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On-line Access: 2025-09-26

Received: 2025-04-28

Revision Accepted: 2025-08-11

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Journal of Zhejiang University SCIENCE B

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Reduced NGF mediates arsenic-induced mitochondrial dynamic imbalance and neuronal damage both in vivo and in vitro


Author(s):  Xinbo MA, Liu YANG, Xinhua SHAO, Jia CUI, Ziqiao GUAN, Man LV, Shuaifei YANG, Na FANG, Yang LIU, Yanhui GAO, Xiaona LIU, Yanmei YANG

Affiliation(s):  Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, China; more

Corresponding email(s):  xiaonaliu_2013@163.com, yangyanmei@hrbmu.edu.cn

Key Words:  Arsenic; Nerve growth factor (NGF); Mitochondrial dynamics; Neurotoxicity; Phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT)


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Xinbo MA, Liu YANG, Xinhua SHAO, Jia CUI, Ziqiao GUAN, Man LV, Shuaifei YANG, Na FANG, Yang LIU, Yanhui GAO, Xiaona LIU, Yanmei YANG. Reduced NGF mediates arsenic-induced mitochondrial dynamic imbalance and neuronal damage both in vivo and in vitro[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2500216

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%A Xinbo MA
%A Liu YANG
%A Xinhua SHAO
%A Jia CUI
%A Ziqiao GUAN
%A Man LV
%A Shuaifei YANG
%A Na FANG
%A Yang LIU
%A Yanhui GAO
%A Xiaona LIU
%A Yanmei YANG
%J Journal of Zhejiang University SCIENCE B
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doi="https://doi.org/10.1631/jzus.B2500216"

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A1 - Jia CUI
A1 - Ziqiao GUAN
A1 - Man LV
A1 - Shuaifei YANG
A1 - Na FANG
A1 - Yang LIU
A1 - Yanhui GAO
A1 - Xiaona LIU
A1 - Yanmei YANG
J0 - Journal of Zhejiang University Science B
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Abstract: 
Arsenic exposure is known to cause cognitive deficits, although the underlying mechanisms are yet to be explored. In this study, we investigated the role of nerve growth factor (NGF), a neuroprotective factor, in arsenic-induced cognitive impairment. In mouse models exposed to 25 mg/L and 50 mg/L sodium arsenite (NaAsO2), we observed neuronal damage accompanied by the downregulation of NGF, decreased phosphorylation of phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), reduced phosphorylation of the mitochondrial fission protein dynamin-related protein 1 (Drp1), and downregulation of the mitochondrial fusion protein optic atrophy 1 (OPA1). Similarly, the downregulation of NGF, inactivation of the PI3K/AKT signaling pathway, mitochondrial dynamics imbalance (dysregulation of mitochondrial fission and fusion processes), and increased apoptosis were observed in HT-22 cells exposed to 4 μmol/L NaAsO2. NGF overexpression mitigated these arsenic-induced alterations, while the protective effect of NGF against arsenic toxicity was reduced by LY294002, a PI3K/AKT pathway inhibitor. These findings suggest that a decrease in NGF mediates the arsenic-disrupted mitochondrial dynamics via inhibiting the PI3K/AKT pathway, ultimately impairing cognitive function.

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