ArticleNeurotoxicology and teratology
The organophosphate insecticide diazinon and aging: Neurobehavioral and mitochondrial effects in zebrafish exposed as embryos or during aging.
Article in Neurotoxicology and teratology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- Environmental Mixture Toxicity of Guanitoxin and Organophosphates in Zebrafish: from Developmental and Neurobehavioral Phenotypes to Transcriptomic Responses.Environmental science & technology · 2026Article
- Impact of pesticide diazinon on gastric cancer cell lines and the alteration of cholinergic and serotonergic pathway genes affecting cell proliferation.Scientific reports · 2025Article
- Zebrafish as an Integrative Model for Central Nervous System Research: Current Advances and Translational Perspectives.Life (Basel, Switzerland) · 2025Review
- Article
- Developmental exposure of zebrafish to neonicotinoid pesticides: Long-term effects on neurobehavioral function.Neurotoxicology · 2023Article
- Organophosphate Insecticide Toxicity in Neural Development, Cognition, Behaviour and Degeneration: Insights from Zebrafish.Journal of developmental biology · 2022Review
- Embryonic exposure to benzo[a]pyrene causes age-dependent behavioral alterations and long-term metabolic dysfunction in zebrafish.Neurotoxicology and teratologyArticle
- Embryonic exposures to cadmium and PAHs cause long-term and interacting neurobehavioral effects in zebrafish.Neurotoxicology and teratologyArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Organophosphate (OP) compounds comprise one of the most widely used classes of insecticides worldwide. OPs have been shown to have negative human health impacts, particularly developmental neurotoxicity. However, neurotoxic impacts in later adulthood and during the aging process are relatively uncharacterized. The present study examined diazinon (DZN), an OP, to determine the neurobehavioral consequences, in addition to mitochondrial dysfunction on a macroscale (whole organism basal respiration) and on a microscale (whole organ mitochondrial respiration), using zebrafish (ZF) as a model. One group of 14-month-old adult ZF were exposed acutely as adults (0.4, 1.25, and 4.0 μM) for five days and tested as adults, and another group was exposed developmentally 5-120 h post-fertilization (70, 210, and 700 nM) and tested at larval, adolescent, adult, and aging life stages. ZF exposed acutely as adults did not display many significant neurobehavioral impacts or mitochondrial dysfunction. Conversely, the embryonically exposed ZF showed altered behavioral functions at each stage of life which emerged and attenuated as fish transitioned from each developmental stage to the next. Mitochondrial oxygen consumptions measurement results for developmentally DZN exposed ZF showed significant increases in the low and middle dose groups in organs such as the brain and testes. Overall, there is an indication that early developmental exposure to DZN had continuing adverse neurobehavioral and cellular consequences throughout their lives well into adulthood and aging periods.
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