Involvement of Mitophagy in Aluminum Oxide Nanoparticle–Induced Impairment of Learning and Memory in Mice

Huang, Tao; Guo, Weiwei; Wang, Yanhong; Chang, Lijun; Shang, Nan; Chen, Jin; Fan, Rong; Zhang, Lan; Gao, Xiaocheng; Niu, Qiao; Zhang, Qinli

doi:10.1007/s12640-020-00283-0

Cited by 24 publications

(14 citation statements)

References 69 publications

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“…Several studies have proposed that mitochondrial dysfunction may play a critical role in the toxic effects of Al, including neurotoxicity [ 197 , 208 ]. Rao et al [ 209 ] have shown that the ROS formation and mitochondrial respiratory activity, as well as glutathione depletion, were increased in the glial cells after being treated with Al for 24 h. Other groups have also depicted that Al exposure increased ROS formation and impaired the cytochrome c oxidase, which impaired mitochondrial functions in various neuronal cell types, including PC12 [ 210 , 211 , 212 ], SH-SY5Y neuroblastoma cells [ 213 , 214 ], and rat and cerebellar granule neuronal cells [ 42 , 215 ].…”

Section: Molecular Mechanisms Of Metal-induced Mitochondrial Dysfunctionmentioning

confidence: 99%

“…In addition, their other study also suggested that Al exposure decreased MnSOD and aconitase activities in different regions of the rat brain [ 220 ]. Additionally, transmission electron microscope results showed that Al exposure caused mitochondrial swelling and vacuolization structures, and thus increased the diameter of mitochondria in the hippocampus nerve cells of mice and rats [ 208 , 219 ]. Finally, Al exposure upregulated the autophagy-related proteins LC3-II and Beclin-1, while downregulating p62 expression, suggesting that Al-induced learning and memory impairments may be related to mitophagy [ 208 ].…”

Section: Molecular Mechanisms Of Metal-induced Mitochondrial Dysfunctionmentioning

confidence: 99%

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Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Cheng

Yang

Tao

et al. 2021

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.

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Section: Molecular Mechanisms Of Metal-induced Mitochondrial Dysfunctionmentioning

confidence: 99%

Section: Molecular Mechanisms Of Metal-induced Mitochondrial Dysfunctionmentioning

confidence: 99%

Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Cheng

Yang

Tao

et al. 2021

Toxics

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“…AlNPs induced oxidative stress in the cerebral cortex as evidenced by marked reduction of SOD activity and significant elevation of MDA level. Significant pathological changes in the ultra-structure and function of mitochondria were also recorded (Huang et al, 2021).…”

Section: Neurotoxicitymentioning

confidence: 98%

“…ATPase activity was markedly inhibited in the kidney and brain but no discernible change in ATPase activity in the intestine was recorded (Canli et al, 2019b). Huang et al (2021) treated female mice, through a nasal drip three times per day, with 50 nm AlNPs at doses of 25, 50, and 75 mg/kg for 30 days. The results revealed that AlNPs impaired the spatial learning and memory in mice.…”

Section: Neurotoxicitymentioning

confidence: 99%

Potential Toxic Effects of Aluminum Nanoparticles: An overview

Elkhadrawy¹,

Abou-Zeid²,

El-Borai³

et al. 2021

Journal of Current Veterinary Research

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Alumina (aluminum oxide) nanoparticles (AlNPs) have been categorized among the most important nano-metals, with wide applications in many fields as in food, agriculture, industry, engineering, pharmacy, medicine and others. The extensive use of AlNPs results in a massive release of them into the environment resulting in potential adverse impacts on animals and human health. Toxicokinetic studies demonstrated the rapid absorption and the systemic distribution of AlNPs to different organs. AlNPs mainly induced their toxic damage by induction of oxidative stress and mitochondrial dysfunction. Cellular accumulation of AlNPs resulted in interaction with cell components and binding with proteins and genetic materials (DNA and RNA) with producing other different chemical compounds resulting in cellular oxidative damage. Also, AlNPs induced cell death by disrupting the integrity of the mitochondrial membrane, depleting the mitochondrial thiols, activating apoptotic caspases (9 and 3) and generating more ROS. Previous in vivo and in vitro studies revealed hepato-, nephro-, myocardial, reproductive and neuro-toxic effects of AlNPs. Moreover, AlNPs exert inflammatory, apoptotic and geno-toxic effects. The aim here is to spot on previous studies demonstrating the toxic effects of AlNPs.

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“…Treated with aluminaNPs could also decrease the ratio of active to total level of Akt while increased GSK-3β level in the hippocampus [ 39 ]. Furthermore, spatial learning and memory impairment induced by aluminaNPs could be related to mitophagy, as indicated by increases in LC3-II and Beclin-1 activity in the hippocampal CA3 area of mice [ 11 ]. Previous studies have also reported that aluminaNPs can cause oxidative stress and inflammatory events in mouse brains [ 7 , 40 ].…”

Section: Introductionmentioning

confidence: 99%

Aluminium oxide nanoparticles compromise spatial memory performance and proBDNF-mediated neuronal function in the hippocampus of rats

Liu

2022

Part Fibre Toxicol

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Background Alumina nanoparticles (aluminaNPs), which are widely used in a range of daily and medical fields, have been shown to penetrate blood-brain barrier, and distribute and accumulate in different brain areas. Although oral treatment of aluminaNPs induces hippocampus-dependent learning and memory impairments, characteristic effects and exact mechanisms have not been fully elucidated. Here, male adult rats received a single bilateral infusion of aluminaNPs (10 or 20 µg/kg of body weight) into the hippocampal region, and their behavioral performance and neural function were assessed. Results The results indicated that the intra-hippocampus infusions at both doses of aluminaNPs did not cause spatial learning inability but memory deficit in the water maze task. This impairment was attributed to the effects of aluminaNP on memory consolidation phase through activation of proBDNF/RhoA pathway. Inhibition of the increased proBDNF by hippocampal infusions of p75NTR antagonist could effectively rescue the memory impairment. Incubation of aluminaNPs exaggerated GluN2B-dependent LTD induction with no effects on LTD expression in hippocampal slices. AluminaNP could also depress the amplitude of NMDA-GluN2B EPSCs. Meanwhile, increased reactive oxygen specie production was reduced by blocking proBDNF-p75NTR pathway in the hippocampal homogenates. Furthermore, the neuronal correlate of memory behavior was drastically weakened in the aluminaNP-infused groups. The dysfunction of synaptic and neuronal could be obviously mitigated by blocking proBDNF receptor p75NTR, implying the involvement of proBDNF signaling in aluminaNP-impaired memory process. Conclusions Taken together, our findings provide the first evidence that the accumulation of aluminaNPs in the hippocampus exaggeratedly activates proBDNF signaling, which leads to neural and memory impairments.

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Involvement of Mitophagy in Aluminum Oxide Nanoparticle–Induced Impairment of Learning and Memory in Mice

Cited by 24 publications

References 69 publications

Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Potential Toxic Effects of Aluminum Nanoparticles: An overview

Aluminium oxide nanoparticles compromise spatial memory performance and proBDNF-mediated neuronal function in the hippocampus of rats

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