Glutathione S-transferases as antioxidant defence agents confer pyrethroid resistance in Nilaparvata lugens

2001 ◽  
Vol 357 (1) ◽  
pp. 65-72 ◽  
Author(s):  
John G. VONTAS ◽  
Graham J. SMALL ◽  
Janet HEMINGWAY
Keyword(s):  
Lipid Peroxidation ◽  
Pyrethroid Resistance ◽  
Brown Planthopper ◽  
Nilaparvata Lugens ◽  
Metabolic Inhibitors ◽  
Main Role ◽  
Pyrethroid Insecticides ◽  
Glutathione S Transferases

Selection of a laboratory colony of the brown planthopper Nilaparvata lugens with the pyrethroids permethrin and λ-cyhalothrin increased its resistance to both insecticides. Biochemical analysis and synergistic studies with metabolic inhibitors indicated that elevated glutathione S-transferases (GSTs) with a predominant peroxidase activity conferred resistance to both pyrethroids, whereas esterases conferred part of the resistance to permethrin. Purified esterases hydrolysed permethrin at a slow rate, but incubation of either pyrethroid or their primary metabolites with partially purified GSTs had no effect on the metabolic profile. Although GSTs were sensitive to inhibition by both pyrethroids, they did not serve as binding proteins, as previously hypothesized [Grant and Matsumura (1988) Insect Biochem. 18, 615–622]. We demonstrate that pyrethroids, in addition to their neurotoxic effect, induce oxidative stress and lipid peroxidation in insects. Pyrethroid exposure induced lipid peroxides, protein oxidation and depleted reduced glutathione. Elevated GSTs in the resistant strains attenuated the pyrethroid-induced lipid peroxidation and reduced mortality, whereas their in vivo inhibition eliminated their protective role. We therefore hypothesize that the main role of elevated GSTs in conferring resistance in N. lugens is through protecting tissues from oxidative damage. Our study extends the GSTs' range of efficacy to pyrethroid insecticides and possibly explains the role of elevated GSTs in other pyrethroid-resistant insects.

Establishing the role of detoxifying enzymes in field-evolved resistance to various insecticides in the brown planthopper (Nilaparvata lugens) in South India

2015 ◽  
Vol 24 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Vijayakumar Maheshwari Malathi ◽  
Sushil K. Jalali ◽  
Dandinashivara K. Sidde Gowda ◽  
Muthugounder Mohan ◽  
Thiruvengadam Venkatesan
Keyword(s):  
South India ◽  
Brown Planthopper ◽  
Nilaparvata Lugens ◽  
Detoxifying Enzymes

Egg mortality of the brown planthopper, Nilaparvata lugens (Homoptera: Delphacidae) and green leafhoppers, Nephotettix spp. (Homoptera: Cicadellidae), on rice in Sri Lanka

1991 ◽  
Vol 81 (2) ◽  
pp. 161-167 ◽  
Author(s):  
S.V. Fowler ◽  
M.F. Claridge ◽  
J.C. Morgan ◽  
I.D.R. Peries ◽  
L. Nugaliyadde
Keyword(s):  
Sri Lanka ◽  
Spatial Scales ◽  
Brown Planthopper ◽  
Nilaparvata Lugens ◽  
Egg Parasitoids ◽  
Dependent Relationship ◽  
Egg Density ◽  
Egg Parasitism ◽  
A Minor

AbstractRice plants, infested with eggs of Nilaparvata lugens (Stål) or Nephotettix spp. in laboratory cultures, were used to trap egg parasitoids in rice fields at two sites over a period of four days in Sri Lanka. Levels of egg parasitism per plant varied from 0 to 54% in N. lugens and 45 to 100% in Nephotettix spp. Egg predation was a minor cause of mortality, but attack by a species of Panstenon (Hymenoptera: Pteromalidae) killed up to 18% Nilaparvata lugens eggs. N. lugens eggs were parasitized by Anagrus sp. nr flaveolus Waterhouse, A. optabilis (Perkins) (Hymenoptera: Mymaridae) and Oligosita sp. (Hymenoptera: Trichogrammatidae). Nephotettix spp. eggs were parasitized by two species of Gonatocerus (Hymenoptera: Mymaridae) and one of Paracentrobia (Hymenoptera: Trichogrammatidae). There was no overlap in field host range between the two parasitoid assemblages. Gonatocerus spp. and Paracentrobia spp. seldom attacked the same Nephotettix sp. egg batch, suggesting the possibility that these species compete in the field. Overall egg parasitism of Nilaparvata lugens was positively related to host egg density at the spatial scale of the rice plant, but unrelated at the tiller or batch scale. Nephotettix spp. egg parasitism showed a negative density dependent relationship at the spatial scales of the tiller and plant and no relationship at the batch level. The potential role of these egg parasitoids in preventing outbreaks of hopper pests in Sri Lanka is discussed.

scholarly journals Transcriptomic Profiling of Rice Reveals Positive Role of OsNCED3 in Rice Resistance Against Brown Planthopper

2021 ◽  
Author(s):  
Litong Sun ◽  
Yongyan Liu ◽  
Ali Noman ◽  
Lin Chen ◽  
Jitong Li ◽  
...  
Keyword(s):  
Higher Plants ◽  
Abiotic Stress Tolerance ◽  
Brown Planthopper ◽  
Nilaparvata Lugens ◽  
Positive Role ◽  
Differential Expression Genes ◽  
Loss Index ◽  
Rate Limiting ◽  
Aba Biosynthesis

Abstract Background: Exogenous abscisic acid (ABA) could improve rice resistance to brown planthopper (BPH) Nilaparvata lugens. The 9-cis-epoxycarotenoid dioxygenase (NCED) is the rate-limiting enzyme for ABA biosynthesis in higher plants. In rice, OsNCED3 gene promoted ABA synthesis and improved abiotic stress tolerance, but the function of OsNCED3 in regulating rice defense against BPH remains unclear. Results: In this study, the average injury level, functional plant loss index and EPG results of rice conferred that insect-resistance of OE rice lines was significantly higher than that of WT. Then transcriptome analysis of overexpression (OE), RNA interference (RNAi) and wild type (WT) of OsNCED3 in Zhonghua11 rice lines after BPH infestation were performed. Seventeen RNA libraries were obtained from OE, RNAi and WT rice lines at 12 h post BPH infestation. The number of all differential expression genes (DEGs) between OE and WT or RNAi and WT were mostly up-regulated. These accounted for more than 75% of the total number of DEGs for each other. The number of DEGs between RNAi and WT rice lines fed by BPH increased significantly, higher than that between OE and WT, and most of these DEGs were related to the adversity stress and the biosynthesis of JA (jasmonic acid).Conclusions: overexpression of OsNCED3 gene could improve rice resistance to BPH.

scholarly journals Adaptation by the Brown Planthopper to Resistant Rice: A Test of Female-Derived Virulence and the Role of Yeast-like Symbionts

Insects ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 908
Author(s):  
Finbarr G. Horgan ◽  
Ainara Peñalver Cruz ◽  
Arriza Arida ◽  
Jedeliza B. Ferrater ◽  
Carmencita C. Bernal
Keyword(s):  
Rice Variety ◽  
Brown Planthopper ◽  
Female Parent ◽  
Nilaparvata Lugens ◽  
Resistant Variety ◽  
Weak Evidence ◽  
Manipulative Experiments ◽  
Genetic Mechanisms ◽  
Nilaparvata Lugens Stål

The adaptation by planthoppers to feed and develop on resistant rice is a challenge for pest management in Asia. We conducted a series of manipulative experiments with the brown planthopper (Nilaparvata lugens (Stål)) on the resistant rice variety IR62 (BPH3/BPH32 genes) to assess behavioral and bionomic changes in planthoppers exhibiting virulence adaptation. We also examined the potential role of yeast-like symbionts (YLS) in virulence adaptation by assessing progeny fitness (survival × reproduction) following controlled matings between virulent males or females and avirulent males or females, and by manipulating YLS densities in progeny through heat treatment. We found virulence-adapted planthoppers developed faster, grew larger, had adults that survived for longer, had female-biased progeny, and produced more eggs than non-selected planthoppers on the resistant variety. However, feeding capacity—as revealed through honeydew composition—remained inefficient on IR62, even after 20+ generations of exposure to the resistant host. Virulence was derived from both the male and female parents; however, females contributed more than males to progeny virulence. We found that YLS are essential for normal planthopper development and densities are highest in virulent nymphs feeding on the resistant host; however, we found only weak evidence that YLS densities contributed more to virulence. Virulence against IR62 in the brown planthopper, therefore, involves a complex of traits that encompass a series of behavioral, physiological, and genetic mechanisms, some of which are determined only by the female parent.

scholarly journals Roles of Lipid Peroxidation-Derived Electrophiles in Pathogenesis of Colonic Inflammation and Colon Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Lei Lei ◽  
Jianan Zhang ◽  
Eric A. Decker ◽  
Guodong Zhang
Keyword(s):  
Colorectal Cancer ◽  
Lipid Peroxidation ◽  
Critical Role ◽  
Redox Stress ◽  
Colonic Inflammation ◽  
Colon Tumorigenesis ◽  
Inflammatory Bowel

Redox stress is a common feature of gut disorders such as colonic inflammation (inflammatory bowel disease or IBD) and colorectal cancer (CRC). This leads to increased colonic formation of lipid-derived electrophiles (LDEs) such as 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), trans, trans-2,4-decadienal (tt-DDE), and epoxyketooctadecenoic acid (EKODE). Recent research by us and others support that treatment with LDEs increases the severity of colitis and exacerbates the development of colon tumorigenesis in vitro and in vivo, supporting a critical role of these compounds in the pathogenesis of IBD and CRC. In this review, we will discuss the effects and mechanisms of LDEs on development of IBD and CRC and lifestyle factors, which could potentially affect tissue levels of LDEs to regulate IBD and CRC development.

Erastin induces ferroptosis via ferroportin-mediated iron accumulation in endometriosis

2020 ◽  
Author(s):  
Yajie Li ◽  
Xinliu Zeng ◽  
Dingheng Lu ◽  
Minuo Yin ◽  
Meirong Shan ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Lipid Peroxidation ◽  
Cell Viability ◽  
Stromal Cells ◽  
Morphological Changes ◽  
Iron Accumulation ◽  
Blue Staining ◽  
Endometrial Stromal Cells

Abstract STUDY QUESTION Could erastin activate ferroptosis to regress endometriotic lesions? SUMMARY ANSWER Erastin could induce ferroptosis to regress endometriotic lesions in endometriosis. WHAT IS KNOWN ALREADY Ectopic endometrial stromal cells (EESCs) are in an iron overloading microenvironment and tend to be more sensitive to oxidative damage. The feature of erastin-induced ferroptosis is iron-dependent accumulation of lethal lipid reactive oxygen species (ROS). STUDY DESIGN, SIZE, DURATION Eleven patients without endometriosis and 21 patients with endometriosis were recruited in this study. Primary normal and ectopic endometrial stromal cells were isolated, cultured and subjected to various treatments. The in vivo study involved 10 C57BL/6 female mice to establish the model of endometriosis. PARTICIPANTS/MATERIALS, SETTING, METHODS The markers of ferroptosis were assessed by cell viability, lipid peroxidation level and morphological changes. The cell viability was measured by colorimetric method, lipid peroxidation levels were measured by flow cytometry, and morphological changes were observed by transmission electron microscopy. Immunohistochemistry and western blot were used to detect ferroportin (FPN) expression. Prussian blue staining and immunofluorescent microscopy of catalytic ferrous iron were semi-quantified the levels of iron. Adenovirus-mediated overexpression and siRNA-mediated knockdown were used to investigate the role of FPN on erastin-induced ferroptosis in EESCs. MAIN RESULTS AND THE ROLE OF CHANCE EESCs were more susceptible to erastin treatment, compared to normal endometrial stromal cells (NESCs) (P<0.05). Treatment of cultured EESCs with erastin dramatically increased the total ROS level (P<0.05, versus control), lipid ROS level (P<0.05, versus NESCs) and intracellular iron level (P<0.05, versus NESCs). The cytotoxicity of erastin could be attenuated by iron chelator, deferoxamine (DFO), and ferroptosis inhibitors, ferrostatin-1 and liproxstatin-1, (P<0.05, versus erastin) in EESCs. In EESCs with erastin treatment, shorter and condensed mitochondria were observed by electron microscopy. These findings together suggest that erastin is capable to induce EESC death by ferroptosis. However, the influence of erastin on NESCs was slight. The process of erastin-induced ferroptosis in EESCs accompanied iron accumulation and decreased FPN expression. The overexpression of FPN ablated erastin-induced ferroptosis in EESCs. In addition, knockdown of FPN accelerated erastin-induced ferroptosis in EESCs. In a mouse model of endometriosis, we found ectopic lesions were regressed after erastin administration. LARGE SCALE DATA N/A LIMITATIONS, REASONS FOR CAUTION This study was mainly conducted in primary human endometrial stromal cells. Therefore, the function of FPN in vivo need to be further investigated. WIDER IMPLICATIONS OF THE FINDINGS Our findings reveal that erastin may serve as a potential therapeutic treatment for endometriosis. STUDY FUNDING/COMPETING INTEREST(S) This research did not receive any specific grant from funding agencies in the public, commercial or not-for-profit sectors. The authors declare no conflict of interest.

scholarly journals Regulation of Expression and Latency in BLV and HTLV

Viruses ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1079
Author(s):  
Aneta Pluta ◽  
Juan P. Jaworski ◽  
Renée N. Douville
Keyword(s):  
Gene Expression ◽  
Transcription Initiation ◽  
Spastic Paraparesis ◽  
Viral Gene ◽  
Regulation Of Transcription ◽  
Main Role ◽  
Regulation Of Expression ◽  
Incurable Cancer

Human T-lymphotrophic virus type 1 (HTLV-1) and Bovine leukemia virus (BLV) belong to the Deltaretrovirus genus. HTLV-1 is the etiologic agent of the highly aggressive and currently incurable cancer adult T-cell leukemia (ATL) and a neurological disease HTLV-1-associated myelopathy (HAM)/tropical spastic paraparesis (TSP). BLV causes neoplastic proliferation of B cells in cattle: enzootic bovine leucosis (EBL). Despite the severity of these conditions, infection by HTLV-1 and BLV appear in most cases clinically asymptomatic. These viruses can undergo latency in their hosts. The silencing of proviral gene expression and maintenance of latency are central for the establishment of persistent infection, as well as for pathogenesis in vivo. In this review, we will present the mechanisms that control proviral activation and retroviral latency in deltaretroviruses, in comparison with other exogenous retroviruses. The 5′ long terminal repeats (5′-LTRs) play a main role in controlling viral gene expression. While the regulation of transcription initiation is a major mechanism of silencing, we discuss topics that include (i) the epigenetic control of the provirus, (ii) the cis-elements present in the LTR, (iii) enhancers with cell-type specific regulatory functions, (iv) the role of virally-encoded transactivator proteins, (v) the role of repressors in transcription and silencing, (vi) the effect of hormonal signaling, (vii) implications of LTR variability on transcription and latency, and (viii) the regulatory role of non-coding RNAs. Finally, we discuss how a better understanding of these mechanisms may allow for the development of more effective treatments against Deltaretroviruses.

Role of lipid peroxidation in H2O2-induced renal epithelial (LLC-PK1) cell injury

1995 ◽  
Vol 268 (1) ◽  
pp. F30-F38 ◽  
Author(s):  
A. K. Salahudeen
Keyword(s):  
Lipid Peroxidation ◽  
Renal Cell ◽  
Time Course ◽  
Cell Injury ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
In Vivo Studies ◽  
Sequence Of Events

The exact sequence of events or mechanisms by which H2O2 induces renal cell injury remains undetermined. Specifically, whether the attendant lipid peroxidation is a cause or an effect remains unclear. Employing H2O2 and LLC-PK1 cells, we tested the hypothesis that lipid peroxidation is a seminal event and that its inhibition is cytoprotective. In a time course study, lipid peroxidation (thiobarbituric acid reaction) and degradation (release of [3H]arachidonic acid) preceded H2O2-induced cytolysis (51Cr and lactate dehydrogenase release). The role of preceding lipid peroxidation in cytolysis was examined with lipid radical scavengers. alpha-Tocopherol and lazaroid compound 2-methyl aminochroman dose-dependently inhibited H2O2-induced lipid peroxidation and prevented cytolysis. 2-Methyl aminochroman cytoprotection was associated with blockade of lipid degradation. 21-Aminosteroid, another lazaroid, also inhibited lipid peroxidation and prevented cytolysis. These findings provide evidence that lipid alterations contribute to H2O2-mediated LLC-PK1 injury and, for the first time, demonstrate the potency of lazaroids in a renal cell line. In vivo studies with lazaroids may define the role of lipid peroxidation in acute renal injury models.

scholarly journals Change in geomagnetic field intensity alters migration-associated traits in a migratory insect

2020 ◽  
Vol 16 (4) ◽  
pp. 20190940
Author(s):  
Guijun Wan ◽  
Ruiying Liu ◽  
Chunxu Li ◽  
Jinglan He ◽  
Weidong Pan ◽  
...  
Keyword(s):  
Field Intensity ◽  
Geomagnetic Field ◽  
Brown Planthopper ◽  
Nilaparvata Lugens ◽  
Primary Energy ◽  
Migration Route ◽  
Variable Environments ◽  
Insect Migration ◽  
Cryptochrome 1

Geomagnetic field (GMF) intensity can be used by some animals to determine their position during migration. However, its role, if any, in mediating other migration-related phenotypes remains largely unknown. Here, we simulated variation in GMF intensity between two locations along the migration route of a nocturnal insect migrant, the brown planthopper Nilaparvata lugens , that varied by approximately 5 µT in field intensity. After one generation of exposure, we tested for changes in key morphological, behavioural and physiological traits related to migratory performance, including wing dimorphism, flight capacity and positive phototaxis. Our results showed that all three morphological and behavioural phenotypes responded to a small difference in magnetic field intensity. Consistent magnetic responses in the expression of the phototaxis-related Drosophila-like cryptochrome 1 ( Cry1 ) gene and levels of two primary energy substrates used during flight, triglyceride and trehalose, were also found. Our findings indicate changes in GMF intensity can alter the expression of phenotypes critical for insect migration and highlight the unique role of magnetoreception as a trait that may help migratory insects express potentially beneficial phenotypes in geographically variable environments.

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