S-nitrosylating protein disulphide isomerase mediates α-synuclein aggregation caused by methamphetamine exposure in PC12 cells

Wu, Xiaofang; Wang, Aifeng; Chen, Ling; Huang, Enping; Xie, Wei‐Bing; Liu, Chao; Huang, Weiye; Chen, Chuanxiang; Qiu, Pingming; Wang, Huijun

doi:10.1016/j.toxlet.2014.07.026

Cited by 29 publications

(22 citation statements)

References 47 publications

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“…Indeed, α-synuclein knock-down in SH-SY5Y cells or in rats can protect against METH-induced toxicity (Chen et al, 2013;Tai et al, 2014). It is also of interest to note that S-nitrosylating protein disulphide isomerase may mediate METH-induced α-synuclein aggregation and that inhibition of this enzyme may offer a therapeutic potential (Wu et al, 2014).…”

Section: Page 33 Of 82mentioning

confidence: 99%

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

Moratalla

Khairnar

Simola

et al. 2017

Progress in Neurobiology

188

122

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Amphetamine-related drugs, such as 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine (METH), are popular recreational psychostimulants. Several preclinical studies have demonstrated that, besides having the potential for abuse, amphetamine-related drugs may also elicit neurotoxic and neuroinflammatory effects. The neurotoxic potentials of MDMA and METH to dopaminergic and serotonergic neurons have been clearly demonstrated in both rodents and non-human primates. This review summarizes the species-specific cellular and molecular mechanisms involved in MDMA and METH-mediated neurotoxic and neuroinflammatory effects, along with the most important behavioral changes elicited by these substances in experimental animals and humans. Emphasis is placed on the neuropsychological and neurological consequences associated with the neuronal damage. Moreover, we point out the gap in our knowledge and the need for developing appropriate therapeutic strategies to manage the neurological problems associated with amphetamine-related drug abuse.

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Section: Page 33 Of 82mentioning

confidence: 99%

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

Moratalla

Khairnar

Simola

et al. 2017

Progress in Neurobiology

188

122

View full text Add to dashboard Cite

show abstract

“…MA abuse results in depression and psychosis and MA-induced psychotic symptoms often transform into schizophrenia [1,2]. Thus, MA induced psychosis is considered to be a model for schizophrenia in vivo [2] Moreover, long-lasting MA exposure increases the risk of Parkinson's disease [3] and MA exposure in vitro is used to establish the model of Parkinson's disease [4]. Given the association of MA neurotoxicity with psychosis and neurodegenerative diseases, it is crucial to elucidate the molecular underpinnings of MA toxicity.…”

Section: Introductionmentioning

confidence: 99%

Lithium protects against methamphetamine-induced neurotoxicity in PC12 cells via Akt/GSK3β/mTOR pathway

Zhu

Zhang

et al. 2015

Biochemical and Biophysical Research Communications

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“…However, with meth, autophagy is increased (Kanthasamy et al, 2006;Kongsuphol et al, 2009;Lin et al, 2012;Nopparat et al, 2010;Pitaksalee et al, 2015). There are supporting evidence to suggest increased oxidative stress/reduced glutathione levels Wu et al, 2014;Xuan-Khanh Thi et al, 2015) and mitochondrial dysfunction Suwanjang et al, 2010;Xuan-Khanh Thi et al, 2015). It has been reported that meth binds to the N-terminus of alphasynuclein and triggers a conformational change in alpha-synuclein (Tavassoly & Lee, 2012); accumulation of alpha-synuclein has also been observed after 24h exposure of 3 mM meth .…”

Section: Methamphetaminementioning

confidence: 99%

“…The most studied key downstream event is apoptotic cell death (Irie et al, 2011;Kanthasamy et al, 2006;Kongsuphol et al, 2009;Lin et al, 2012;Nopparat et al, 2010;Pitaksalee et al, 2015;Shivalingappa et al, 2012;Suwanjang et al, 2010;Wu et al, 2014;Xuan-Khanh Thi et al, 2015), and ER stress (Irie et al, 2011) as well as activation of JNK (Nopparat et al, 2010) have been implicated as preceding events to apoptotic cell death.…”

Section: Methamphetaminementioning

confidence: 99%

Systematic literature review on Parkinson's disease and Childhood Leukaemia and mode of actions for pesticides

Choi¹,

Polcher²,

Joas³

2016

EFSA Supporting Publications

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This report presents the outcomes of a systematic review (SR) identifying the mechanisms and chemicals involved in the pathogenesis of Parkinson's disease (PD) and childhood leukaemia (CL). This work serves as a basis for defining and mapping the causal linkages between a molecular initiating event (MIE) and a final adverse outcome (AO) that are relevant for the development of a prototype adverse outcome pathway (AOP) for assessing risk factors for PD and CL. Search for literature from 1990 to present was conducted using Web of Science, PubMed and TOXNET, and relevant references were selected using established inclusion/exclusion criteria and ranked using a set of quality control factors.For PD, 7,384 individual references were identified to be relevant for PD pathogenesis and chemicals associated with PD. Dopaminergic neurodegeneration in the substantia nigra leading to locomotor deficits was identified as the AO in PD. Other identified key events in PD pathogenesis include mitochondrial dysfunction, cellular accumulation of alpha-synuclein and oxidative stress. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, rotenone and paraquat are some chemicals identified to be associated with PD pathogenesis.For CL, 1,988 individual references were identified to be relevant for CL pathogenesis and chemicals associated with CL. Chromosomal translocation, genetic damage/mutation and hyperdiploidy are considered as driving forces of CL. Except for infant leukaemia, CL pathogenesis requires a 'two-hit' model with an initiating event occurring in utero followed by a secondary hit potentially occurring after birth. Potential MIEs leading to these driving mechanisms include aberrant DNA topoisomerase II activity and erroneous DNA repair. Epigenetics appears to also play an influential role in CL pathogenesis. Benzene, bioflavonoids and organophosphates are some chemicals identified to be implicated in CL pathogenesis.The challenges of developing AOPs for these two diseases and the data gaps identified from the outcomes of this SR are also elaborated in this report. The present document has been produced and adopted by the bodies identified above as authors. This task has been carried out exclusively by the authors in the context of a contract between the European Food Safety Authority and the authors, awarded following a tender procedure. The present document is published complying with the transparency principle to which the Authority is subject. It may not be considered as an output adopted by the Authority. The European Food Safety Authority reserves its rights, view and position as regards the issues addressed and the conclusions reached in the present document, without prejudice to the rights of the authors. KEY WORDSSystematic Review, Parkinson Disease, Childhood Leukaemia, Pathogenesis, Chemicals, Pesticides, Adverse Outcome Pathway SUMMARYThe aim of this project was to perform a systematic review (SR) to collect relevant publications related to the mechanisms involved in the pathogenesis of Parkinson's disease (PD)...

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S-nitrosylating protein disulphide isomerase mediates α-synuclein aggregation caused by methamphetamine exposure in PC12 cells

Cited by 29 publications

References 47 publications

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

Amphetamine-related drugs neurotoxicity in humans and in experimental animals: Main mechanisms

Lithium protects against methamphetamine-induced neurotoxicity in PC12 cells via Akt/GSK3β/mTOR pathway

Systematic literature review on Parkinson's disease and Childhood Leukaemia and mode of actions for pesticides

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