The Sources of Reactive Oxygen Species and Its Possible Role in the Pathogenesis of Parkinson’s Disease

Weng, Minrui; Xie, Xiaoji; Liu, Chao; Lim, Kah‐Leong; Zhang, Chengwu; Lin, Li

doi:10.1155/2018/9163040

Cited by 67 publications

(69 citation statements)

References 101 publications

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“…Mitochondrial dysfunction, genetic, and environmental factors can generate oxidative stress, and inflammation is a neuroprotective response to diverse types of tissue damage. If the tissue is inflamed, it causes an increase of ROS, which can lead to cell death [ 46 , 47 ]. The oxidative stress modifies the inflammatory response, thus, when there is a redox balance, the inflammatory response is a defense mechanism; when there is a redox imbalance, the signaling pathways that modulate the immune system are altered, leading to dysregulation of the immune response [ 48 ].…”

Section: Role Of Oxidative Stressmentioning

confidence: 99%

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Corona

2020

Antioxidants

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Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder of childhood. Although abnormalities in several brain regions and disturbances of the catecholaminergic pathway have been demonstrated, the pathophysiology of ADHD is not completely understood, but as a multifactorial disorder, has been associated with an increase in oxidative stress and neuroinflammation. This review presents an overview of factors that increase oxidative stress and neuroinflammation. The imbalance between oxidants and antioxidants and also the treatment with medications are two factors that can increase oxidative damage, whereas the comorbidity between ADHD and inflammatory disorders, altered immune response, genetic and environmental associations, and polymorphisms in inflammatory-related genes can increase neuroinflammation. Evidence of an association with these factors has become valuable for research on ADHD. Such evidence opens up new intervention routes for the use of natural products as antioxidants that could have potential as a treatment against oxidative stress and neuroinflammation in ADHD.

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Section: Role Of Oxidative Stressmentioning

confidence: 99%

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Corona

2020

Antioxidants

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“…However, this report is inconsistent with experiments published elsewhere [ 60 ]. Partial mitochondrial dysfunction, as seen in rho- yeast petites is linked to the symptoms of Parkinson’s disease (PD) [ 12 , 13 ]. Neuronal cell death in PD, as in α-syn-induced yeast apoptosis, occurs from complete loss of mitochondrial function [ 14 , 15 ].…”

Section: Resultsmentioning

confidence: 99%

“…Partial mitochondrial dysfunction, as seen in ρ − yeast petites, is linked to the symptoms of Parkinson’s disease (PD) [ 12 , 13 ]. Ρ − yeast cells also share greatly diminished activity of the mitochondrial electron transport chain with dopaminergic neurons of patients who have Parkinson’s disease (PD).…”

Section: Introductionmentioning

confidence: 99%

Apoptosis, Induced by Human α-Synuclein in Yeast, Can Occur Independent of Functional Mitochondria

Akintade

Chaudhuri

2020

Cells

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Human α-synuclein expression in baker’s yeast reportedly induces mitochondria-dependent apoptosis. Surprisingly, we find that, under de-repressing conditions of the inducible MET25/GAL1 promoters, yeast cells expressing chromosomally-integrated copies of the human α-synuclein gene are not killed, but spontaneously form respiration-deficient rho-minus (ρ−) petites. Although yeast cells can undergo cell death (apoptosis) from loss of mitochondrial function, they can also survive without functional mitochondria. Such cells are referred to as ρ0 or ρ− petites. This study reports that minimal expression of human α-synuclein in yeast, from MET25/GAL1 promoter, gives rise to ρ− petites. Interestingly, the full expression of α-synuclein, from the same promoters, in α-synuclein-triggered ρ− petites and also in ρ0 petites (produced by treating ρ+ cells with the mutagen ethidium bromide) initiates apoptosis. The percentages of petites increase with increasing α-synuclein gene copy-number. ρ− petites expressing α-synuclein from fully-induced MET25/GAL1 promoters exhibit increased ROS levels, loss of mitochondrial membrane potential, and nuclear DNA fragmentation, with increasing copies of α-synuclein. Our results indicate that, for the first time in yeast, α-synuclein-triggered apoptosis can occur independently of functional mitochondria. The observation that α-synuclein naturally forms petites and that they can undergo apoptosis may have important implications in understanding the pathogenesis of Parkinson’s disease.

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“…The pathogenic mechanisms of PD causing the degeneration of the nigrostriatal DA system still remain unclear, however, it is well known that the upregulation of risk factors is involved in the pathogenesis and progression of PD [ 4 , 5 , 6 , 7 ], and the following circumstances are highly responsible for the onset of PD: neuroinflammation [ 8 , 9 ], mismanagement of apoptosis [ 10 , 11 , 12 ] and autophagy [ 10 , 11 , 12 , 13 ], genetic mutations [ 5 , 14 ], neurotrophic support failure [ 6 , 8 , 15 , 16 , 17 ], and oxidative stress [ 5 , 18 , 19 ]. In particular, oxidative stress is considered to be a key risk factor of PD due to the vulnerability of DA neurons to oxidative stress caused by the excessive production of reactive oxygen species (ROS; free radicals) [ 14 , 20 , 21 ], resulting from the dopamine metabolism [ 22 , 23 ], mitochondrial dysfunction [ 14 , 19 , 24 ], neuroinflammation [ 3 , 8 , 9 , 25 ], and iron accumulation [ 26 , 27 ] in the SN.…”

Section: Introductionmentioning

confidence: 99%

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

et al. 2020

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Oxidative stress reflects an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense systems, and it can be associated with the pathogenesis and progression of neurodegenerative diseases such as multiple sclerosis, stroke, and Parkinson’s disease (PD). The application of antioxidants, which can defend against oxidative stress, is able to detoxify the reactive intermediates and prevent neurodegeneration resulting from excessive ROS production. There are many reports showing that numerous flavonoids, a large group of natural phenolic compounds, can act as antioxidants and the application of flavonoids has beneficial effects in the adult brain. For instance, it is well known that the long-term consumption of the green tea-derived flavonoids catechin and epigallocatechin gallate (EGCG) can attenuate the onset of PD. Also, flavonoids such as ampelopsin and pinocembrin can inhibit mitochondrial dysfunction and neuronal death through the regulation of gene expression of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Additionally, it is well established that many flavonoids exhibit anti-apoptosis and anti-inflammatory effects through cellular signaling pathways, such as those involving (ERK), glycogen synthase kinase-3β (GSK-3β), and (Akt), resulting in neuroprotection. In this review article, we have described the oxidative stress involved in PD and explained the therapeutic potential of flavonoids to protect the nigrostriatal DA system, which may be useful to prevent PD.

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The Sources of Reactive Oxygen Species and Its Possible Role in the Pathogenesis of Parkinson’s Disease

Cited by 67 publications

References 101 publications

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Role of Oxidative Stress and Neuroinflammation in Attention-Deficit/Hyperactivity Disorder

Apoptosis, Induced by Human α-Synuclein in Yeast, Can Occur Independent of Functional Mitochondria

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

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