ArticleJournal of biochemical and molecular toxicology2015
Role of calcium and calpain in the downregulation of voltage-gated sodium channel expression by the pyrethroid pesticide deltamethrin.
Article in Journal of biochemical and molecular toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Pesticides in Honeybee Products-Determination of Pesticides in Bee Pollen, Propolis, and Royal Jelly from Polish Apiary.Molecules (Basel, Switzerland) · 2025Article
- Protective effects of rutin against deltamethrin-induced hepatotoxicity and nephrotoxicity in rats via regulation of oxidative stress, inflammation, and apoptosis.Environmental science and pollution research international · 2021Article
- Effects of Deltamethrin Acute Exposure on Nav1.6 Channels and Medium Spiny Neurons of the Nucleus Accumbens.Toxicology · 2020Article
- Calcium Homeostasis: A Potential Vicious Cycle of Bone Metastasis in Breast Cancers.Frontiers in oncology · 2020Review
- Developmental pyrethroid exposure causes long-term decreases of neuronal sodium channel expression.Neurotoxicology · 2017Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated sodium channels (Na(v)) are essential for initiation and propagation of action potentials. Previous in vitro studies reported that exposure to the Na(v) toxins veratridine and α scorpion toxin cause persistent downregulation of Na(v) mRNA in vitro. However the mechanism of this downregulation is not well characterized. Here, we report that the type-II pyrethroid deltamethrin, which has a similar mechanism as these toxins, elicited an approximate 25% reduction in Na(v) 1.2 and Na(v) 1.3 mRNA in SK-N-AS cells. Deltamethrin-induced decreases of Na(v) mRNA were blocked with the Na(v) antagonist tetrodotoxin, demonstrating a primary role for interaction with Na(v). Pre-treatment with the intracellular calcium chelator BAPTA-AM and the calpain inhibitor PD-150606 also prevented these decreases, identifying a role for intracellular calcium and calpain activation. Because alterations in Na(v) expression and function can result in neurotoxicity, additional studies are warranted to determine whether or not such effects occur in vivo.
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