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 The green peach aphid Myzus persicae perform better on pre-infested Chinese cabbage Brassica pekinensis by enhancing host plant nutritional quality

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
He-He Cao ◽  
Hui-Ru Liu ◽  
Zhan-Feng Zhang ◽  
Tong-Xian Liu
Keyword(s):  
Chinese Cabbage ◽  
Myzus Persicae ◽  
Green Peach Aphid ◽  
Marker Genes ◽  
Plant Leaves ◽  
Resistance Level ◽  
Aphid Infestation ◽  
Phloem Sap ◽  
Brassica Pekinensis ◽  
Plant Nutritional Quality

Abstract The green peach aphid, Myzus persicae Sulzer, is a notorious pest on vegetables, which often aggregates in high densities on crop leaves. In this study, we investigated whether M. persicae could suppress the resistance level of Chinese cabbage Brassica pekinensis. M. persicae performed better in terms of weight gain (~33% increase) and population growth (~110% increase) when feeding on previously infested (pre-infested) Chinese cabbage compared with those on non-infested plants. However, when given a choice, 64% of the aphids preferred to settle on non-infested leaves, while 29% of aphids chose pre-infested leaves that had a 2.9 times higher concentration of glucosinolates. Aphid feeding significantly enhanced the amino acid:sugar ratio of phloem sap and the absolute amino acid concentration in plant leaves. Aphid infestation significantly increased the expression levels of salicylic acid (SA) marker genes, while it had marginal effects on the expression of jasmonate marker genes. Exogenously applied SA or methyl jasmonate had no significant effects on M. persicae performance, although these chemicals increased glucosinolates concentration in plant leaves. M. persicae infestation increase amino acid:sugar ratio and activate plant defenses, but aphid performed better on pre-infested plants, suggesting that both nutrition and toxics should be considered in insect-plant interaction.

scholarly journals Mutations in Aspergillus fumigatus Resulting in Reduced Susceptibility to Posaconazole Appear To Be Restricted to a Single Amino Acid in the Cytochrome P450 14α-Demethylase

2003 ◽  
Vol 47 (2) ◽  
pp. 577-581 ◽  
Author(s):  
Paul A. Mann ◽  
Raulo M. Parmegiani ◽  
Shui-Qing Wei ◽  
Cara A. Mendrick ◽  
Xin Li ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Aspergillus Fumigatus ◽  
Single Point ◽  
Point Mutations ◽  
Drug Accumulation ◽  
Resistant Isolate ◽  
Single Amino Acid ◽  
Single Point Mutation ◽  
Genes Encoding ◽  
Moderately Resistant

ABSTRACT To better understand the molecular basis of posaconazole (POS) resistance in Aspergillus fumigatus, resistant laboratory isolates were selected. Spontaneous mutants arose at a frequency of 1 in 108 and fell into two susceptibility groups, moderately resistant and highly resistant. Azole resistance in A. fumigatus was previously associated with decreased drug accumulation. We therefore analyzed the mutants for changes in levels of transcripts of genes encoding efflux pumps (mdr1 and mdr2) and/or alterations in accumulation of [14C]POS. No changes in either pump expression or drug accumulation were detected. Similarly, there was no change in expression of cyp51A or cyp51B, which encode the presumed target site for POS, cytochrome P450 14α-demethylase. DNA sequencing revealed that each resistant isolate carried a single point mutation in residue 54 of cyp51A. Mutations at the same locus were identified in three clinical A. fumigatus isolates exhibiting reduced POS susceptibility but not in susceptible clinical strains. To verify that these mutations were responsible for the resistance phenotype, we introduced them into the chromosome of a POS-susceptible A. fumigatus strain under the control of the glyceraldehyde phosphate dehydrogenase promoter. The transformants exhibited reductions in susceptibility to POS comparable to those exhibited by the original mutants, confirming that point mutations in the cyp51A gene in A. fumigatus can confer reduced susceptibility to POS.

scholarly journals Evidence that the androgen receptor mediates sexual differentiation of mouse renal cytochrome P450 expression

1991 ◽  
Vol 278 (2) ◽  
pp. 499-503 ◽  
Author(s):  
C J Henderson ◽  
C R Wolf
Keyword(s):  
Cytochrome P450 ◽  
Androgen Receptor ◽  
Sexual Dimorphism ◽  
Mammalian Species ◽  
Cytochrome P450s ◽  
Transcriptional Level ◽  
P450 Gene ◽  
P450 Expression ◽  
Male Phenotype ◽  
Circulating Levels

We have previously shown that sexual dimorphism in the expression of mouse renal cytochrome P450s is mediated by androgens, probably at a transcriptional level [Henderson, Scott, Yang & Wolf (1990), Biochem. J. 266, 675-681]. In the present study we show that this effect is already observed for most isoenzymes at only 2-3 weeks of age, as is the ability to induce or suppress expression with exogenous testosterone. The testosterone responsiveness did, however, exhibit age- as well as dose-dependency. Intriguingly, the effects of androgen took up to 8 days to become maximized, and the dose of testosterone needed to convert the female into the male phenotype was much higher than the circulating levels normally found in males. Studies using testicular feminized (Tfm) male mice, which carry an androgen receptor defect, showed them to have the female kidney cytochrome P450 phenotype, and these animals were not responsive to testosterone treatment. These data demonstrate the involvement of the androgen receptor in the regulation process. Taken together, our results indicate that the androgen receptor does not interact directly with the P450 genes, but initiates a cascade of events leading to the changes in cytochrome P450 gene expression. Significant differences were observed in the degree of sexual dimorphism in kidney P450 expression in other mammalian species. The significance of these findings in relation to the observed sexual dimorphism in other species is discussed.

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 Evaluation and optimization of the protocols for measuring cytochrome P450 activity in aphids

2018 ◽  
Author(s):  
He-He Cao ◽  
Tong-Xian Liu
Keyword(s):  
Cytochrome P450 ◽  
Acyrthosiphon Pisum ◽  
Green Peach Aphid ◽  
Rhopalosiphum Padi ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Inhibitory Effect ◽  
Homogenization Method ◽  
Cytochrome P450 Enzymes ◽  
Cytochrome P450 Activity ◽  
P450 Activity

AbstractCytochrome P450 enzymes play major roles in insect detoxification of plant toxins and insecticides. However, measuring P450 activity in aphids has variable success, and a reliable method is not available yet. In this study, we evaluated and optimized the method for measuring P450 activity in aphids using the 7-ethoxycoumarin as the substrate. First, we found that nicotinamide adenine dinucleotide phosphate and protective agents are not needed in the aphid P450 activity assay, and homogenizing the green peach aphid,Myzus persicae, in the microplate resulted in significantly higher P450 activities than those in Eppendorf tube. Homogenizing aphids in Eppendorf tube could grind tissues thoroughly and released uncharacterized compounds that could inhibit aphid and pig liver P450 activities, whereas aphids in the microplate likely could not be thoroughly ground and thus released fewer such inhibitors. Then, the microplate homogenization method was optimized to follows: one or two aphids were put into one well of the microplate and ground in phosphate buffer using pipette tips for 20 cycles, followed by addition of 7-ethoxycoumarin, and then incubated for 1 h at room temperature, after which glycine buffer-ethanol mixture was added to stop the reaction. This method is also suitable for the pea aphid,Acyrthosiphon pisum, and the bird cherry □oat aphid,Rhopalosiphum padi.These results emphasize the importance of considering inhibitory effect of endogenous compounds in insects on their P450 activity and provide one possible method to reduce this inhibitory effect.

scholarly journals 180. THE CONSEQUENCES OF ACRYLAMIDE EXPOSURE ON THE MALE GERMLINE

2010 ◽  
Vol 22 (9) ◽  
pp. 98
Author(s):  
B. J. Nixon ◽  
B. Nixon ◽  
S. D. Roman
Keyword(s):  
Gene Expression ◽  
Dna Damage ◽  
Cytochrome P450 ◽  
Germ Cells ◽  
Dietary Exposure ◽  
Cytochrome P450 Enzymes ◽  
Male Germ Cells ◽  
P450 Gene ◽  
Male Germline ◽  
Future Outcomes

Acrylamide is a common industrial compound that has recently been identified in cooked, carbohydrate-rich foods such as potato chips, breads and cereals. Acrylamide has been found to be a reproductive toxin in rodents, eliciting male infertility and transgenerational toxicity through the male germline; thus dietary exposure to the compound may have consequences for male fertility and reproduction in humans. The aim of this project was to elucidate the mechanisms of acrylamide toxicity in male germ cells of mice. Freshly isolated early male germ cells were exposed to acrylamide and assessed for cell viability and aberrant morphology. DNA damage in these cells was also investigated using a modified version of the Comet Assay, which allows for adduct specificity. Significant increases in cell death or aberrant morphology were not observed following acrylamide exposure (1 µM, 18 hours). However, a significant increase in DNA damage (125% increase in mean tail DNA assessed by Comet) was identified; which may originate from either the metabolic conversion of acrylamide to glycidamide, leading to glycidamide adducts, or from oxidative stress. Additionally, the regulation of cytochrome P450 gene expression was measured using real time PCR and early male germ cells were found to upregulate gene expression of cytochrome P450 enzymes in response to acrylamide exposure. Collectively, these results support a genotoxic mode of action of acrylamide toxicity, in addition to potential oxidative damage in male germ cells. However, the mechanism by which acrylamide elicits toxicity in germ cells requires further investigation. Future outcomes of this research may provide insight into factors necessary for the healthy development of offspring and aid in the risk assessment of dietary acrylamide exposure in humans.

scholarly journals Amplification of a Cytochrome P450 Gene Is Associated with Resistance to Neonicotinoid Insecticides in the Aphid Myzus persicae

PLoS Genetics ◽  
2010 ◽  
Vol 6 (6) ◽  
pp. e1000999 ◽  
Author(s):  
Alin M. Puinean ◽  
Stephen P. Foster ◽  
Linda Oliphant ◽  
Ian Denholm ◽  
Linda M. Field ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Myzus Persicae ◽  
Cytochrome P450 Gene ◽  
P450 Gene ◽  
Neonicotinoid Insecticides

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 Mechanisms of retinoid resistance in leukemic cells: possible role of cytochrome P450 and P-glycoprotein

Blood ◽  
1996 ◽  
Vol 87 (2) ◽  
pp. 725-733 ◽  
Author(s):  
M Kizaki ◽  
H Ueno ◽  
Y Yamazoe ◽  
M Shimada ◽  
N Takayama ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Cellular Proliferation ◽  
Acquired Resistance ◽  
Cell Types ◽  
Leukemic Cells ◽  
Cytochrome P450 Enzymes ◽  
P450 Gene ◽  
P Glycoprotein ◽  
Clinical Resistance ◽  
Differentiation And Proliferation

Retinoic acid (RA) regulates the differentiation and proliferation of a wide variety of different cell types and all-trans RA induces complete remission in a high proportion of patients with acute promyelocytic leukemia (APL). However, clinical resistance to retinoids may develop and poses a serious problem for differentiation-inducing therapy. We studied the effects of RA in combination with a cytochrome P450 inhibitor (clotrimazole) and a P-glycoprotein antagonist (verapamil) on cell growth and differentiation of RA-resistant HL-60 cells and fresh RA-resistant leukemic cells from two APL patients. RA-resistant HL-60 cells and APL cells differentiated to mature granulocytes when cultured with all-trans RA and either clotrimazole and verapamil but not with either of the agents alone. These findings were confirmed in these cells by their increased expression of CD11b antigen and migration- inhibitory factor-related protein-8/14 mRNAs and decreased levels of c- myc mRNA. These combinations also markedly decreased the number of viable cells and inhibited cellular proliferation. After isolation of microsomes, measurements showed that levels of cytochrome P450 activities in both wild-type and RA-resistant HL-60 cells were almost comparable. Moreover, expression of the CYP1A1-type cytochrome P450 gene could not be detected in either cell type. However, RA-resistant HL-60 cells and APL cells, but not RA-sensitive HL-60 cells and APL cells, expressed multidrug-resistance-1 gene transcripts. Taken together, acquired resistance to RA may be explained in part by drug metabolism in leukemic cells. Possible mechanisms for accelerated clearance of RA include the induction of non-CYP1A1 cytochrome P450 enzymes and P-glycoprotein.

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