effectively target outdoor and early biting vectors, complementing the still effective conventional tools. Although this approach has garnered attention, development of ivermectin resistance is a potential pitfall. Herein, we evaluate the potential role of xenobiotic pumps and cytochrome P450 enzymes in protecting mosquitoes against ivermectin by active efflux and metabolic detoxification, respectively. Methods We determined the lethal concentration 50 for ivermectin in colonized Anopheles gambiae; then we used chemical inhibitors and inducers of xenobiotic pumps and cytochrome P450 enzymes in combination with ivermectin to probe the mechanism of ivermectin detoxification. Results Dual inhibition of xenobiotic pumps and cytochromes was found to have a synergistic effect with ivermectin, greatly increasing mosquito mortality. Inhibition of xenobiotic pumps alone had no effect on ivermectin-induced mortality. Induction of xenobiotic pumps and cytochromes may confer partial protection from ivermectin. Conclusion There is a clear pathway for development of ivermectin resistance in malaria vectors. Detoxification mechanisms mediated by cytochrome P450 enzymes are more important than xenobiotic pumps in protecting mosquitoes against ivermectin.

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