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- W4380320511 abstract "Because triclosan (TCS) has been confirmed to cause severe neurotoxicity, it is urgent to disclose the underlying toxicity mechanisms at varying levels. TCS exposure resulted in a series of malformations in larval zebrafish, including reduced neurons, blood-vessel ablation and abnormal neurobehavior. Apoptosis staining and the upregulated expression of proapoptotic genes demonstrated that TCS induced neuronal apoptosis and neurotransmitter disorders. By integrating RT-qPCR analysis with the effects of pathway inhibitors and agonists, we found that TCS triggered abnormal regulation of neuron development-related functional genes, and suppressed the BDNF/TrkB signaling pathway. TCS inhibited total m6A-RNA modification level by activating the demethylase ALKBH5, and induced neurodevelopmental toxicity based on the knockdown experiments of alkbh5 and molecular docking. The main novelties of this study lies in: (1) based on specific staining and transgenic lines, the differential neurotoxicity effects of TCS were unravelled at individual, physiological, biochemical and molecular levels in vivo; (2) from a epigenetics viewpoint, the decreasing m6A methylation level was confirmed to be mediated by alkbh5 upregulation; and (3) both homology modeling and molecular docking evidenced the targeting action of TCS on ALKBH5 enzyme. These findings open a novel avene for TCS's risk assessment and early intervention of the contaminant-sourcing diseases." @default.
- W4380320511 created "2023-06-13" @default.
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- W4380320511 date "2023-09-01" @default.
- W4380320511 modified "2023-10-14" @default.
- W4380320511 title "Mechanistic exploration on neurodevelopmental toxicity induced by upregulation of alkbh5 targeted by triclosan exposure to larval zebrafish" @default.
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- W4380320511 doi "https://doi.org/10.1016/j.jhazmat.2023.131831" @default.
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