The cytoskeleton as a non-cholinergic target of organophosphate compounds

• Published in: Chemico-biological interactions Vol. 346; p. 109578
• Main Authors: Hernandez-Toledano, David, Vega, Libia
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01-09-2021
• Subjects: Actin; Adducts; Cytoskeleton; Non-cholinergic mechanism; Organophosphate; Tubulin; AChE; DEDTP; OP; GTP; CPO; NM IIA; PTM; Non-cholinergic mechanism; ABP; GDP; Tubulin; Organophosphate; MAPs; Actin; ROS; Cytoskeleton; ATP; Adducts
• ISSN: 0009-2797; 1872-7786
• DOI: 10.1016/j.cbi.2021.109578

Current organophosphate (OP) toxicity research now considers potential non-cholinergic mechanisms for these compounds, since the inhibition of acetylcholinesterase (AChE) cannot completely explain all the adverse biological effects of OP. Thanks to the development of new strategies for OP detection, some potential molecular targets have been identified. Among these molecules are several cytoskeletal proteins, including actin, tubulin, intermediate filament proteins, and associated proteins, such as motor proteins, microtubule-associated proteins (MAPs), and cofilin. in vitro, ex vivo, and some in vivo reports have identified alterations in the cytoskeleton following OP exposure, including cell morphology defects, cells detachments, intracellular transport disruption, aberrant mitotic spindle formation, modification of cell motility, and reduced phagocytic capability, which implicate the cytoskeleton in OP toxicity. Here, we reviewed the evidence indicating the cytoskeletal targets of OP compounds, including their strategies, the potential effects of their alterations, and their possible participation in neurotoxicity, embryonic development, cell division, and immunotoxicity related to OP compounds exposure.
•Cytoskeleton and related proteins are non-cholinergic targets for organophosphates.•Organophosphates exposure can modify cytoskeleton-dependent cell functions.•Cytoskeleton disruption may be related to chronic organophosphates exposure effects .