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PLoS One. 2017; 12(1): e0170836.
Published online 2017 Jan 26. doi:10.1371/journal.pone.0170836
Yallappa Rajashekar1,2 and Thimmappa Shivanandappa1,3,*
Frederic Marion-Poll, Editor
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Decalesides are a new class of natural insecticides which are toxic to insects by contact via the tarsal gustatory chemosensilla. The symptoms of their toxicity to insects and the rapid knockdown effect suggest neurotoxic action, but the precise mode of action and the molecular targets for decaleside action are not known. We have presented experimental evidence for the involvement of sodium pump inhibition in the insecticidal action of decaleside in the cockroach and housefly. The knockdown effect of decaleside is concomitant with the in vivo inhibition of Na+, K+ -ATPase in the head and thorax. The lack of insecticidal action by experimental ablation of tarsi or blocking the tarsal sites with paraffin correlated with lack of inhibition of Na+- K+ ATPase in vivo. Maltotriose, a trisaccharide, partially rescued the toxic action of decaleside as well as inhibition of the enzyme, suggesting the possible involvement of gustatory sugar receptors. In vitro studies with crude insect enzyme preparation and purified porcine Na+, K+ -ATPase showed that decaleside competitively inhibited the enzyme involving the ATP binding site. Our study shows that the insecticidal action of decaleside via the tarsal gustatory sites is causally linked to the inhibition of sodium pump which represents a unique mode of action. The precise target(s) for decaleside in the tarsal chemosensilla and the pathway linked to inhibition of sodium pump and the insecticidal action remain to be understood.
In view of the environmental and ecological concerns, human health hazards, and increasing insect resistance, many insecticides have been banned or replaced by newer chemicals . Mode of action of the major chemical classes of insecticides involves mainly three target sites in the nervous system: acetylcholinesterase, an enzyme of critical importance in the transmission of nerve impulse (organophosphorus and carbamates), voltage-gated sodium channels across the nerve membrane (pyrethoids and DDT), and the acetylcholine receptor (neonicotinoids) [1–5]. Selective insecticides such as juvenile hormone mimics (fenoxycarb and pyriproxyfen), ecdysone agonists and chitin synthesis inhibitors (Diflubenzuron) act on insect- specific targets that disrupt reproduction and development [6–8]. Among the insecticides derived from natural sources, azadirachtin, from the Indian neem tree, is a feeding deterrent and an insect growth regulator that suppresses fecundity, moulting, pupation and adult emergence [9–10]. Compounds that selectively act on the insect nicotinic acetylcholine receptor (neonicotinoids), such as imidacloprid, acetamiprid and thiomethaxam are among the modern insecticides used in pest management [11–13]. Avermectins, the insecticides of microbial origin, target GABA-gated chloride channels [14–15], whereas, the diamide insecticide acts on the ryanodine receptor [16–17]. Spinosyns, a new class of insecticides derived from actinomycetes, show high selectivity and low mammalian toxicity with eco-friendly behaviour [18–19].
Recent addition to the natural insecticides are decaleside I and II, novel trisaccharides isolated from the roots of Decalepis hamiltonii (Wight and Arn.) that are toxic to several insect species by contact with the tarsal gustatory sites but not toxic by oral or topical application [20–21]. This intriguing nature of the insecticidal action of these natural insecticides seems to involve new, unknown target(s) in insects. The insect toxicity of decaleside in the contact bioassay based on the symptoms and behaviour indicated neurotoxic nature somewhat similar to that of pyrethroids . The knockdown effect and mortality and symptoms suggest that decalesides may act on neural/neuromuscular targets via gustatory chemosensilla [21–22]. In insects, the axons of the gustatory receptor neurons from the chemosensilla directly report to the thoracic-abdominal and subesophageal ganglion as in the case of Drosophila [23–24]. Therefore, we hypothesised that the possible mode of action of decaleside on the chemosensilla may involve interference with the neuronal transmission of nerve impulse that could lead to the knock down effect. The biochemical basis of the insecticidal action of decalesides, however, is not known at present.
Na+, K+ -ATPase, or sodium pump, is a transmembrane ion motive enzyme most important in cellular ion regulation and maintenance of membrane potential by regulating the movement of Na+ and K+ ions across the cell membrane [25–28] which is coupled to ATP hydrolysis. Na+, K+ -ATPase, a highly conserved heterodimeric protein consisting of alpha and beta subunits with a transmembrane segment and the subunits combine to give tissue specific isoforms of the enzyme . It is a target for natural toxins such as cardenolides from plants and bufodienolides from plants, animals, and palytoxin from marine organisms [29–30]. The natural toxins cardenolides and bufadienolides bind to the alpha subunit interfering with the cellular functions by disrupting the cat ion exchange across the cell membrane . The highly toxic palytoxin, in a unique action, binds to the N-terminal side of the alpha subunit of the sodium pump, converting it to a ion channel resulting in K+ efflux, Na+ influx and membrane depolarisation [31–35]. Recently, it has been reported that palytoxin isolated from the red alga, Chondria armata was extremely toxic to cockroach when injected  suggesting the possibility that Na+, K+ -ATPase could be a potential target for newer insecticides. A preliminary observation in our study we found in vivo inhibition of Na+, K+ -ATPase in decaleside-treated insects, which led to the present study wherein we present experimental evidence that Na+, K+ -ATPase (sodium pump) is involved in the insecticidal action of decaleside in insects, which leads us to postulate novel mode of action for these unique natural insecticides.
Materials and Methods
The purified enzyme, sodium potassium adenosine triphosphatase (from porcine cerebral cortex), adenosine triphosphate (ATP), bovine serum albumin (BSA) and Ouabain were purchased from Sigma chemical Co., (St. Louis MO, USA). Other chemicals were purchased from Sisco Research Laboratory Mumbai, India. Decaleside I and II were isolated and characterized (purity, 99%) from the roots of Decalepis hamiltonii as reported earlier .
Housefly (Musca domestica) were reared in a mixture of sterilized bran, milk powder and water, and the adults were allowed free access to water and thick paste of condensed milk and milk powder . The German cockroach (Blatella germanica) was reared in plastic tubes with harborages, with dry food (biscuits) and water provided ad libitum . Insect cultures were maintained at 25.0 ± 2.5°C and 70% RH with a photoperiod of 12:12 (L: D).
Knockdown effect, defined as the state of intoxication and partial paralysis with lack of movement which usually precedes death by exposure to decaleside I and II, was investigated in contact bioassays using adults of the cockroach and housefly. A 1 ml solution (in methanol) each of the decalesides containing known concentration of the compounds was applied on Whatman No.1 (9cm) filter paper and placed in a glass Petri dish and the solvent was allowed to evaporate for 10 min under airflow with a fan, followed by the release of 10 adult cockroaches or 20 houseflies into each dish. The control filter paper discs were treated with the solvent only. Methanol as solvent was chosen for the ease of evaporation. Each treatment consisted of four replicates. The knockdown of insects was recorded after 45 min exposure. The dosages ranged from 0.004 to 0.272 mg/cm2, and the effective dosages were chosen based on trial experiments. Four replicates were used for each dosage. KD50 (50% knockdown in 24 h exposure) were determined from the dose-response data using probit regression analysis .
Decaleside I and II (0.008–0.270 mg/cm2) solutions (1ml) were sprayed on to filter paper and the control groups received only the solvent as described earlier. The solvent was allowed to evaporate for 10 min followed by the release of 10 unsexed adults of B. germanica and M. domestica separately into glass petri dishes (9cm diameter) at 25.0 ± 2.5°C. Four replicates were used for each dosage. Effective dosage for 50% knockdown effect (KD50) (45 min, exposure) was determined from the dose-response data using probit regression analysis .
Cockroaches or houseflies (10 per replicate) were released into Petri dish containing decaleside treated filter paper at KD50 dose (0.07 mg/cm2). The number of insects knocked-down was recorded for 0–60 min exposure.
In vivo inhibition of Na+, K+ -ATPase in relation to knockdown effect
Dose-response study: The KD25, KD50, and KD90 doses of decaleside I and II were determined by exposing the insects (cockroach and housefly) for 45 min in contact bioassay. In the case of houseflies, the head and thorax were frozen for the enzyme assay, whereas, for cockroaches, the brain (cerebral ganglia) and the coxal muscle were dissected out and used.
Time-course study: Insects were exposed to the KD50 dose of decalesides in the contact bioassay and removed at various exposure time intervals (15, 30, 45 and 60 min). The tissues of the insects were dissected and assayed as described above.
Na+, K+-ATPase assay
The tissues were homogenised in 0.1M tris-HCl buffer (pH 7.4), and centrifuged at 10, 000 x g for 15 min at 4°C and the supernatant was used for the assay of Na+, K+–ATPase . The reaction mixture contained NaCl (0.14M), KCl (14mM), MgCl2 (3mM), ethylenediamine tetra-acetic acid (EDTA, 2mM), to which the enzyme (50μl) was added with or without 1mM ouabain in a final volume of 1ml and pre-incubated at 37°C for 10 min. The reaction was started by adding 50μl of ATP (1.5mM), incubated for 30 min at 37°C and the reaction was stopped by the addition of 0.5ml of ice-cold 10% trichloroacetic acid and centrifuged at 5000 rpm for 10 min and the phosphate content (Pi) in the supernatant was estimated . The enzyme ATPase hydrolyses ATP to ADP and Pi (inorganic phosphate), and the specific activity of Na+, K+-ATPase was calculated as ouabain-inhibitable activity and expressed as Pi (μg)/mg protein.
Tarsi-mediated contact toxicity in relation to Na+, K+ -ATPase inhibition
Requirement of direct contact of decaleside with the tarsi in the legs for the insecticidal action has been experimentally demonstrated by surgical ablation of the tarsi or blocking by molten wax, as reported earlier . In order to test if the tarsi-mediated insecticidal action involves sodium pump inhibition, the activity of Na+, K+-ATPase activity was investigated in relation to the knockdown effect. The experimental procedures have been described earlier . Insects were treated with decaleside by direct application of 1mg aqueous solution with or without surgical ablation, and, wax treatment and the knockdown effect(0–45 min) and inhibition of Na+, K+-ATPase activity were determined.
Effect of hydrolysis of decaleside on the insecticidal activity and Na+, K+-ATPase activity
Chemical and enzymatic hydrolysis of decaleside and its effect on insect toxicity has been described earlier . In this study, effect of hydrolysis on in vivo inhibition of Na+, K+-ATPase activity in relation to the knockdown effect was investigated.
Effect of sugars on the insecticidal action of decaleside in relation to Na+, K+-ATPase inhibition
Since some sugars interfere with the insect toxicity of decaleside, we undertook to study if it involves sodium pump inhibition. The contact bioassay procedures with or without sugars on the toxicity have been described earlier . The activity of Na+, K+ -ATPase was assayed in the treated and control insects as described above.
In vitro inhibition of Na+, K+ -ATPase
In vitro inhibition of the enzyme, Na+, K+ -ATPase by decalesides in the tissues of houseflies, cockroaches (crude preparation) and the purified enzyme (porcine cerebral cortex) was studied. The enzyme was pre incubated with decaleside I and II (10μm– 1mM) at 37°C for 30 min, followed by the addition of 50μl of ATP (1.5mM), and incubated for 30 min at 37°C. The reaction was stopped by the addition of 1ml of ice-cold 10% trichloroacetic acid and centrifuged. Phosphate content in the supernatant was estimated . The enzyme activity with or without ouabain (1mM) in the reaction mixture was calculated, and the inhibition of Na+, K+ -ATPase was determined. IC50 were calculated by regression analysis.
Protein content was measured by the method of Lowry et al.  using BSA as the standard.
The data was analysed using one-way Anova (p < 0.05) using Statplus 2007 software. The data was expressed as means ± SE. Probit analysis was used for calculating KD50 .
In vivo inhibition of Na+, K+–ATPase in relation to insect toxicity
Na+, K+ -ATPase activities in insects exposed to KD25, KD50 and KD90 doses of decaleside I and II was markedly inhibited in a dose-dependent manner in the housefly (head and thorax) (Fig 1A, 1B and 1C) and cockroach (brain and coaxial muscle) (S1A and S1B Fig). The in vivo enzyme inhibition was dose-dependent and correlated with the knockdown effect measured at 45 min of exposure in the contact bioassay.
Dose-dependent in vivo inhibition of Na+, K+-ATPase by decalesides in relation to insecticidal activity in the house fly.
A) % Knockdown effect (n = 4, error bars, s.e.m.). B) Decaleside I (control activity: head = 38.03 μg Pi / mg protein; thorax = 45.8 μg Pi / mg protein) (n = 4, error bars, s.e.m.).C) Decaleside II (control activity: head = 33.15 μg Pi / mg protein; thorax = 45.4 μg Pi / mg protein) (n = 4, error bars, s.e.m.).
Inhibition of Na+, K+ -ATPase markedly increased with time in insects exposed to KD50 dose of decalesides (Fig 2A, 2B and 2C), and closely correlated with the knockdown effect (S2A and S2B Fig).
Time-course of in vivo inhibition of Na+, K+-ATPase in relation to knockdown of housefly treated with decalesides.
A) % Knockdown effect (n = 4, error bars, s.e.m.). B) Decaleside I (control activity: head = 61.6 μg Pi / mg protein; thorax = 38.6 μg Pi / mg protein) (n = 4, error bars, s.e.m.), and C) Decaleside II (control activity: head = 74.02 μg Pi / mg protein; thorax = 47.82 μg Pi / mg protein) (n = 4, error bars, s.e.m.).
Experiments in which recovery of the insects exposed to KD50 dose of decaleside I and II was monitored for 60–300 min after exposure, showed that recovery from knock-down effect also correlated with the recovery of the enzyme inhibition in vivo (S3A, S3B, S3C, S3D, S4A, S4B, S4C and S4D Figs).
Effect of tarsal ablation and wax treatment
Both tarsal ablation and wax treatment of the tarsi in cockroaches abolished the toxic action of decaleside II as evident by lack of knockdown effect and, there was no in vivo inhibition of Na+, K+ -ATPase in the brain as well as coxal muscle of cockroaches (Fig 3A and 3B) or wax treatment (Fig 3C and 3D). However, in the respective control groups, toxicity correlated with Na+, K+ -ATPase inhibition.
Experimental demonstration of the tarsi-mediated knockdown effect of decaleside II in relation to inhibition of Na+, K+ -ATPase activity in the brain of German cockroach.
A, B: Effect of tarsal ablation on the a) Knockdown, b) Na+, K+ ATPase activity of decaleside II, I) Intact insects, II) Intact insects + decaleside II, III) Tarsii ablated + decaleside II (n = 4, error bars, s.e.m.). C, D: Effect of wax application on c) Knockdown, d) Na+, K+ ATPase activity in the brain of Blatella germanica exposed to KD50 (0.07 mg/cm2) of decaleside II, by contact bioassay. I) Intact insects, II) wax treated (solvent control), III) Intact insects + decaleside II, IV) wax treated + decaleside II. (n = 4, error bars, s.e.m.).
The effect of direct application on the tarsi
Direct application of decaleside to the tarsi of the first pair of legs induced knockdown effect and caused enzyme inhibition in the cockroaches, whereas wax application on the tarsi protected against the toxicity and, there was no enzyme inhibition (S5A and S5B Fig.).
Effect of hydrolysis
In cockroaches exposed to KD50 concentration of the hydrolyzed (chemical and enzymatic) decaleside II, there was no toxicity as evident from the absence of knock down. Also, there was no inhibition of Na+, K+ -ATPase in the brain of cockroaches showing correlation with lack of toxicity of the hydrolyzed sample of decaleside II (Fig 4A and 4B).
Effect of hydrolysis of decaleside II on the knockdown and inhibition of Na+, K+ ATPase activity in the brain of Blatella germanica exposed to KD50 (0.07 mg/cm2) of decaleside II by contact bioassay.
A) Knockdown, B) Inhibition of Na+, K+ ATPase of activity. I) Control (without hydrolysis), II) Acid hydrolysis, III) β-Galactosidase, IV) α-Glucosidase. (n = 4, error bars, s.e.m.) One-way ANOVA, ***P < 0.001.
Effect of sugars
Experiments in which cockroaches were exposed to decaleside treated paper with or without various sugars, showed that sugars interfered with the toxicity as measured by the knockdown effect, which correlated with the decreased inhibition of Na+, K+ -ATPase enzyme in the brain in vivo (Fig 5A and 5B). However, treatment with the amino acid (glycine) had no effect on the knockdown effect of decaleside II, which correlated with the lack of Na+, K+ -ATPase inhibition (Fig 5A and 5B). Among the sugars, maltotriose, a trisaccharide, was most effective in rescuing the knockdown effect of decaleside II and Na+, K+ -ATPase inhibition. The dose-dependent protective effect of maltotriose against toxicity (knock-down) of decaleside II correlated with inhibition of Na+, K+ -ATPase in the brain in vivo (Fig 5C and 5D).
Effect of sugars on the knockdown and inhibition of Na+, K+ ATPase activity in the brain of Blatella germanica exposed to KD50 (0.07 mg/cm2) of decaleside II by contact bioassay.
A, B: A) Knockdown, B) Inhibition of Na+, K+ ATPase: I. Decaleside II, II. Decaleside II + Glycine, III. Decaleside II + Glucose, IV. Decaleside II + Xylose, V. Decaleside II + Trehalose, VI. Decaleside II + Raffinose, VII. Decaleside II + Melezitose, VIII. decaleside II + Maltotriose in 1:1 equimolar concentration. C, D: Effect (dose-response) of maltotriose on the C) Knockdown, D) Inhibition of Na+, K+ ATPase activity: I. Decaleside II, II. Decaleside II + Maltotriose (1:0.1), III. Decaleside II + Maltotriose (1:0.25), IV. Decaleside II + Maltotriose (1:0.5), V. Decaleside II + Maltotriose (1:0.75), VI. Decaleside II + Maltotriose in 1:1 equimolar concentration.
In vitro inhibition
Both decaleside I and II were inhibitors of Na+, K+ -ATPase from the tissues of house fly, cockroach and the purified enzyme from the porcine cerebral cortex. The enzyme inhibition was concentration-dependant (Fig 6A, 6B, 6C, 6D and 6E). IC50 determined for the house fly, cockroach, and the purified Na+, K+ -ATPase indicated that decaleside I and II were more potent inhibitors of Na+, K+ -ATPase than ouabain (S1 Table).
In vitro inhibition of Na+, K+ ATPase by decaleside I and II in comparison with that of ouabain.
A, B : cockroach brain and thorax, respectively (control activity: head = 29.33 μg Pi / mg protein; thorax = 88.5 μg Pi / mg protein); C, D : house fly head and thorax, respectively (control activity: head = 73.6 μg Pi / mg protein; thorax = 97.42 μg Pi / mg protein ); E: Purified Na+, K+ ATPase (porcine cerebral cortex, sigma); IC50: Ouabain, 25.4 × 10-5M; Decaleside I, 10.5 × 10-5M; Decaleside II, 9.5 × 10-5M.
Type of inhibition
Kinetic studies showed that the Km (ATP) shifted with the increased concentration of the inhibitors indicating that the inhibition was competitive as evident from the Lineweaver-Burk plot (S6A, S6B, S6C and S6D Fig). Similar results were found with the purified Na+, K+ -ATPase from porcine cerebral cortex, indicating the competitive type of inhibition (S7A and S7B Fig).
Our study has demonstrated that Na+, K+ -ATPase is severely inhibited in insects (both house fly and cockroaches) exposed to decaleside I and II in the contact bioassay. The in vivo inhibition closely correlated (r = >0.9) with the knockdown effect of decaleside I and II in dose-response and time-course studies. The in vivo inhibition was seen in both head and thorax in the case of house fly and the nervous (ganglion) and muscle tissue in cockroaches exposed to decaleside. Further, experimental evidence shows that the inhibition of Na+, K+ -ATPase requires contact of the insect leg (tarsi) with insecticide treated surface, since no inhibition was seen in insects with tarsi ablated. The same was demonstrated with the application of wax on the tarsi, wherein toxic action of decaleside was abolished. In these experiments in which contact with tarsi for the insecticidal action of decaleside is required, also show concomitant inhibition of Na+, K+ -ATPase in vivo. The results lead us to conclude that tarsi-mediated insect toxicity of decaleside involves Na+, K+ -ATPase inhibition. Our results are the first report of a natural insecticide (novel trisaccharides) showing Na+, K+ -ATPase as the target in its mode of action. The molecular mechanisms involved in the insecticidal action of decaleside via the gustatory chemosensilla that lead to the knock-down effect, the toxic outcome finally leading to mortality, are not clear at present. Our results show that the insects exposed to decaleside, are initially hyperactive indicating neural excitation, which is followed by knockdown effect, symptoms somewhat similar to that of pyrethoids, suggesting a neurotoxic effect [43–44]. The basic difference, however, is that the decaleside action is mediated by contact with tarsi, unlike that of pyrethoids which act by contact at any point of the body surface of insects. It is known that pyrethroids act by interfering with the voltage gated sodium channels in the neurons which causes hyper excitation leading to knockdown [45–47]. In the case of decaleside action, inhibition of sodium pump is clearly demonstrated in our studies. The following hypothesis is proposed in order to explain the mode of action of decaleside via the gustatory receptors: on contact with the gustatory (sugar) receptors (step I) causes inhibition of sodium pump (step II) which is responsible for the hyperactivity due to increased neuronal excitation caused by excessive Na+ concentration (step III) finally leading to knockdown effect and mortality. Electrophysiological evidence is needed to support this hypothesis.
Our study shows that some of the sugars particularly maltotriose, a trisaccharide, interferes with the insecticidal activity of decaleside implying the involvement of sugar receptors in the gustatory chemosensilla which is also concomitant with the Na+, K+ -ATPase inhibition in vivo. Whether specific gustatory receptor neurons mediate the action of decaleside action needs to be investigated.
Our in vitro studies of Na+, K+ -ATPase from the insect tissues as well as the purified enzyme indicate that the inhibition is competitive type which suggests that decaleside is interacting with the ATP binding site of the enzyme. It is known that the ATP binding site of Na+, K+ -ATPase in the plasma membrane is interior to the cell unlike the ouabain binding site which is to the exterior [25, 48–49]. The difference in the IC50 values for the in vitro inhibition of the insect enzyme versus the purified enzyme could be attributed to the crude enzyme preparation from insect tissue and it is not clear if the binding sites for decaleside on the enzyme are different. Future investigations on insecticidal action of decalesides targeting the gustatory (sugar) receptors and the neurons will open up a new field for scientific inquiry in order to unravel the mechanisms involved in their toxic action in insects. Decalesides, therefore, represent novel natural insecticidal molecules with a unique mode of action.
In vivo inhibition of Na+, K+-ATPase in the cockroach by decaleside II (contact bioassay).
A: % Knockdown. B: Dose-dependent in vivo inhibition of Na+, K+-ATPase in the cockroach by Decaleside II (control activity: Brain = 58.03 μg Pi / mg protein; Coxal muscle = 65.8 μg Pi / mg protein).
Click here for additional data file.(295K, tif)
Correlation between knockdown effect and Na+, K+ ATPase inhibition in vivo in house fly (A) and cockroach (B) treated with decaleside II in a dose-response study.
Click here for additional data file.(343K, tif)
Time-course of in vivo inhibition of Na+, K+-ATPase in Blatella germanica by decaleside II.
A) % Knockdown, B) Na+, K+ ATPase activity of decaleside II in Blatella germanica exposure at 1mg/leg (fore legs) by topical application (control activity: brain = 68.03 μg Pi / mg protein; coxal muscle = 75.8 μg Pi / mg protein). C) % Knockdown, D) Na+, K+ ATPase activity of decaleside II in Blatella germanica exposure at KD50 (0.07 mg/cm2) by contact bioassay (control activity: brain = 73.4.03 μg Pi / mg protein; coxal muscle = 78.8 μg Pi / mg protein).
Click here for additional data file.(505K, tif)
Time-course of in vivo inhibition of Na+, K+-ATPase in relation to recovery from knockdown of house flies treated with decaleside I and II at KD50 concentration (0.032 mg/cm2) (starting time point after exposure was 45 min from which recovery was monitored).
A) Recovery from knockdown of decaleside I;B) Recovery of Na+, K+-ATPase inhibition (control activity: head = 37.56 μg Pi / mg protein; thorax = 17.4 μg Pi / mg protein). C) Recovery from knockdown of decaleside II;D) Recovery of Na+, K+-ATPase inhibition (control activity: head = 37.56 μg Pi / mg protein; thorax = 17.4 μg Pi / mg protein).
Click here for additional data file.(390K, tif)
Effect of direct topical application of decaleside II on the tarsi with or without wax treatment on A) Knockdown, B) Na+, K+ ATPase activity in contact bioassay.
I) Control (no wax), II) Control (no wax) + decaleside II (1mg/insect), III) wax treated on tarsi (+ solvent), IV) with wax treated tarsi + decaleside II (1mg/insect) (n = 4, error bars, s.e.m.), One-way ANOVA, ***P < 0.001.
Click here for additional data file.(540K, tif)
Kinetics of in vitro inhibition of Na+, K+ ATPase in brain and coxal muscle of German cockroach: The double reciprocal (Linweaver-Burk) plot.
Brain: A, Decaleside I; B, Decaleside II. Coxal muscle: C, Decaleside I; D, Decaleside II.
Click here for additional data file.(723K, tif)
Kinetics of in vitro inhibition of the purified (porcine cerebral cortex) Na+, K+ ATPase: The double reciprocal (Linweaver-Burk) plot.
A) Decaleside I; B) Decaleside II.
Click here for additional data file.(353K, tif)
In vitro inhibition (IC50) of Na+, K+ ATPase by decaleside I and II in the house fly, cockroach and purified Na+, K+ ATPase (porcine cerebral cortex).
Click here for additional data file.(103K, pdf)
The authors wish to thank the Director of the institute for his keen interest in this study.
The authors received no specific funding for this work.
All relevant data are within the paper and its Supporting Information files.
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Articles from PLOS ONE are provided here courtesy of PLOS
What is the mode of action of DDT? ›
What is the mechanism of action of DDT? DDT affects the nervous system by interfering with normal nerve impulses (2). DDT causes the nerve cells to repeatedly generate an impulse which accounts for the repetitive body tremors seen in exposed animals (2).What is the mode of action of insecticide? ›
Many insecticides act upon the insect's nervous system (e.g., cholinesterase inhibition), while others act as growth regulators or endotoxins. Most act on neurons by causing a sodium/potassium imbalance preventing normal transmission of nerve impulses.What is the mode of entry of insecticides? ›
Insecticides can be classified according to their mode of entry into the insect as 1) stomach poisons, 2) contact poisons, or 3) fumigants. However, many insecticides belong to more than one category when grouped in this way, limiting its usefulness.What is the mode of action of lannate insecticide? ›
It is a carbamate insecticide that works by inhibiting cholinesterase. This means that it causes overstimulation of nerves and muscles, which results in paralysis and death for insects.What enzyme does DDT inhibit? ›
DDT is known as a non-genotoxic hepatocarcinogen and has been shown to induce microsomal enzymes through activation of constitutive androstane receptor (CAR) and to inhibit gap junctional intercellular communication (GJIC) in the rodent liver.How does DDT work as an insecticide? ›
It is an insecticide that kills insects by disrupting their nervous systems. DDT was effective and popular for several reasons. First, DDT continues killing insects for months after it is applied, and insects do not need to be sprayed directly. If an insect crawls on a surface with DDT, it will die.What are the 4 main modes of action of insecticides? ›
Brown (1951) has classified insecticides into five groups, based on mode of action: (l) physical poisons, (2) protoplasmic poisons, (3) respiratory poisons, (4) nerve poisons, and (5) poisons of a more general nature.
Mode of action of the major chemical classes of insecticides involves mainly three target sites in the nervous system: acetylcholinesterase, an enzyme of critical importance in the transmission of nerve impulse (organophosphorus and carbamates), voltage-gated sodium channels across the nerve membrane (pyrethoids and ...What inhibitor is used as an insecticide? ›
The most widely used types are insecticides as cholinesterase (ChE) inhibitor, mainly organophosphorous compounds and carbamates (WHO 1991).How do you determine the mode of entry? ›
A company must properly evaluate country risk before deciding on an entry mode. This would include an evaluation of political, economic and market related risks as well as exchange rate risk.
What are the modes of entry? ›
The five most common modes of international-market entry are exporting, licensing, partnering, acquisition, and greenfield venturing. Each of these entry vehicles has its own particular set of advantages and disadvantages.What are the basic modes of entry? ›
|Type of Entry||Advantages|
|Exporting||Fast entry, low risk|
|Licensing and Franchising||Fast entry, low cost, low risk|
|Partnering and Strategic Alliance||Shared costs reduce investment needed, reduced risk, seen as local entity|
|Acquisition||Fast entry; known, established operations|
LANNATE® LV is a broad spectrum insecticide registered in a wide range of field, fruit and vegetable crops. LANNATE® LV is particularly active on many Lepidopterous pests as an ovicide, larvicide and adulticide. LANNATE® LV is primarily a contact insecticide giving rapid knockdown effects on insects.Is lannate insecticide systemic? ›
8. GENERAL DESCRIPTION: A systemic, contact and ingested insecticide and nematode killer.How does insecticide spray work? ›
The active ingredients in bug spray are designed to mask or hide the scent of carbon dioxide so insects can't find you. For additional repellant power, bug sprays also include scents that bugs find repulsive to keep them even further away.Is DDT a competitive inhibitor? ›
The inhibition by DDT was noncompetitive, maximum at acid pH and independent of temperature. The inhibition was counteracted by exogenous phosphatidylcholine and phosphatidylethanolamine.Is pesticide an enzyme inhibitor? ›
Pesticides mostly, exert toxicity by inhibiting the enzyme acetylcholinesterase (AChE)  which degrades acetylcholine (ACh), an essential neurotransmitter in the central nervous system (CNS) of insects, rodents, and humans .How do insects become resistant to DDT? ›
Genetics and intensive application of insecticides are responsible for the rapid development of resistance in many insects and mites. Selection by an insecticide allows some insects with resistance genes to survive and pass the resistance trait on to their offspring.How does DDT affect sodium channels? ›
DDT and pyrethroids preferably bind to open sodium channels and stabilize the open state, causing prolonged currents. In contrast, SCBIs block sodium channels by binding to the inactivated state.What happens when DDT is sprayed in the environment? ›
DDT was canceled because it persists in the environment, accumulates in fatty tissues, and can cause adverse health effects on wildlife (4). In addition, resistance occurs in some insects (like the house fly) who develop the ability to quickly metabolize the DDT (1).
What is DDT What was it used for quizlet? ›
DDT, or para-dichlorodiphenyltrichloroethane, was used as an insecticide. It was widely used in the 1950s and 60s, and environmental concentration rose, which lead to affecting birds reproductive capabilities.What is classification of mode of action? ›
The Mode of Action Classification scheme is a key part of IRAC's global IRM strategy. IRAC promotes the use of a Mode of Action (MoA) Classification of insecticides and acaricides as the basis for effective and sustainable resistance management. Actives are allocated to specific groups based on their target site.What is insecticide resistance mode of action? ›
Insecticide resistance is defined by the Insecticide Resistance Action Committee (IRAC)  as 'a heritable change in the sensitivity of a pest population that is reflected in the repeated failure of a product to achieve the expected level of control when used according to the label recommendation for that pest ...What are the 4 types of pesticides and what organisms do they work for? ›
Microbial pesticides are microorganisms that kill, inhibit, or out-compete pests, including insects or other microorganism pests. Molluscicides kill snails and slugs. Nematicides kill nematodes (microscopic, worm-like organisms that feed on plant roots). Ovicides kill eggs of insects and mites.How are pesticides classified on the basis of their mode of action? ›
However the most common way to classify them is based on their chemical structure, identifying four main groups: organochlorines, organophosphates, carbamates, and pyrethroids.What are the three 3 mechanisms of plant resistance to insects? ›
Plant resistance can be categorized into three categories: antibiosis, antixenosis or non-preference, and tolerance.What are the three types of pesticides and what do they have an effect on? ›
- Herbicides destroy or control weeds and other unwanted vegetation. They are commonly used on lawns.
- Insecticides kill or control insects. ...
- Fungicides control fungi and can be used on plants or other surfaces where mold or mildew grow.
Pyrethrum is a highly effective natural insecticide. It is used in all manner of insect pests.Which enzyme used as a insecticide? ›
Organophosphate triesters, such as parathion and diazinon, are potent acetylcholinesterase (AChE) inhibitors and have been widely used as insecticides around the world.Which insecticide is responsible for inhibition of cholinesterase enzymes? ›
Carbamates are a group of chemicals that, like organophosphates, are commonly used as insecticides. They also inhibit cholinesterase.
How do you do the mode method? ›
To find the mode manually, arrange the numbers in ascending or descending order, then count how often each number appears. The number that appears most often is the mode. It's now easy to see which numbers appear most often.What are the methods of determining mode? ›
- A. Mode = 2 Median – 3 Mean.
- B. Mode = 2 Median + 3 Mean.
- C. Mode = 2 Median – 2 Mean.
- D. Mode = 3 Median + 2 mean.
There are two major types of market entry modes: equity and non-equity. The non-equity modes category includes export and contractual agreements. The equity modes category includes joint ventures and wholly owned subsidiaries.What are the 6 types of entry modes? ›
What are the six types of entry modes? The six types of entry modes are export, licensing, franchising, wholly-owned ventures, Greenfield strategy, and Mergers and Acquisitions.Why entry mode is important? ›
The choice of entry mode is an important strategic decision for SMEs as it involves committing resources in different target markets with different levels of risk, control, and profit return.Which is the most appropriate mode of entry? ›
Detailed Solution. Exporting is the most appropriate mode of entry in international business to an enterprise with little experience in international markets. Explanation: One of the critical decisions in international marketing is the mode of entering the foreign market.What are the types of intermediate mode of entry? ›
Intermediate entry modes include a variety of arrangements, such as licensing, franchising, management contracts, turnkey contracts, joint ventures and technical know-how or coproduction arrangements.What is licensing mode of entry? ›
Licensing is a type of market entry whereby a company in one country transfers the right of a company in another country to use its unique production processes, patents, trademarks, technological achievements, and other valuable skills for a fee that is established under the contract.What is acquisition entry mode? ›
An acquisitionAn international entry mode in which a firm gains control of another firm by purchasing its stock, exchanging stock, or, in the case of a private firm, paying the owners a purchase price. is a transaction in which a firm gains control of another firm by purchasing its stock, exchanging the stock for its ...Which is the best chemical for thrips? ›
Greenhouse thrips is readily controlled with thorough application of contact sprays such as horticultural oil, natural pyrethrins (plus piperonyl butoxide), or insecticidal soaps to the underside of infested leaves.
How long does permethrin last on plants? ›
If permethrin is applied to plants, it may stay on the leaves for between 1 and 3 weeks.How long does permethrin last on trees? ›
Permethrin SFR 36.8% is an insecticide concentrate and used to create a residual barrier to eliminate a broad range of insects both indoors and outdoors. This product creates a strong insecticidal barrier for about 90 days indoors and 30 day outdoors that is safe to use around pets and livestock.Which insecticide has systemic action? ›
Neonicotinoids and fipronil belong to a wide family of substances jointly referred to as the “systemic insecticides” due to their systemic properties, some carbamate and organophosphorus substances, however, can also act systemically (Sanchez-Bayo et al.What makes an insecticide systemic? ›
What are Systemic Insecticides? Systemic pesticides (whether insecticides, fungicides, herbicides or other pesticides) are absorbed by and transported through plants. Systemic insecticides can render some or all of a plant toxic to insects that feed on plant tissue.What are the 4 types of insecticides? ›
- Organic insecticides.
- Synthetic insecticides.
- Inorganic insecticides.
- Miscellaneous compounds.
Preventative treatment for ants, cockroaches, and other common pests: 15 to 30 minutes. Removal of active ant or cockroach infestations: 90 to 120 minutes or more depending on the extent of the infestation.How long does it take for insecticide to work? ›
In most cases, you can expect to see a significant and noticeable reduction in pest activity within one to two days. The exact timeframe depends on the pest we're dealing with along with the choice of materials necessary to provide the best long-term results.How does DDT work against malaria? ›
DDT is used in IRS by spraying indoor surfaces with a coating of DDT. This residual coating prevents malaria transmission as a spatial repellent or contact irritant or by killing mosquitoes (indicating more than one mode of action), effectively preventing or interrupting transmission (Grieco et al.What is DDT and what is its effect on the ecosystem? ›
DDE decreases the reproductive rate of birds by causing eggshell thinning and embryo deaths (14). DDT is highly toxic to aquatic animals (14). DDT affects various systems in aquatic animals including the heart and brain (14). DDT is highly toxic to fish (14).Does DDT still prevent malaria? ›
Some people canvass its anti-malarial benefits while others cite its harmful effects on the environment and human health. It is banned in some countries even as many others use it to control mosquitoes that cause malaria.
Is DDT banned in the US? ›
The United States banned the use of DDT in 1972. Some countries outside the United States still use DDT to control of mosquitoes that spread malaria. DDT and its related chemicals persist for a long time in the environment and in animal tissues.What are 3 benefits of using DDT? ›
It was initially used with great effect to combat malaria, typhus, and the other insect-borne human diseases among both military and civilian populations. It also was effective for insect control in crop and livestock production, institutions, homes, and gardens.How DDT affects the organisms along the food chain? ›
When an animal consumes food having DDT residue, the DDT accumulates in the tissue of the animal by a process called bioaccumulation. The higher an animal is on the food chain (e.g. tertiary consumer such as seals), the greater the concentration of DDT in their body as a result of a process called biomagnification.Does DDT break down quickly in the environment? ›
DDT lasts a very long time in soil. Half the DDT in soil will break down in 2–15 years. Some DDT will evaporate from soil and surface water into the air, and some is broken down by sunlight or by microscopic plants or animals in soil or surface water.What are the modes of insecticide resistance? ›
Insecticide resistance can be divided into two major types: behavioral resistance and physiological resistance [1, 79]. In behavioral resistance, the insect populations may develop the ability to avoid or reduce lethal insecticide exposure .How did insects become resistant to DDT quizlet? ›
The rapid rise in the percentage of mosquitoes resistant to DDT was most likely caused by natural selection in which mosquitoes resistant to DDT could survive and reproduce, while other mosquitoes could not.How can we prevent insecticide resistance? ›
- Minimize Pesticide Use. Minimizing pesticide use is fundamental to pesticide resistance management. ...
- Avoid Tank Mixes. Avoid combinations (mixes) of two insecticides or miticides in a single application. ...
- Avoid Persistent Chemicals. ...
- Use Long-term Rotations.
The agricultural runoff that contains DDT when sent into the water body results in water pollution and it causes the destruction o aquatic flora and fauna. Thus, spraying of DDT results in air, soil and water pollution.Why doesn t everyone stop using DDT and change over to using biodegradable insecticides? ›
Due to the inability of DDT to be broken down by microbes it remains present in the environment and is a major cause of insecticide pollution. DDT is removed from human use because no enzyme is yet discovered which is capable of acting on it.