Comparative neurochemical and neurobehavioral effects of repeated chlorpyrifos exposures in young and adult rats
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Cited by (105)
Berberine affords protection against oxidative stress and apoptotic damage in F1 generation of wistar rats following lactational exposure to chlorpyrifos
2021, Pesticide Biochemistry and PhysiologyCitation Excerpt :This is in accordance with the experiments of Kondakala et al. (2017) and Ouardi et al. (2019) who reported a dose dependent effect of chlorpyrifos on AChE activity as at higher doses a significant inhibition was observed contrary to the lower doses and acute treatments. Rapid recovery of brain AChE activity following exposure is maybe due to spontaneous reactivation of the phosphorylated enzyme or de novo protein synthesis (Chakraborti et al., 1993). An important element of this study concerning cellular apoptosis focused more specifically on DNA damage-induced apoptosis.
Intrinsic and extrinsic factors that can modify toxicity
2020, An Introduction to Interdisciplinary Toxicology: From Molecules to ManChemical warfare agents and the nervous system
2020, Handbook of Toxicology of Chemical Warfare AgentsPossible Mechanisms of Developmental Neurotoxicity of Organophosphate Insecticides
2018, Advances in NeurotoxicologyOxidative Stress, Unfolded Protein Response, and Apoptosis in Developmental Toxicity
2015, International Review of Cell and Molecular BiologyCitation Excerpt :For instance, neonatal rats are more sensitive to the organophosphate, chlorpyrifos, than adults (Chakraborti et al., 1993). Chlorpyrifos has been shown to cause neurobehavioral defects following early exposure in mammals (Chakraborti et al., 1993; Chanda and Pope, 1996). It has also been linked to aberrant behavior, spinal curvature, pericardial edema, and mortality in zebrafish embryos (Kienle et al., 2009), whereas exposed frogs displayed tail flexure and decreased neuromuscular activity (Bonfanti et al., 2004).