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  1. Article ; Online: The role of mTORC1/TFEB axis mediated lysosomal biogenesis and autophagy impairment in fluoride neurotoxicity and the intervention effects of resveratrol.

    Tang, Huayang / Hou, Haoqi / Song, Li / Tian, Zhiyuan / Liu, Wenhui / Xia, Tao / Wang, Aiguo

    Journal of hazardous materials

    2024  Volume 467, Page(s) 133634

    Abstract: Elevated exposures to fluoride have been linked to neurological diseases. Identifying mechanisms of fluoride neurotoxicity and finding ways for prevention and treatment of epidemic fluorosis are important issues of public health. In this study, fluoride ... ...

    Abstract Elevated exposures to fluoride have been linked to neurological diseases. Identifying mechanisms of fluoride neurotoxicity and finding ways for prevention and treatment of epidemic fluorosis are important issues of public health. In this study, fluoride inhibited TFEB nuclear translocation by activating p-mTORC1/p-p70S6K, thus inhibiting lysosomal biogenesis, leading to dysfunctional lysosome accumulation, which further negatively affected autophagosome and lysosome fusion, thus impairing autophagy degradation, evidenced by the blocked conversion of LC3II to LC3I, and the increased p62 levels. Interestingly, RSV alleviated rats' cognition by improving fluoride-induced nerve damage and promoted lysosomal biogenesis demonstrated by the increased nucleus translocation of TFEB via inhibiting p-mTORC1 and p-p70S6K, the decreased expression of LC3II and p62. Collectively, we clarified the correlation between fluoride neurotoxicity and mTORC1/TFEB-mediated lysosomal biogenesis and autophagy. Meanwhile, RSV appeared to be a promising drug for the prevention and treatment of epidemic fluorosis.
    MeSH term(s) Animals ; Rats ; Fluorides/toxicity ; Resveratrol ; Ribosomal Protein S6 Kinases, 70-kDa ; Neurotoxicity Syndromes/drug therapy ; Neurotoxicity Syndromes/prevention & control ; Autophagy ; Lysosomes ; Mechanistic Target of Rapamycin Complex 1 ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
    Chemical Substances Fluorides (Q80VPU408O) ; Resveratrol (Q369O8926L) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; TFEB protein, rat ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
    Language English
    Publishing date 2024-01-28
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1491302-1
    ISSN 1873-3336 ; 0304-3894
    ISSN (online) 1873-3336
    ISSN 0304-3894
    DOI 10.1016/j.jhazmat.2024.133634
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: ZLN005 alleviates PBDE-47 induced impairment of mitochondrial translation and neurotoxicity through PGC-1α/ERRα axis.

    Tian, Zhiyuan / Li, Jing / Tang, Huayang / Liu, Wenhui / Hou, Haoqi / Wang, Chenxi / Li, Dongjie / Chen, Gaoshuai / Xia, Tao / Wang, Aiguo

    Journal of hazardous materials

    2024  Volume 471, Page(s) 134331

    Abstract: Recent studies are identified the mitochondria as critical targets of 2, 2', 4, 4'-tetrabromodiphenyl ether (PBDE-47) induced neurotoxicity. This study aimed at examining the impact of PBDE-47 exposure on mitochondrial translation, and its subsequent ... ...

    Abstract Recent studies are identified the mitochondria as critical targets of 2, 2', 4, 4'-tetrabromodiphenyl ether (PBDE-47) induced neurotoxicity. This study aimed at examining the impact of PBDE-47 exposure on mitochondrial translation, and its subsequent effect on PBDE-47 neurotoxicity. The Sprague-Dawley (SD) rat model and neuroendocrine pheochromocytoma (PC12) cells were adopted for the measurements of mitochondrial ATP levels, mitochondrial translation products, and expressions of important mitochondrial regulators, such as required meiotic nuclear division 1 (RMND1), estrogen-related receptor α (ERRα), and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α). To delve into the role of PGC-1α/ERRα axis in mitochondrial translation, 2-(4-tert-butylphenyl) benzimidazole (ZLN005) was employed. Both cellular and animal model results shown that PBDE-47 impeded PGC-1α/ERRα axis and mitochondrial translation. PBDE-47 suppressed mitochondrial function in rat hippocampus and PC12 cells by decreasing relative mitochondrial DNA (mtDNA) content, mitochondrial translation products, and mitochondrial ATP levels. Particularly, ZLN005 reversed PBDE-47 neurotoxicity by enhancing mitochondrial translation through activation of PGC-1α/ERRα axis, yet suppressing PGC-1α with siRNA attenuates its neuroprotective effect in vitro. In conclusion, this work highlights the importance of mitochondrial translation in PBDE-47 neurotoxicity by presenting results from cellular and animal models and suggests a potential therapeutic approach through activation of PGC-1α/ERRα axis. ENVIRONMENTAL IMPLICATION: PBDEs have attracted extensive attention because of their high lipophilicity, persistence, and detection levels in various environmental media. Increasing evidence has shown that neurodevelopmental disorders in children are associated with PBDE exposure. Several studies have also found that perinatal PBDE exposure can cause long-lasting neurobehavioral abnormalities in experimental animals. Our recent studies have also demonstrated the impact of PBDE-47 exposure on mitochondrial biogenesis and dynamics, leading to memory and neurobehavioral deficits. Therefore, we explore whether the pathological mechanism of PBDE-47-induced neurotoxicity involves the regulation of mitochondrial translation through the PGC-1α/ERRα axis.
    Language English
    Publishing date 2024-04-16
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1491302-1
    ISSN 1873-3336 ; 0304-3894
    ISSN (online) 1873-3336
    ISSN 0304-3894
    DOI 10.1016/j.jhazmat.2024.134331
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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