Mode of Action of Insecticides

Roan, C. C.; Hopkins, Teri

doi:10.1146/annurev.en.06.010161.002001

Cited by 40 publications

(7 citation statements)

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“…Lutta and Shulman (1956) distinguished several stages of I. ricinus poisoning but the criteria of the stages were rather indistinct. Roan and Hopkins (1961) gave more determinate criteria of insect poisoning and distinguished six stages of the post-treatment period. We worked out these criteria and stages for tick poisoning in detail so that they precisely describe all changes in terms of tick behavior.…”

Section: Stages Of Tick Poisoningmentioning

confidence: 99%

Potential risk of pathogen transmission by acaricide-poisoned ticks

Uspensky

Ioffe-uspensky

2006

International Journal of Medical Microbiology

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Section: Stages Of Tick Poisoningmentioning

confidence: 99%

Potential risk of pathogen transmission by acaricide-poisoned ticks

Uspensky

Ioffe-uspensky

2006

International Journal of Medical Microbiology

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“…As to the site of loss, depletion of body fluids is usually attributed to increased regurgitation and excretion (Mobius & Wedekind, 1934; Klinger, 1936;Ludwig, 1946;Jochem, 1953Jochem, , 1956 Roan & Hopkins, 1961;Roberts et al, 1969), possibly after redistribution of the available water from the blood to the gut (Jochem, 1956;Hopkins, Rao & Ameel, 1970). Losses may also occur by increased transpiration through the spiracles (Ingram, 1955), through the integumental membranes of the body wall (Ludwig, 1946), and through the general integument (Buck & Keister, 1949;Chadbourne & Rainwater, 1953;Ingram, 1955).…”

Section: (3) Insecticide-induced Water Lossmentioning

confidence: 99%

Insecticides: Their Route of Entry, Mechanism of Transport and Mode of Action

Gerolt

1983

Biological Reviews

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Summary (1) The assumption that the circulatory system of the insect is instrumental in transporting insecticides to their site of action appeared not to be based on good evidence. On the contrary, experiments specifically designed to test the hypothesis provided ample evidence to refute the idea. Salient points to disprove the haemolymph route of entry can be summed up as follows: (a) A topically applied dose of insecticide does not readily penetrate the insect and the minor fraction that does so is largely retained in the body wall. The small amount that actually passes into the blood is too small to cause symptoms of toxicity if injected into the haemocoel. (b) The amount of insecticide present in the haemolymph (and CNS) does not appear to have any bearing on toxicity ‐ internally introduced insecticides are, in fact, basically very much less toxic than those externally applied. Where injected doses appear to be more toxic than equal amounts topically applied, this is due to the boosting effect of organic solvent carriers. Tests with parabiotically joined insects provide support for the view that haemolymph‐borne insecticide is of no consequence. (c) The topographical proximity of the locus of external application with the site of action (the thoracic ganglia) seems to be important irrespective of the general direction of the blood flow, and this should not be so if the circulatory system was instrumental in the transport of insecticide. (d) The introduction into the haemocoel of material such as olive oil, which is an excellent absorbent for insecticides, does not affect the toxicity (speed of action) of externally applied compounds to a significant extent. It should have a pronounced effect if haemolymph‐borne insecticide were an essential element in the process of poisoning. (e) As judged by speed of action, blocking of the blood circulation does not hamper the insecticide's movement to the site of action. (2) Only two other feasible routes remain. (a) The insecticide might reach the CNS via peripheral nerves and nerve cord, but the results of histochemical assays of cholinesterase inhibition in the insect's CNS make the idea improbable for organo‐phosphates. The nerve route is also incompatible with the observation that a wax barrier blocked the movement in and over the body wall so as to delay the onset of symptoms of toxicity, as such a barrier would not hinder movement into lateral nerves near the locus of application. (6) The only other feasible alternative, i.e. entry by means of lateral transport via the integument of the body wall and tracheae, is supported by autoradiographic and other evidence which showed the insecticide to accumulate in the tracheal system. It is further supported by the fact that inter‐tracheal introduction is faster acting than topical treatment, indicating that the tracheal system offers a very effective pathway to the internal organs. (3) Regarding the mechanism of entry, earlier reviews and text books maintain this to be associated exclusively with penetration into and thr...

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“…There is some evidence that unrelated environmental stresses, whether insecticidal or non-specific, produce analogous effects in insects by the release into the body fluids of pharmacologically active substances of unknown chemical identity (Roan & Hopkins, 1961;Sternburg, 1963). Stress of adults and nymphs of the cotton stainer Dysdercus fasciatus Sign, due to crowding resulted in changes in life span, fecundity and body size (Hodjat, 1969), and unrelated stresses due to sublethal doses of insecticides, poor diet or starvation would, therefore, be expected to have similar effects.…”

Section: Introductionmentioning

confidence: 99%

Effects of sublethal doses of insecticides and of diet and crowding on Dysdercus fasciatus Sign. (Hem., Pyrrhocoridae)

Hodjat

1971

Bull. Entomol. Res.

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The effects of sublethal doses of insecticides and unrelated environmental stresses on Dysdercus fasciatus Sign, were studied in the laboratory. Dieldrin applied topically to fifth-instar nymphs at 02–0·6 μg/individual increased egg production, at 0·8–60 μg/individual decreased egg production, and at 0·6–60 μg/individual decreased fertility. Applied to adults, dieldrin at 2–4 μg/individual reduced egg production, and at 0·02–0 08 μg/individual (males) and 0·2–0·8 μg/individual (females) shortened the life span. In a separate experiment, dieldrin at 0·2 μg/individual reduced egg production when applied to fourth-instar nymphs, but had no effect on fifth-instar nymphs or adults. p.p'DDT at 6 μg/individual applied topically to unmated females increased egg production. Exposure of all life stages to 0·06 mg DDT/ litre for two generations was followed by increased egg production and fertility: shorter exposure at 1 mg DDT/litre had no effect, and at 6–20 mg/litre egg production and fertility were reduced. Rearing on boiled cotton seed resulted in small adults with low gg production and fertility, the eggs being longer than normal. Crowding nymphs (24 individuals/200-ml cage) had the same effect on the size of the resultant adults. Starvation caused low egg production and fertility. Fluttering of males during a free fall (a measure of activity) was increased by crowding (maximum at 2 individuals/cage), by topically applied dieldrin at 0·04–0·08 μg/individual and DDT at 3–5 μg/individual, by two-generation exposure to 0·06 mg DDT/litre, but not by feeding on boiled cotton seed.

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Mode of Action of Insecticides

Cited by 40 publications

References 0 publications

Potential risk of pathogen transmission by acaricide-poisoned ticks

Potential risk of pathogen transmission by acaricide-poisoned ticks

Insecticides: Their Route of Entry, Mechanism of Transport and Mode of Action

Effects of sublethal doses of insecticides and of diet and crowding on Dysdercus fasciatus Sign. (Hem., Pyrrhocoridae)

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