MiADMSA reverses impaired mitochondrial energy metabolism and neuronal apoptotic cell death after arsenic exposure in rats

Dwivedi, Nidhi; Mehta, Ashish; Yadav, Abhishek; Binukumar, B.; Gill, Kiran Dip; Flora, Swaran J.S.

doi:10.1016/j.taap.2011.04.004

Cited by 66 publications

(41 citation statements)

References 57 publications

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“…Several mechanisms have been proposed, including effects on mitochondrial enzyme activity, free radical formation, and the permeability transition pore [8,[10][11][12]. Indeed, our previous studies have shown arsenite-induced apoptosis via the mitochondrial pathway [20,21].…”

Section: Melatonin Attenuates Arsenite-induced Mitochondrial Lossmentioning

confidence: 99%

“…An oxidative mechanism is reportedly involved in the arsenite-induced neurotoxicity [5][6][7][8][9][10][11]. In support of this notion, arsenics have been shown to induce oxidative stress, including free radical formation, glutathione depletion, lipid peroxidation, and mitochondrial impairment [5][6][7][8][9][10][11][12]. Antioxidative strategies have been suggested for arsenics-induced neurotoxicity [13][14][15][16][17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Melatonin Attenuates Arsenite-induced Mitochondrial Lossmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Teng¹,

Tai²,

Huang

et al. 2015

Mol Neurobiol

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“…These early events, along with diminished ATP levels, could be co-related with the later events of the release of cytochrome c into cytosol, altered bax/bcl-2 ratio, and increased caspase-3 activity. 29) In addition, Lu et al recently reported that inorganic arsenic induces reactive oxygen species, causing neuronal cell death via both c-Jun N terminal kinase/extracellular signal-regulated kinase (JNK/ERK)-mediated mitochondria-dependent and GRP 78/CHOP-triggered apoptosis pathways. 30) These results indicate that exposure to inorganic arsenic at least contributes to neuronal cell death via a mitochondrial dependent pathway.…”

Section: Sodium Arsenite Induces Neural Cell Death Via a Mitochondriamentioning

confidence: 99%

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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“…Superoxide ion constantly generated during cellular metabolism gets converted to hydrogen peroxide (H 2 O 2 ) and other ROS. Under physiological conditions, the maintenance of an appropriate level of intracellular ROS is important in keeping redox balance and signaling cellular proliferation [44]. ROS produced within mitochondria presents almost 90% of the total ROS produced in the cell.…”

Section: Mitochondrial Energy Metabolism and Ageingmentioning

confidence: 99%

Investigation on the Mechanism of Qi-Invigoration from a Perspective of Effects of Sijunzi Decoction on Mitochondrial Energy Metabolism

Li¹

2012

Alternative Medicine

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MiADMSA reverses impaired mitochondrial energy metabolism and neuronal apoptotic cell death after arsenic exposure in rats

Cited by 66 publications

References 57 publications

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

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

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

Investigation on the Mechanism of Qi-Invigoration from a Perspective of Effects of Sijunzi Decoction on Mitochondrial Energy Metabolism

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