Role of miRNAs in mediating organophosphate compounds induced toxicity

Dehghan, Hajar; Farkhondeh, Tahereh; Darroudi, Majid; Yousefizadeh, Shahnaz; Samarghandian, Saeed

doi:10.1016/j.toxrep.2023.01.007

Cited by 3 publications

(1 citation statement)

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“…Therefore, dysregulation of this pathway compromises the cellular defense mechanism against oxidative stress, exacerbating the toxic impact of oxidative stress in the presence of CP. [ 164 ] Another study by Weldon et al found significant differences in the expression of six miRNAs (miR‐133b, miR‐28‐5p, miR‐518d‐3p, miR‐517b‐3p, miR‐597, and miR‐223‐3p) in farmworkers during the post‐harvesting season, indicating their potential as novel biomarkers for the pesticide exposure. The binding of Ach, functioning of enzymes, and, neurological processes such as neurotransmitter functioning and binding of receptors are all regulated by these miRNAs.…”

Section: Effect Of Opps On Glial Cellsmentioning

confidence: 99%

Implications of organophosphate pesticides on brain cells and their contribution toward progression of Alzheimer's disease

Yadav,

Kaur,

Yadav

et al. 2024

J Biochem & Molecular Tox

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The most widespread neurodegenerative disorder, Alzheimer's disease (AD) is marked by severe behavioral abnormalities, cognitive and functional impairments. It is inextricably linked with the deposition of amyloid β (Aβ) plaques and tau protein in the brain. Loss of white matter, neurons, synapses, and reactive microgliosis are also frequently observed in patients of AD. Although the causative mechanisms behind the neuropathological alterations in AD are not fully understood, they are likely influenced by hereditary and environmental factors. The etiology and pathogenesis of AD are significantly influenced by the cells of the central nervous system, namely, glial cells and neurons, which are directly engaged in the transmission of electrical signals and the processing of information. Emerging evidence suggests that exposure to organophosphate pesticides (OPPs) can trigger inflammatory responses in glial cells, leading to various cascades of events that contribute to neuroinflammation, neuronal damage, and ultimately, AD pathogenesis. Furthermore, there are striking similarities between the biomarkers associated with AD and OPPs, including neuroinflammation, oxidative stress, dysregulation of microRNA, and accumulation of toxic protein aggregates, such as amyloid β. These shared markers suggest a potential mechanistic link between OPP exposure and AD pathology. In this review, we attempt to address the role of OPPs on altered cell physiology of the brain cells leading to neuroinflammation, mitochondrial dysfunction, and oxidative stress linked with AD pathogenesis.

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Section: Effect Of Opps On Glial Cellsmentioning

confidence: 99%