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Bioallethrin

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Per Eriksson – 1st expert on this subject based on the ideXlab platform

  • comparison of single and repeated exposure to low doses of pyrethroids permethrin and Bioallethrin during neonatal brain development on adult spontaneous behaviour
    51st Annual Meeting of Society of Toxicology San Francisco March 11-15 2012, 2012
    Co-Authors: Sonja Buratovic, Anders Fredriksson, Kevin Crofton, Henrik Viberg, Per Eriksson

    Abstract:

    Permethrin and Bioallethrin belong to the Type 1 class of pyrethroid pesticides. The primary mechanism of action is interference with nerve membrane sodium channels that results in increased neuronal activity. We have earlier reported on developmental neurotoxic effects after repeated, PND 10 to PND16, neonatal exposure to pyrethroids. The effects were manifested as altered spontaneous behavior, hyperactivity and reduced cognitive function and changes in cholinergic muscarinic/nicotinic receptors in the cerebral cortex of neonatal and adult mice. The present study was undertaken to compare repeated and single exposure to permethrin and Bioallethrin during the neonatal brain growth spurt (BGS) on adult spontaneous behavior in a novel home environment. Neonatal NMRI male mice were given permethrin, orally (0.55; 3.3; 6.6 mg/kg bw/day) on PND 10-14, or just a single oral dose of 6.6 mg/kg bw on PND 10. Bioallethrin was given as a single oral dose of 0.7 mg/kg bw on PND 10, and compared to earlier published data on repeated exposure. Mice serving as controls received the 20 % fat emulsion vehicle. Spontaneous behavior test (locomotion, rearing, total activity) in 2-month-old mice revealed a significant higher activity in mice exposed to repeated doses of 6.6 mg permethrin, as well in mice just receiving a single 6.6 mg dose of permethrin. No significant difference was observed between repeated and single exposure. A single dose of 0.7 mg Bioallethrin on PND 10 caused the same effects as a repeated dose of 0.7 mg between PND 10 to PND 16. This demonstrates that a single dose of these pyrethroids can cause the same developmental neurotoxic effects as that seen following repeated doses over one week during the neonatal BGS period in mouse. This research provides is consistent with previous findings that exposure during the BGS can result in persistent behavioral defects.

  • DDT and pyrethroids-ecotoxicological considerations
    Comparative Biochemistry and Physiology Part C: Comparative Pharmacology, 2004
    Co-Authors: Per Eriksson

    Abstract:

    Abstract 1. 1. DDT, and a DDT metabolite, DDOH, conjugated to palmitic acid, DDOH-PA, as well as Bioallethrin and deltamethrin have all been shown to affect muscarinic cholinergic receptors (MAChR) in the neonatal mouse brain after administration to 10-day-old mice during the period of rapid brain growth. 2. 2. This early exposure has also been shown to lead to permanent changes in cholinergic and behavioural variables in the animals as adults.

  • neonatal exposure to a single low dose of a type 1 pyrethroid Bioallethrin affects spontaneous behaviour and learning in adult mice of different strains
    , 2004
    Co-Authors: Celia Fischer, Anders Fredriksson, Per Eriksson

    Abstract:

    Neonatal exposure to a single low dose of a type 1 pyrethroid (Bioallethrin) affects spontaneous behaviour and learning in adult mice of different strains

David M Soderlund – 2nd expert on this subject based on the ideXlab platform

  • differential state dependent modification of inactivation deficient nav1 6 sodium channels by the pyrethroid insecticides s Bioallethrin tefluthrin and deltamethrin
    Neurotoxicology, 2012
    Co-Authors: Samantha J Mccavera, David M Soderlund

    Abstract:

    Pyrethroid insecticides disrupt nerve function by modifying the gating kinetics of transitions between the conducting and nonconducting states of voltage-gated sodium channels. Pyrethroids modify rat Nav1.6 + β1 + β2 channels expressed in Xenopus oocytes in both the resting state and in one or more states that require channel activation by repeated depolarization. The state dependence of modification depends on the pyrethroid examined: deltamethrin modification requires repeated channel activation, tefluthrin modification is significantly enhanced by repeated channel activation, and S-Bioallethrin modification is unaffected by repeated activation. Use-dependent modification by deltamethrin and tefluthrin implies that these compounds bind preferentially to open channels. We constructed the rat Nav1.6Q3 cDNA, which contained the IFM/QQQ mutation in the inactivation gate domain that prevents fast inactivation and results in a persistently open channel. We expressed Nav1.6Q3 + β1 + β2 sodium channels in Xenopus oocytes and assessed the modification of open channels by pyrethroids by determining the effect of depolarizing pulse length on the normalized conductance of the pyrethroid-induced sodium tail current. Deltamethrin caused little modification of Nav1.6Q3 following short (10 ms) depolarizations, but prolonged depolarizations (up to 150 ms) caused a progressive increase in channel modification measured as an increase in the conductance of the pyrethroid-induced sodium tail current. Modification by tefluthrin was clearly detectable following short depolarizations and was increased by long depolarizations. By contrast modification by S-Bioallethrin following short depolarizations was not altered by prolonged depolarization. These studies provide direct evidence for the preferential binding of deltamethrin and tefluthrin (but not S-Bioallethrin) to Nav1.6Q3 channels in the open state and imply that the pyrethroid receptor of resting and open channels occupies different conformations that exhibit distinct structure–activity relationships.

  • divergent actions of the pyrethroid insecticides s Bioallethrin tefluthrin and deltamethrin on rat nav1 6 sodium channels
    Toxicology and Applied Pharmacology, 2010
    Co-Authors: David M Soderlund

    Abstract:

    Abstract We expressed rat Na v 1.6 sodium channels in combination with the rat β 1 and β 2 auxiliary subunits in Xenopus laevis oocytes and evaluated the effects of the pyrethroid insecticides S –Bioallethrin, deltamethrin, and tefluthrin on expressed sodium currents using the two-electrode voltage clamp technique. S –Bioallethrin, a type I structure, produced transient modification evident in the induction of rapidly decaying sodium tail currents, weak resting modification (5.7% modification at 100 μM), and no further enhancement of modification upon repetitive activation by high-frequency trains of depolarizing pulses. By contrast deltamethrin, a type II structure, produced sodium tail currents that were ~ 9-fold more persistent than those caused by S –Bioallethrin, barely detectable resting modification (2.5% modification at 100 μM), and 3.7-fold enhancement of modification upon repetitive activation. Tefluthrin, a type I structure with high mammalian toxicity, exhibited properties intermediate between S –Bioallethrin and deltamethrin: intermediate tail current decay kinetics, much greater resting modification (14.1% at 100 μM), and 2.8-fold enhancement of resting modification upon repetitive activation. Comparison of concentration–effect data showed that repetitive depolarization increased the potency of tefluthrin ~ 15-fold and that tefluthrin was ~ 10-fold more potent than deltamethrin as a use-dependent modifier of Na v 1.6 sodium channels. Concentration–effect data from parallel experiments with the rat Na v 1.2 sodium channel coexpressed with the rat β 1 and β 2 subunits in oocytes showed that the Na v 1.6 isoform was at least 15-fold more sensitive to tefluthrin and deltamethrin than the Na v 1.2 isoform. These results implicate sodium channels containing the Na v 1.6 isoform as potential targets for the central neurotoxic effects of pyrethroids.

  • evidence for a separate mechanism of toxicity for the type i and the type ii pyrethroid insecticides
    Neurotoxicology, 2009
    Co-Authors: Charles B Breckenridge, David M Soderlund, Larry R Holden, Nicholas C Sturgess, Myra L Weiner, Larry P Sheets, Dana Sargent, Jinsung Choi, Steve Symington, Marshall J Clark

    Abstract:

    Abstract Neurotoxicity and mechanistic data were collected for six α-cyano pyrethroids (β-cyfluthrin, cypermethrin, deltamethrin, esfenvalerate, fenpropathrin and λ-cyhalothrin) and up to six non-cyano containing pyrethroids (bifenthrin, S-Bioallethrin [or allethrin], permethrin, pyrethrins, resmethrin [or its cis-isomer, cismethrin] and tefluthrin under standard conditions. Factor analysis and multivariate dissimilarity analysis were employed to evaluate four independent data sets comprised of (1) fifty-six behavioral and physiological parameters from an acute neurotoxicity functional observatory battery (FOB), (2) eight electrophysiological parameters from voltage clamp experiments conducted on the Na v 1.8 sodium channel expressed in Xenopus oocytes, (3) indices of efficacy, potency and binding calculated for calcium ion influx across neuronal membranes, membrane depolarization and glutamate released from rat brain synaptosomes and (4) changes in chloride channel open state probability using a patch voltage clamp technique for membranes isolated from mouse neuroblastoma cells. The pyrethroids segregated into Type I (T-syndrome—tremors) and Type II (CS syndrome—choreoathetosis with salivation) groups based on FOB data. Of the α-cyano pyrethroids, deltamethrin, λ-cyhalothrin, cyfluthrin and cypermethrin arrayed themselves strongly in a dose-dependent manner along two factors that characterize the CS syndrome. Esfenvalerate and fenpropathrin displayed weaker response profiles compared to the non-cyano pyrethroids. Visual clustering on multidimensional scaling (MDS) maps based upon sodium ion channel and calcium influx and glutamate release dissimilarities gave similar groupings. The non-cyano containing pyrethroids were arrayed in a dose-dependent manner along two different factors that characterize the T-syndrome. Bifenthrin was an outlier when MDS maps of the non-cyano pyrethroids were based on sodium ion channel characteristics and permethrin was an outlier when the MDS maps were based on calcium influx/glutamate release potency. Four of six α-cyano pyrethroids (λ-cyfluthrin, cypermethrin, deltamethrin and fenpropathrin) reduced open chloride channel probability. The R-isomers of λ-l-cyhalothrin reduced open channel probability whereas the S-isomers, antagonized the action of the R-isomers. None of the non-cyano pyrethroids reduced open channel probability, except Bioallethrin, which gave a weak response. Overall, based upon neurotoxicity data and the effect of pyrethroids on sodium, calcium and chloride ion channels, it is proposed that Bioallethrin, cismethrin, tefluthrin, bifenthrin and permethrin belong to one common mechanism group and deltamethrin, λ-cyhalothrin, cyfluthrin and cypermethrin belong to a second. Fenpropathrin and esfenvalerate occupy an intermediate position between these two groups.

Anders Fredriksson – 3rd expert on this subject based on the ideXlab platform

  • comparison of single and repeated exposure to low doses of pyrethroids permethrin and Bioallethrin during neonatal brain development on adult spontaneous behaviour
    51st Annual Meeting of Society of Toxicology San Francisco March 11-15 2012, 2012
    Co-Authors: Sonja Buratovic, Anders Fredriksson, Kevin Crofton, Henrik Viberg, Per Eriksson

    Abstract:

    Permethrin and Bioallethrin belong to the Type 1 class of pyrethroid pesticides. The primary mechanism of action is interference with nerve membrane sodium channels that results in increased neuronal activity. We have earlier reported on developmental neurotoxic effects after repeated, PND 10 to PND16, neonatal exposure to pyrethroids. The effects were manifested as altered spontaneous behavior, hyperactivity and reduced cognitive function and changes in cholinergic muscarinic/nicotinic receptors in the cerebral cortex of neonatal and adult mice. The present study was undertaken to compare repeated and single exposure to permethrin and Bioallethrin during the neonatal brain growth spurt (BGS) on adult spontaneous behavior in a novel home environment. Neonatal NMRI male mice were given permethrin, orally (0.55; 3.3; 6.6 mg/kg bw/day) on PND 10-14, or just a single oral dose of 6.6 mg/kg bw on PND 10. Bioallethrin was given as a single oral dose of 0.7 mg/kg bw on PND 10, and compared to earlier published data on repeated exposure. Mice serving as controls received the 20 % fat emulsion vehicle. Spontaneous behavior test (locomotion, rearing, total activity) in 2-month-old mice revealed a significant higher activity in mice exposed to repeated doses of 6.6 mg permethrin, as well in mice just receiving a single 6.6 mg dose of permethrin. No significant difference was observed between repeated and single exposure. A single dose of 0.7 mg Bioallethrin on PND 10 caused the same effects as a repeated dose of 0.7 mg between PND 10 to PND 16. This demonstrates that a single dose of these pyrethroids can cause the same developmental neurotoxic effects as that seen following repeated doses over one week during the neonatal BGS period in mouse. This research provides is consistent with previous findings that exposure during the BGS can result in persistent behavioral defects.

  • neonatal exposure to a single low dose of a type 1 pyrethroid Bioallethrin affects spontaneous behaviour and learning in adult mice of different strains
    , 2004
    Co-Authors: Celia Fischer, Anders Fredriksson, Per Eriksson

    Abstract:

    Neonatal exposure to a single low dose of a type 1 pyrethroid (Bioallethrin) affects spontaneous behaviour and learning in adult mice of different strains

  • changes in behavior and muscarinic receptor density after neonatal and adult exposure to Bioallethrin
    Neurobiology of Aging, 1998
    Co-Authors: Ulrika Talts, Anders Fredriksson, Per Eriksson

    Abstract:

    Abstract Throughout life, mammals are exposed to environmental toxicants, some of which have acute effects on the nervous system. Early, low-dose exposure in combination with later re-exposure and possible interference with normal aging have been little studied. The present study revealed increased susceptibility in adult mice, exposed neonatally to a low dose of the insecticide Bioallethrin, to renewed exposure to Bioallethrin as adults. Ten-day-old Naval Medical Research Institute male mice received Bioallethrin orally (0.7 mg per kg body weight per day for 7 days). When aged 5 months they were given the same dose of Bioallethrin by gavage. Twenty-four hours after the last administration, a spontaneous motor activity test revealed significant aberrations in mice exposed both neonatally and as adults to Bioallethrin. The density of muscarinic receptors was significantly increased. When aged 7 months, spontaneous behavioral disturbances and muscarinic receptor changes persisted and learning and memory deficits had developed. These results indicate that neonatal exposure to Bioallethrin has the potential to increase susceptibility of the adult mouse to a new exposure at a dosage that does not have any effect in animals treated neonatally with vehicle.