Influence of dosing volume on the neurotoxicity of bifenthrin

Wolansky, Marcelo Javier; McDaniel, Katherine L.; Moser, Virginia C.; Crofton, Kevin M.

doi:10.1016/j.ntt.2007.01.007

Cited by 41 publications

(37 citation statements)

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“…1) is one of the most potent commercialized pyrethroids to date, with LD 50 values of about 53 mg/kg in female rats and 70 mg/kg in male rats after oral gavage (Wolansky et al, 2006;Wolansky and Harrill, 2008). Bifenthrin, as low as 10 mg/kg, produces type I pyrethroid-like episodes of head and whole-body shakes, a strong and prolonged tremorigenic response, hyperthermia, vocalizations, prostration, and, at doses .28 mg/kg, it eventually triggers convulsions and death (Holton et al, 1997;Wolansky et al, 2007). This dose range corresponds to a brain concentration of bifenthrin of about 550-650 ng/g of brain tissue .…”

Section: Introductionmentioning

confidence: 99%

Nanomolar Bifenthrin Alters Synchronous Ca²⁺Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity

et al. 2014

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Bifenthrin, a relatively stable type I pyrethroid that causes tremors and impairs motor activity in rodents, is broadly used. We investigated whether nanomolar bifenthrin alters synchronous Ca 21 oscillations (SCOs) necessary for activity-dependent dendritic development. Primary mouse cortical neurons were cultured 8 or 9 days in vitro (DIV), loaded with the Ca 21 indicator Fluo-4, and imaged using a Fluorescence Imaging Plate Reader Tetra. Acute exposure to bifenthrin rapidly increased the frequency of SCOs by 2.7-fold (EC 50 5 58 nM) and decreased SCO amplitude by 36%. Changes in SCO properties were independent of modifications in voltage-gated sodium channels since 100 nM bifenthrin had no effect on the whole-cell Na 1 current, nor did it influence neuronal resting membrane potential. The L-type Ca 21 channel blocker nifedipine failed to ameliorate bifenthrin-triggered SCO activity. By contrast, the metabotropic glutamate receptor (mGluR)5 antagonist MPEP [2-methyl-6-(phenylethynyl)pyridine] normalized bifenthrin-triggered increase in SCO frequency without altering baseline SCO activity, indicating that bifenthrin amplifies mGluR5 signaling independent of Na 1 channel modification. Competitive [AP-5; (2)-2-amino-5-phosphonopentanoic acid] and noncompetitive (dizocilpine,10R)- (1)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate]) N-methyl-D-aspartate antagonists partially decreased both basal and bifenthrin-triggered SCO frequency increase. Bifenthrin-modified SCO rapidly enhanced the phosphorylation of cAMP response element-binding protein (CREB). Subacute (48 hours) exposure to bifenthrin commencing 2 DIV-enhanced neurite outgrowth and persistently increased SCO frequency and reduced SCO amplitude. Bifenthrin-stimulated neurite outgrowth and CREB phosphorylation were dependent on mGluR5 activity since MPEP normalized both responses. Collectively these data identify a new mechanism by which bifenthrin potently alters Ca 21 dynamics and Ca 21-dependent signaling in cortical neurons that have long term impacts on activity driven neuronal plasticity.

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Section: Introductionmentioning

confidence: 99%

Nanomolar Bifenthrin Alters Synchronous Ca²⁺Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity

et al. 2014

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“…Kim et al (2008) also detected deltamethrin (10 mg/kg dose) in brain out to 48 h. The levels of bifenthrin in brain began to decrease 24-h postadministration. Peak motor activity effects of bifenthrin in the rat occur at 4-h postadministration when the dosing volume is 1 mL/kg (Wolansky et al, 2006(Wolansky et al, , 2007. This is the same volume used in this study.…”

Section: Discussionmentioning

confidence: 99%

“…For both experiments, rats were administered bifenthrin at a dose of 0.3 or 3 mg/kg in corn oil (1 mL/kg) by oral (po) gavage. Our group has used corn oil as a vehicle for the oral administration of pyrethroids in several studies (Godin et al, 2010;Tornero-Velez et al, 2012;Wolansky et al, 2006Wolansky et al, , 2007. The high dose of bifenthrin is equivalent to an oral dose that decreases motor activity in a rat by 30% (Wolansky et al, 2006).…”

Section: Methodsmentioning

confidence: 99%

“…corn oil, glycerol formal) (Crofton et al, 1995;Kim et al, 2007) and vehicle volume (e.g. 1 vs. 5 mL) (Wolansky et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

“…Our laboratory and collaborators used this rat strain in several neurotoxicology and disposition studies (Crofton et al, 1995;Godin et al, 2010;Scollon et al, 2011;Tornero-Velez et al, 2012;Wolansky et al, 2006Wolansky et al, , 2007. We administered bifenthrin by oral gavage at two dose levels and studied the tissue disposition of parent compound out to 21 days.…”

Section: Introductionmentioning

confidence: 99%

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Tissue time course and bioavailability of the pyrethroid insecticide bifenthrin in the Long-Evans rat

et al. 2015

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1. Pyrethroids are neurotoxic and parent pyrethroid appears to be toxic entity. This study evaluated the oral disposition and bioavailability of bifenthrin in the adult male Long-Evans rat. 2. In the disposition study, rats were administered bifenthrin (0.3 or 3 mg/kg) by oral gavage and serially sacrificed (0.25 h to 21 days). Blood, liver, brain and adipose tissue were removed. In the bioavailability study, blood was collected serially from jugular vein cannulated rats (0.25 to 24 h) following oral (0.3 or 3 mg/kg) or intravenous (0.3 mg/kg) administration of bifenthrin. Tissues were extracted and analyzed for bifenthrin by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). 3. Bifenthrin concentration in blood and liver peaked 1-2-h postoral administration and were approximately 90 ng/ml (or g) and 1000 ng/ml (or g) for both tissues at 0.3 and 3 mg/kg, respectively. Bifenthrin was rapidly cleared from both blood and liver. Brain concentrations peaked at 4-6 h and were lower than in blood at both doses (12 and 143 ng/g). Bifenthrin in adipose tissue peaked at the collected time points of 8 (157 ng/g) and 24 (1145 ng/g) h for the 0.3 and 3 mg/kg doses, respectively and was retained 21 days postoral administration. Following intravenous administration, the blood bifenthrin concentration decreased bi-exponentially, with a distribution half-life of 0.2 h and an elimination half-life of 8 h. Bifenthrin bioavailability was approximately 30%. These disposition and kinetic bifenthrin data may decrease uncertainties in the risk assessment for this pyrethroid insecticide.

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Insecticides

Tosti,

Metruccio,

Moretto

2023

Patty's Toxicology

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Insecticides include a variety of compounds that act against different target species targeting different receptors, enzymes or functions. Hence, there are many chemical groups that also present different species specificity and toxicity for humans. They are used in agriculture, in public health to fight against vectors of disease or nuisance insects, and in veterinary medicine. Some, for example, avermectins, are also used in human medicine. In general, they act on different molecular targets within the nervous system with variable species specificity. For instance, carbamates inhibit acetylcholinesterase (AChE) without significant differences in potency between insects and mammals, while there is a significantly higher sensitivity to neonicotinoids of insects' nicotinic receptors as compared to mammalian ones. Also, significant differences in metabolism are responsible of the low toxicity of pyrethroids to mammalians as compared to insects. Application of insecticides is usually upwards; hence, human exposure during their application may be higher than that following the application of herbicides. Factors that impact on the level of exposure include the amount of active ingredient per hectare, water volume (dilution), the protective equipment used. Dermal exposure is considered to be the most relevant, inhalation accounting for about 10% of total exposure. The Insecticide Resistance Action Committee (IRAC) lists mode of actions and related compounds ( www.irac‐online.org ). It will not be possible to deal with all compounds in this chapter. Therefore, groups with significant current uses will be dealt with. In addition, organophosphates are considered in a separate chapter.

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Influence of dosing volume on the neurotoxicity of bifenthrin

Cited by 41 publications

References 41 publications

Nanomolar Bifenthrin Alters Synchronous Ca²⁺Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity

Nanomolar Bifenthrin Alters Synchronous Ca²⁺Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity

Tissue time course and bioavailability of the pyrethroid insecticide bifenthrin in the Long-Evans rat

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Influence of dosing volume on the neurotoxicity of bifenthrin

Cited by 41 publications

References 41 publications

Nanomolar Bifenthrin Alters Synchronous Ca2+Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity

Nanomolar Bifenthrin Alters Synchronous Ca2+Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity

Tissue time course and bioavailability of the pyrethroid insecticide bifenthrin in the Long-Evans rat

Insecticides

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Product

Resources

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Nanomolar Bifenthrin Alters Synchronous Ca²⁺Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity

Nanomolar Bifenthrin Alters Synchronous Ca²⁺Oscillations and Cortical Neuron Development Independent of Sodium Channel Activity