Negative Temperature Coefficient Of Toxicity Research Articles

Temperature Effects on λ-Cyhalothrin Toxicity in Insecticide-Susceptible and Resistant German Cockroaches (Dictyoptera: Blattellidae)

Pre- and post-treatment temperature effects on -cyhalothrin toxicity were determined in insecticide-susceptible and resistant German cockroach, Blattella germanica (L.), strains. Acclimation at 19, 26, or 31C for 10 days before insecticide treatment had no effect on l- cyhalothrin toxicity in either strain. No differences were observed in aldrin epoxidase and glutathione S-transferase activities when “Orlando” (susceptible) cockroaches were incubated for 10 days at 19, 26, and 31C. When temperature treatment followed insecticide application, a negative temperature coefficient of toxicity (greater toxicity at lower temperature) toward l- cyhalothrin was observed for the Orlando but not the kdr-type resistant “Village Green” cockroaches. Piperonyl butoxide synergized l- cyhalothrin in “Orlando” cockroaches 3 and 5-fold at 26 and 31C, respectively. Conversely, piperonyl butoxide pre-treatment did not cause a significant reduction in the LD 50 value in the “Village Green” strain regardless of temperature.

Influence of Treatment Technique on the Temperature-Toxicity Relationships of cis- and trans-Permethrin in the Cabbage Looper (Lepidoptera: Noctuidae)

The toxicity of cis - and trans -permethrin to third instar cabbage loopers, Trichoplusia ni (Hubner), was determined at 15.6, 26.7, and 37.8°C by two treatment techniques. Whether applied topically or incorporated into the diet of the larvae, both isomers showed a negative temperature coefficient of toxicity between 15.6 and 37.8°C. However, temperature coefficients between 15.6 and 26.7°C and between 26.7 and 37.8°C varied. Data indicate that the method of application of a pyrethroid can affect its temperature-toxicity relationship.

Effect of temperature on pyrethroid action to kdr-type house fly adults

The actions of DDT and some pyrethroids on the kdr-type 228e2b and susceptible SRS strains of Musca domestica L. were examined at five temperatures from 15 to 35°C. The two classes of insecticides showed a negative temperature coefficient of toxicity for both strains, although high resistance was detected over the temperature range examined. Penetration of (1RS)-trans-[ 14C]-permethrin was positively correlated to temperature. Both permethrin and cypermethrin showed negative temperature coefficients on the exposed thoracic ganglia from the two strains. There was a slight difference in qualitative nerve response patterns of femur motor nerve preparations of the two strains to DDT and two types of pyrethroids applied to the exposed thoracic ganglia: The pattern of DDT is similar to that of pyrethroids with type I action rather than type II action. It is concluded that increased nerve sensitivity may be the reason for a negative temperature coefficient of pyrethroid toxicity to the two strains of house flies.

The absorption of cypermethrin in the grasshopper Melanoplus sanguinipes (Fab.): Effects of volatilisation, temperature, age, sex and parasitisation by Malameba locustae (King and Taylor)

AbstractThe residues from metered doses of cypermethrin were recovered from excised portions of grasshopper cuticle to determine losses by volatilisation. Residues from similar doses were also recovered from the cuticles of intact grasshoppers and from whole body homogenates after rinsing the cuticle, to determine rates of absorption and losses from metabolism. Residues were recovered from males and females one week and three weeks after fledging in grasshoppers infected with Malameba locustae and in uninfected ones. They were maintained at 15 or 30°C and sampled from each combination of factors at 4, 8, 16, 24, 30 and 48 h after treatment. There was no measurable loss of cypermethrin by volatilisation up to 72 h after application to excised portions of cuticle at either 15 or 30°C. In all combinations of factors, more cypermethrin was recovered externally (P <0.05) from grasshoppers held at 15°C than those held at 30°C and more from infected grasshoppers than from those that were uninfected. Significantly more cypermethrin was also recovered externally from males than from females (P <0.05) and more from infected one‐week‐old grasshoppers than those that were three weeks old. At 15°C there was a gradual trend towards accumulation of cypermethrin internally, but at 30°C an initial trend towards accumulation was followed by one of decline. Residual cypermethrin recovered could in general be related to the negative temperature coefficient of toxicity, to a decreased sensitivity to cypermethrin in infected grasshoppers and to an increased sensitivity in older grasshoppers.

THE INFLUENCE OF TEMPERATURE ON THE EFFICACY OF THREE PYRETHROID INSECTICIDES AGAINST THE GRASSHOPPER, MELANOPLUS SANGUINIPES (FAB.) (ORTHOPTERA: ACRIDIDAE), UNDER LABORATORY CONDITIONS

AbstractThree pyrethroids, deltamethrin, fenvalerate, and cyfluthrin, were assayed against 2nd-instar nymphs of the grasshopper Melanoplus sanguinipes (Fab.) at 5 dosages and at 5 post-treatment temperatures ranging from 15.6 to 37.8°C. All three showed a negative temperature coefficient of toxicity but there was considerable variation in the pattern of response. Deltamethrin proved to be the most effective and cyfluthrin the least effective, both in terms of the amount of active ingredient required for 90% mortality and in having the lowest negative coefficient, respectively. The extent of the negative temperature coefficient of toxicity was much more pronounced at the LD90 than the LD50. Apparent mortality was recorded at 24, 48, and 72 h post-treatment and with each of the pyrethroids, recovery of some hoppers took place after 24 h. This phenomenon of delayed recovery was greatest at the lower temperatures.

Correlations between in vitro and in vivo mechanisms of pyrethroid insecticide action

Classical neuropharmacological procedures have been used to elucidate insecticide mode of action in vitro. A good deal has thus been learned about pyrethroids but novel techniques have been necessary to explain the toxicology and symptomology. The free-walking, electrode-implanted cockroach technique, which was developed for this purpose, is described. It enabled correlations to be made between symptomology and effects on specific nerves. The negative temperature coefficient of toxicity of allethrin (the first pyrethroid) was explained in terms of repetitive firing in peripheral (sensory) nerves rather than by nerve blockage, which had been suggested from previous in vitro studies. The elucidation of target sites in vivo and the most useful parameter to study, i.e., repetitive firing in nerve axons, enabled the definition of a pyrethroid resistance mechanism in a major insect pest. It also showed two modes of action for permethrin and cypermethrin, its α-cyano analog. A structure-activity relationship for a range of pyrethroids, combining in vitro and in vivo approaches, confirmed two distinct types of pyrethroid action. Studies of poisoning signs and nerve disruptions in vivo in the mouse and cockroach, using diazepam in conjunction with pyrethroids, implicated the GABA-receptor complex as a target for α-CN-phenoxybenzyl pyrethroids. This was confirmed by making conductance measurements in crayfish claw opener muscle fibers in vitro.

Correlations between in Vitro and in Vivo Mechanisms of Pyrethroid Insecticide Action

Correlations between in Vitro and in Vivo Mechanisms of Pyrethroid Insecticide Action. GAMMON, D. W. (1985). Fundam. Appl. Toxicol. 5, 9–23. Classical neuropharmacological procedures have been used to elucidate insecticide mode of action in vitro. A good deal has thus been learned about pyrethroids but novel techniques have been necessary to explain the toxicology and symptomology. The free-walking, electrode-implanted cockroach technique, which was developed for this purpose, is described. It enabled correlations to be made between symptomology and effects on specific nerves. The negative temperature coefficient of toxicity of allethrin (the first pyrethroid) was explained in terms of repetitive firing in peripheral (sensory) nerves rather than by nerve blockage, which had been suggested from previous in Vitro studies. The elucidation of target sites in vivo and the most useful parameter to study, i.e., repetitive firing in nerve axons, enabled the definition of a pyrethroid resistance mechanism in a major insect pest. It also showed two modes of action for permethrin and cypermethrin, its α-cyano analog. A structure-activity relationship for a range of pyrethroids, combining in Vitro and in Vivo approaches, confirmed two distinct types of pyrethroid action. Studies of poisoning signs and nerve disruptions in Vivo in the mouse and cockroach, using diazepam in conjunction with pyrethroids, implicated the GABA-receptor complex as a target for α-CN-phenoxybenzyl pyrethroids. This was confirmed by making conductance measurements in crayfish claw opener muscle fibers in Vitro.

Similar mode of action of pyrethroids and DDT on sodium channel gating in myelinated nerves.

Synthetic pyrethroids are a new class of highly active insecticides with great potential for practical application1. They are generally recognized as neurotoxicants that act directly on excitable membranes2,3. Previous studies have shown that the effect of the pyrethroid allethrin closely resembles that of the classical insecticide dichlorodiphenyl trichloroethane (DDT) in the peripheral nervous system of Xenopus laevis4,5. Both compounds induce intense repetitive activity in sense organs and in myelinated nerve fibres. In the lateral-line sense organ this repetitive activity increases with cooling, a phenomenon that may be related to the negative temperature coefficient of toxicity of DDT6 and pyrethroids7 in insects. In frog node of Ranvier, DDT slows the closing of sodium channels that open during depolarization8,9 so that a prolonged sodium tail current persists after the membrane has been repolarized. We have recently found that the pyrethroid allethrin10 causes a similar sodium tail current in the nodal membrane of Xenopus. Pyrethroids11,12 and DDT13,14 are also known to cause prolongation of the sodium current together with repetitive activity in nerve fibres of invertebrates. The prolonged sodium current is thought to be directly responsible for this repetitive activity3,15, and it has been suggested that the sodium channel in the nerve membrane is the major target site of pyrethroids and DDT-like compounds10,12. We have now investigated the mechanism by which pyrethroids and DDT prolong the sodium current in Xenopus nodal membrane. Our results show that these compounds—despite marked differences in chemical structure—modify sodium channel gating in a strikingly similar way and reduce selectively the rate of closing of the activation gate.

LABORATORY STUDIES ON THE PERSISTENCE AND BEHAVIOUR IN SOIL OF FOUR PYRETHROID INSECTICIDES

AbstractIn direct contact toxicity tests with four pyrethroid and three standard insecticides, using 24–48 h old crickets, Acheta pennsylvanicus (Burmeister), as test insects, carbofuran was most toxic > cypermethrin > fensulfothion > chlorpyrifos > fenvalerate > fenpropanate > permethrin. In moist (5% water) Plainfield sand, using the same test insect, chlorpyrifos was most toxic > carbofuran > fenpropanate > cypermethrin > permethrin > fenvalerate > fensulfothion, i.e. the pyrethroids, although quite strongly adsorbed by soil, were still moderately active as soil insecticides. All pyrethroids were less toxic in muck soil as compared with Plainfield sand, and in air-dry (0.5% water) as compared with moist (5% water) Plainfield sand, with the effects being less on cypermethrin and fenvalerate and greater on permethrin and fenpropanate. None of the pyrethroids was affected by soil type and moisture to the same extent as was carbofuran. Permethrin, fenvalerate, and cypermethrin showed a negative temperature coefficient of toxicity in moist Plainfield sand, being from 1.4 to 1.9× more toxic at 15° than at 32°C. Fenpropanate, like carbofuran, was slightly more toxic at 32° than at 15°C. Generally, soil type, moisture, and temperature had minimal effects on the toxicity of the four pyrethroid insecticides. In persistence studies over 48 weeks, using Plainfield sand, the pyrethroids were more persistent than chlorpyrifos, but less persistent than dieldrin. Under these laboratory conditions, permethrin and fenvalerate were slightly more persistent, while fenpropanate and cypermethrin were as persistent as carbofuran. Trans-isomers of permethrin and cypermethrin declined more quickly in the sand than did the cis-isomers and of the trans-isomers the 1S,trans declined much faster than the 1R,trans while little difference was observed for the corresponding 1S- and 1R,cis-isomers.

Effects of DDT on the cockroach nervous system at three temperatures

AbstractSome effects of DDT on the cockroach nervous system have been correlated with poisoning symptoms, using free‐walking cockroaches with implanted electrodes. Experiments at 16.5°C and 32°C used LD95 doses and at 25°C, an estimated LD95. DDT had excitant actions on each nerve studied; cercal afferent and efferent neurones, and abdominal interneurones. The effects on the central nervous system became more marked as temperature was reduced, despite the smaller quantity of DDT employed, but the excitant actions on the peripheral nervous system were not quantified. It is suggested that the effects of DDT on the cockroach nervous system could account for the negative temperature coefficient of toxicity of DDT.

LABORATORY STUDIES ON THE CONTACT TOXICITY AND ACTIVITY IN SOIL OF FOUR PYRETHROID INSECTICIDES

AbstractThe spectrum of contact toxicity and activity in soil of four pyrethroid insecticides was assessed in the laboratory. Pyrethroids tested were: FMC 33297 (3-phenoxybenzyl (±)-3-(2, 2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylate); Shell WL 41706 (alpha-cyano-3 phenoxybenzyl 2,2,3,3-tetramethylcyclopropanecarboxylate); Shell WL 43467 (alpha-cyano-3-phenoxybenzyl 2-(2,2-dichlorovinyl)-3,3-dimethylcyclopropane-1-carboxylate); and Shell WL 43775 (alpha-cyano-3-phenoxybenzyl-2-(4-chlorophenyl)-3-methyl-1-butyrate). Chlorpyrifos and carbofuran, two broad spectrum contact and soil insecticides were included for comparative purposes. Spectrum of contact toxicity was determined using 24–48 h nymphs of the common field cricket, Acheta pennsylvanicus (Burmeister), 24–48 h onion maggot adults, Hylemya antiqua (Meigen), 3rd instar dark sided cutworms, Euxoa messoria (Harris), northern corn rootworm adults, Diabrotica longicornis (Say), and honeybees, Apis mellifera L. Crickets were used to assess insecticidal activity in soil relative to soil moisture, type, and temperature. The pyrethroids were effective contact insecticides comparable in toxicity and spectrum of activity to chlorpyrifos and carbofuran. They were particularly toxic to the darksided cutworm. They were less effective in mineral soil than chlorpyrifos. WL 43467 showed activity in mineral soil close to that of carbofuran, while the other pyrethroids were less active. Activity in soil was influenced by soil moisture and type. In contrast to the standard insecticides the pyrethroids generally showed a negative temperature coefficient of toxicity in soil.

Influence of Posttreatment Temperature on the Toxicity of Pyrethroid Insecticides12

Posttreatment temperature effects on the toxicity of pyrethroid insecticides applied by direct contact and in soil were assessed. Pyrethrins, resmethrin. FMC 33297 (3-phenoxybenzyl (±)-3-(2,2-dichlorovinyl)-2,2-dimethyl-cyclopropanecarboxylate), Shell WL 41706 (alpha-Cyano-3-phenoxybenzyl 2,2,3,3-tetramethylcyclopropanecarboxylate), and Shell WL 43775 (alpha-Cyano-3-phenoxybenzyl 2-(4-chlorophenyl)-3-methyl-l-butyrate) applied by direct contact were from 2.7 to 3.6 times more toxic to 1st instars of a cricket, Gryllus pennsylvanicus (Burmeister), at 15° as at 32°C. FMC 33297 was 2.6, 3.6, and 7.4 times more toxic at 15° as at 32°C to a flea beetle adult, Phyllotreta cruciferae (Goeze), onion maggot adult, Hylemya antiqua (Meigen), and variegated cutworm, Peridroma saucia (Hübner), respectively. At 15°, 22°, 27°, and 32°C, endosulfan showed a positive, carbaryl a bimodal, and FMC 33297 and DDT a negative temperature coefficient of toxicity. When incorporated into mineral and organic soil FMC 33297 was slightly more toxic to crickets at 15° as compared to 32°C.

Note on the Effects of Temperature and Piperonyl Butoxide on the Toxicity of Carbaryl to Adult Grasshoppers

AbstractTests on adults of the migratory grasshopper, Melanoplus bilituratus (Wlk.), showed carbaryl (1-naphthyl N-methylcarbamate) to have a very marked negative temperature coefficient of toxicity. This was believed to be due to a rapid increase in the rate of detoxification at higher temperatures. The marked synergistic effect of piperonyl butoxide, believed to act by blocking the detoxification process, appeared to confirm this.

Temperature and the action of DDT on the nervous system of Periplaneta americana (L.)

Although the overall effect of DDT on insects is expressed by a negative temperature coefficient of toxicity, the action of DDT on afferent nerves of cockroaches ( Periplaneta americana) has a positive temperature coefficient. In the crural nerve abnormal afferent impulse trains are induced more rapidly and in greater number at high than at low temperature. Decreasing the temperature decreases the numbers of afferent trains slightly, but does not eliminate them. In the central nervous system, impulse trains increase as the temperature decreases, and raising the temperature eliminates them. Impulse trains in the central nervous system can be eliminated by a combination of perfusion and removal of afferent input, but they cannot be eliminated in afferent nerves by saline perfusion. It is concluded that events occurring within the central nervous system are responsible for the overall negative temperature coefficient of DDT-toxicity.

Temperature Coefficient of Toxicity of CertainN-Methylcarbamates Against Honeybees, and the Effect of the Synergist Piperonyl Butoxide

SUMMARYThe toxicity of the carbamate insecticides Sevin(R), Zectran(R) and B 37344 (4-methylthio-3,5-xylyl N-methylcarbamate) to worker honeybees (Apis mellifera) was investigated at 60°, 80° and 90° F. [16,27, 32° C.]. All compounds exhibited a negative temperature coefficient of toxicity. This was most pronounced in Sevin which was 3.81 times as toxic at 60° as at 80° F. Application of the synergist piperonyl butoxide enhanced the toxicity of the carbamates to levels roughly corresponding to their intrinsic toxicity and decreased the influence of the post-treatment temperature on toxicity. The results suggest that a carbamate-detoxification mechanism, sensitive to temperature and the action of piperonyl butoxide, is present in honeybees. The significance of this mechanism deserves further consideration as it might suggest optimum times for the application of the insecticides which would prevent high losses of honeybees.