Inhibition of neurite outgrowth and alteration of cytoskeletal gene expression by sodium arsenite

Aung, Kyaw; Kurihara, Ryohei; Nakashima, Shizuka; Maekawa, Fumihiko; Nohara, Keiko; Kobayashi, Tetsuya; Tsukahara, Shinji

doi:10.1016/j.neuro.2012.09.008

Cited by 52 publications

(41 citation statements)

References 47 publications

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“…31) Overexpression of NF-L causes an abnormal accumulation of neurofilaments in the perikaryal and proximal axons of neurons. 33) In our study, a remarkable increase in the gene expression of NF-L and NF-M proteins was observed in neural cells exposed to sodium arsenite, in which the suppression of neurite outgrowth was also observed 35) (Table 1). These data suggest that alteration to the NF dynamic contributes to arsenic-induced neurite suppression.…”

Section: Disruption Of Cytoskeletal Organization and Neurite Degenerasupporting

confidence: 60%

“…These data suggest that alteration to the NF dynamic contributes to arsenic-induced neurite suppression. We also observed that exposure to sodium arsenite significantly decreased the gene expression of microtubule (Tubulin) and microtubuleassociated protein (Tau) in neural cells 35) (Table 1). Tau is mainly expressed in axonal outgrowth and is essential to the microtubule assembly.…”

Section: Disruption Of Cytoskeletal Organization and Neurite Degeneramentioning

confidence: 64%

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Role of Environmental Chemical Insult in Neuronal Cell Death and Cytoskeleton Damage

Aung

Tsukahara

Maekawa

et al. 2015

Biological & Pharmaceutical Bulletin

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Environmental influences, such as chemical exposure, have long been considered potential risk factors for neurodegenerative disorders, including neuromuscular diseases. However, no definitive links between environmental chemical exposure and a pathogenic mechanism of neurodegenerative disease has yet been established. In this study, we describe that exposure to arsenic, an environmental pollutant naturally found in drinking water, induces neuronal cell death and alteration of morphology, particularly neurite outgrowth and in the cytoskeleton of neurons. Since progressive cell loss accompanied by the alteration of neuronal structures and cytoskeleton is considered the major pathologic feature of neurodegenerative disorders, arsenic-induced neurotoxicity might contribute to an etiologic mechanism of some neurodegenerative diseases. Further, we discuss the importance of in vitro assay, particularly an embryonic toxicity test, for assessing the neurotoxicity of chemicals, because most of chemicals found in our environment remain to be evaluated regarding their neurotoxicity risk for neurodegenerative diseases.

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Section: Disruption Of Cytoskeletal Organization and Neurite Degenerasupporting

confidence: 60%

Section: Disruption Of Cytoskeletal Organization and Neurite Degeneramentioning

confidence: 64%

Role of Environmental Chemical Insult in Neuronal Cell Death and Cytoskeleton Damage

Aung

Tsukahara

Maekawa

et al. 2015

Biological & Pharmaceutical Bulletin

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“…*P<0.05 in As group compared with the control, # P<0.05 in MLT plus As group compared with As group by Kruskal-Wallis test and followed by Mann-Whitney U test as post hoc method levels but also neurite outgrowth [43]. These data indicate that in addition to neuronal cell loss, arsenite compromised neuroplasticity with a concomitant inhibition of neurite growth [44,45]. Moreover, 3-MA attenuated arseniteinduced reduction in α-synuclein levels, suggesting that arsenite-induced autophagy is capable of degrading α-synuclein in the treated primary cultured cortical neurons.…”

Section: Melatonin-induced Neuroprotection and Autophagymentioning

confidence: 87%

Melatonin Ameliorates Arsenite-Induced Neurotoxicity: Involvement of Autophagy and Mitochondria

Teng¹,

Tai²,

Huang

et al. 2015

Mol Neurobiol

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In the present study, the neuroprotective effect of melatonin on arsenite-induced neurotoxicity was investigated in rat primary cultured cortical neurons. Incubation of melatonin prevented arsenite-induced neuronal cell loss in a concentration-dependent manner. Furthermore, melatonin significantly attenuated arsenite-induced elevation in microtubule-associated protein light chain 3 (LC3)-II levels, a biomarker of autophagy. Our fluorescent staining assay showed that melatonin decreased arsenite-induced elevation of co-localized fluorescent puncta of monodansylcadaverine (a specific marker of autophagic vacuoles) and lysotracker red (a specific marker of lysosomes), indicating that melatonin is capable of inhibiting arsenite-induced autophagy and autolysosome formation. Because 3-methyladenine (an autophagic inhibitor) attenuated the arsenite-reduced α-synuclein levels (a protein essential for the neurite outgrowth and synaptic plasticity), melatonin via inhibiting autophagy attenuated the arsenite-reduced α-synuclein levels. At the same time, melatonin ameliorated the arsenite-induced reduction in growth associated protein 43 (a hallmark protein of neurite outgrowth) and discontinuous neurites of rat primary cultured cortical neurons. In addition, melatonin was found to prevent arsenite-induced decreases in cytochrome c oxidase levels (a biomarker of mitochondrial mass) and elevation in co-localized fluorescent puncta of autolysosomes and cytochrome c oxidase. Moreover, melatonin prevented arsenite-induced reduction in peroxisome proliferator-activated receptor gamma co-activator 1 α, a transcriptional co-activator of mitochondrial biosynthesis. Taken together, melatonin may exert its neuroprotective action via inhibiting arsenite-induced autophagy and enhancing mitochondrial biogenesis and thus restoring α-synuclein levels, neuronal integrity, and mitochondrial mass in rat primary cultured cortical neurons.

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“…Rao and Avani (2004) and Chaudhuri et al (1999) also reported increased neurotoxic oxidative stress in mouse brains after oral administration of arsenic trioxide. Aung et al (2013) in an in vitro study suggested the induction of neural apoptosis since neurite outgrowth was suppressed by sodium arsenite. Deficits in spatial memory and in executive and motor function were shown in animal studies (Tolins et al, 2014).…”

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confidence: 99%

Oxidative Balance in Brain After Exposure to Arsenic in Ex Vivo and in Vivo Models.

Bonetto¹,

Lepori²,

Puntarulo³

2017

IJAR

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Inhibition of neurite outgrowth and alteration of cytoskeletal gene expression by sodium arsenite

Cited by 52 publications

References 47 publications

Role of Environmental Chemical Insult in Neuronal Cell Death and Cytoskeleton Damage

Role of Environmental Chemical Insult in Neuronal Cell Death and Cytoskeleton Damage

Melatonin Ameliorates Arsenite-Induced Neurotoxicity: Involvement of Autophagy and Mitochondria

Oxidative Balance in Brain After Exposure to Arsenic in Ex Vivo and in Vivo Models.

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