Methylglyoxal increases dopamine level and leads to oxidative stress in SH-SY5Y cells

Xie, Bijun; Lin, Fuchang; Peng, Lei; Ullah, Kaleem; Wu, Haimei; Qing, Hong; Deng, Yulin

doi:10.1093/abbs/gmu094

Cited by 21 publications

(14 citation statements)

References 33 publications

(34 reference statements)

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“…Xie et al. have shown that MG increases dopamine levels in neuroblastoma cells, a redox‐dependent mechanism that authors have suggested to be involved in the loss of dopaminergic neurons . MG also leads to the formation of the neurotoxin 1‐acetyl‐6,7‐dihydroxyl‐1,2,3,4‐tetrahydroisoquinoline (ADTIQ), by direct reaction with dopamine, which causes hyperglycemia‐related death of dopaminergic neurons .…”

Section: Pathophysiological Relevance Of Methylglyoxal In Metabolic Dmentioning

confidence: 99%

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Matafome

Rodrigues

Sena

et al. 2016

Medicinal Research Reviews

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Glucose and fructose metabolism originates the highly reactive byproduct methylglyoxal (MG), which is a strong precursor of advanced glycation end products (AGE). The MG has been implicated in classical diabetic complications such as retinopathy, nephropathy, and neuropathy, but has also been recently associated with cardiovascular diseases and central nervous system disorders such as cerebrovascular diseases and dementia. Recent studies even suggested its involvement in insulin resistance and beta-cell dysfunction, contributing to the early development of type 2 diabetes and creating a vicious circle between glycation and hyperglycemia. Despite several drugs and natural compounds have been identified in the last years in order to scavenge MG and inhibit AGE formation, we are still far from having an effective strategy to prevent MG-induced mechanisms. This review summarizes the endogenous and exogenous sources of MG, also addressing the current controversy about the importance of exogenous MG sources. The mechanisms by which MG changes cell behavior and its involvement in type 2 diabetes development and complications and the pathophysiological implication are also summarized. Particular emphasis will be given to pathophysiological relevance of studies using higher MG doses, which may have produced biased results. Finally, we also overview the current knowledge about detoxification strategies, including modulation of endogenous enzymatic systems and exogenous compounds able to inhibit MG effects on biological systems.

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Section: Pathophysiological Relevance Of Methylglyoxal In Metabolic Dmentioning

confidence: 99%

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Matafome

Rodrigues

Sena

et al. 2016

Medicinal Research Reviews

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“…Alterations of DA metabolism leading to DA deficiency are responsible for motor disturbance, typical of different diseases conditions (Bagga et al, ; Ishikawa et al, ). In contrast, an excess of DA is neurotoxic because it results in high oxidative stress in neurons (Xie et al, ). Thus, DA production and degradation rates need to be tightly controlled.…”

Section: Introductionmentioning

confidence: 99%

Role of the HIF‐1α/Nur77 axis in the regulation of the tyrosine hydroxylase expression by insulin in PC12 cells

Fiory

Mirra

Nigro

et al. 2018

Journal Cellular Physiology

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Tyrosine hydroxylase (TH), catalyzing the conversion of tyrosine into l‐DOPA, is the rate‐limiting enzyme in dopamine synthesis. Defects in insulin action contribute to alterations of TH expression and/or activity in the brain and insulin increases TH levels in 1‐methyl‐4‐phenylpyridinium (MPP+)‐treated neuronal cells. However, the molecular mechanisms underlying the regulation of TH by insulin have not been elucidated yet. Using PC12 cells, we show for the first time that insulin increases TH expression in a biphasic manner, with a transient peak at 2 hr and a delayed response at 16 hr, which persists for up to 24 hr. The use of a dominant negative hypoxia‐inducible factor 1‐alpha (HIF‐1α) and its pharmacological inhibitor chetomin, together with chromatin immunoprecipitation (ChIP) experiments for the specific binding to TH promoter, demonstrate the direct role of HIF‐1α in the early phase. Moreover, ChIP experiments and transfection of a dominant negative of the nerve growth factor IB (Nur77) indicate the involvement of Nur77 in the late phase insulin response, which is mediated by HIF‐1α. In conclusion, the present study shows that insulin regulates TH expression through HIF‐1α and Nur77 in PC12 cells, supporting the critical role of insulin signaling in maintaining an appropriate dopaminergic tone by regulating TH expression in the central nervous system.

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“…Moreover, salsolinol has also been suggested to act as an endogenous neurotoxin, a molecule stable and difficult to clear out whose accumulation in SH-SY5Y cells may contribute to storage of toxins production of endogenous neurotoxins ( Fig. 7) and overall oxidative stress that could result in neuronal cell death (Xie et al 2014).…”

Section: Ethanol and Tiqsmentioning

confidence: 99%

Not Just from Ethanol. Tetrahydroisoquinolinic (TIQ) Derivatives: from Neurotoxicity to Neuroprotection

2019

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Your article is protected by copyright and all rights are held exclusively by Springer Science+Business Media, LLC, part of Springer Nature. This e-offprint is for personal use only and shall not be self-archived in electronic repositories. If you wish to selfarchive your article, please use the accepted manuscript version for posting on your own website. You may further deposit the accepted manuscript version in any repository, provided it is only made publicly available 12 months after official publication or later and provided acknowledgement is given to the original source of publication and a link is inserted to the published article on Springer's website. The link must be accompanied by the following text: "The final publication is available at link.springer.com". AbstractThe 1,2,3,4-tetrahydroisoquinolines (TIQs) are compounds frequently described as alkaloids that can be found in the human body fluids and/or tissues including the brain. In most circumstances, TIQs may be originated as a consequence of reactions, known as Pictet-Spengler condensations, between biogenic amines and electrophilic carbonyl compounds, including ethanol's main metabolite, acetaldehyde. Several TIQs may also be synthesized enzymatically whilst others may be formed in the body as by-products of other compounds including TIQs themselves. The biological actions of TIQs appear critically dependent on their metabolism, and nowadays, among TIQs, 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), N-methyl-1methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (N-methyl-(R)-salsolinol), 1-[(3,4-dihydroxyphenyl)methyl]-1,2,3,4tetrahydroisoquinoline-6,7-diol (norlaudanosoline or tetrahydropapaveroline or THP) and 1-benzyl-1,2,3,4tetrahydroisoquinoline (1BnTIQ) are considered as those endowed with the most potent neurotoxic actions. However, it remains to be established whether a continuous exposure to TIQs or to their metabolites might carry toxicological consequences in the short-or long-term period. Remarkably, recent findings suggest that some TIQs such as (1-[(4-hydroxyphenyl)methyl]-1,2,3,4tetrahydroisoquinoline-6,7-diol) (higenamine) and 1-methyl-1,2,3,4-tetrahydroisoquinoline (1-MeTIQ) as well as N-methyltetrahydroisoquinoline (N-methyl-TIQ) exert unique neuroprotective and neurorestorative actions. The present review article provides an overview on these aspects of TIQs and summarizes those that presently appear the most significant highlights on this puzzling topic.

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Methylglyoxal increases dopamine level and leads to oxidative stress in SH-SY5Y cells

Cited by 21 publications

References 33 publications

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Role of the HIF‐1α/Nur77 axis in the regulation of the tyrosine hydroxylase expression by insulin in PC12 cells

Not Just from Ethanol. Tetrahydroisoquinolinic (TIQ) Derivatives: from Neurotoxicity to Neuroprotection

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