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Dr. Hong Cheng
Guangxi Medical University

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0 Autophagy
0 Mitochondria
0 transporter
0 metal
0 Neurotixity

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Review
Published: 17 June 2021 in Toxics
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Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. Here, we address contemporary studies on metal-induced mitochondrial dysfunction and its impact on the nervous system.

ACS Style

Hong Cheng; Bobo Yang; Tao Ke; Shaojun Li; Xiaobo Yang; Michael Aschner; Pan Chen. Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders. Toxics 2021, 9, 142 .

AMA Style

Hong Cheng, Bobo Yang, Tao Ke, Shaojun Li, Xiaobo Yang, Michael Aschner, Pan Chen. Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders. Toxics. 2021; 9 (6):142.

Chicago/Turabian Style

Hong Cheng; Bobo Yang; Tao Ke; Shaojun Li; Xiaobo Yang; Michael Aschner; Pan Chen. 2021. "Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders." Toxics 9, no. 6: 142.

Article
Published: 27 March 2021 in Biological Trace Element Research
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Manganese (Mn)-induced neurotoxicity has aroused public concerns for many years, but its precise mechanism is still poorly understood. Herein, we report the impacts of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway in mediating neurological effects induced by manganese sulfate (MnSO4) exposure in PC12 cells. In this study, cells were treated with MnSO4 for 24 h in the absence or presence of LY294002 (a special inhibitor of PI3K). We investigated cell viability and apoptosis signals, as well as levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA). The mRNA levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and Caspase-3 were also quantified through real-time quantitative PCR (RT-qPCR); protein levels of serine/threonine protein kinase (Akt) and forkhead box O3A (Foxo3a) were determined by western blot. Increasing of MnSO4 doses led to decreased SOD, GSH-Px, and CAT activities, while the level of MDA was upregulated. Moreover, cell apoptosis was significantly increased, as the mRNA of Bcl-2 and Caspase-3 was significantly decreased, while Bax mRNA was increased. Phosphorylated Akt (p-Akt) and Foxo3a (p-Foxo3a) were upregulated in a dose-dependent manner. In addition, LY294002 pretreatment reduced the activity of SOD, GSH-Px, and CAT but elevated MDA levels. Meanwhile, LY294002 pretreatment also increased cell apoptosis given the upregulated Bax and Caspase-3 mRNAs and decreased Bcl-2 mRNA. In summary, the PI3K/Akt signaling pathway can be activated by MnSO4 exposure and mediate MnSO4-induced neurotoxicity.

ACS Style

Yanli Tan; Hong Cheng; Cheng Su; Pan Chen; Xiaobo Yang. PI3K/Akt Signaling Pathway Ameliorates Oxidative Stress-Induced Apoptosis upon Manganese Exposure in PC12 Cells. Biological Trace Element Research 2021, 1 -12.

AMA Style

Yanli Tan, Hong Cheng, Cheng Su, Pan Chen, Xiaobo Yang. PI3K/Akt Signaling Pathway Ameliorates Oxidative Stress-Induced Apoptosis upon Manganese Exposure in PC12 Cells. Biological Trace Element Research. 2021; ():1-12.

Chicago/Turabian Style

Yanli Tan; Hong Cheng; Cheng Su; Pan Chen; Xiaobo Yang. 2021. "PI3K/Akt Signaling Pathway Ameliorates Oxidative Stress-Induced Apoptosis upon Manganese Exposure in PC12 Cells." Biological Trace Element Research , no. : 1-12.