scholarly journals Free Radicals, Oxidative Stress and Oxidative Damage in Parkinson's Disease

10.5772/20133 ◽  
2012 ◽  
Author(s):  
Marisa G. ◽  
Ral O. ◽  
Enrique R. ◽  
Jorge A.
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Free Radicals ◽  
Oxidative Damage

scholarly journals Kajian potensi antioksidan dari tanaman herbal dan pengaruhnya terhadap penyakit Parkinson

2021 ◽  
Vol 17 (1) ◽  
pp. 80-95
Author(s):  
Indri Nuraeni Pratiwi ◽  
◽  
Widhya Aligita ◽  
Marita Kaniawati ◽  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Free Radicals ◽  
Neurodegenerative Disorder ◽  
Natural Antioxidants ◽  
Muscle Stiffness ◽  
Literature Study ◽  
Neuron Damage ◽  
Herbal Plants

Background: Parkinson's disease is the most common neurodegenerative disorder affecting more than 10 million people worldwide. This disease is characterized by progressive dopaminergic neuron damage in the substantia nigra. This damage can be triggered by aging and the presence of oxidative stress because of free radicals. Antioxidants can inhibit the formation of free radicals and reduce oxidative stress, so they can be used as an alternative treatment for Parkinson's disease. Objective: This review article aimed to provide information about the antioxidant effects of selected herbal plants on Parkinson's disease. Method: This study used literature study methods sourced from national and international scientific journals published in the last 5 years (2016-2020). Literature search were carried out using databases such as Google Scholar, PubMed®, ScienceDirect, and Garuda Portal. Results: The high content of antioxidants in plants could protect nerve cells from oxidative damage and reduce symptoms such as tremors, muscle stiffness, impaired coordination and motor balance in test animals. Conclusion: Natural antioxidants from herbal plants proved to be able to prevent oxidative stress caused by free radicals and reduce symptoms of Parkinson's disease. Keywords: Parkinson's disease, antioxidants, oxidative stress, herbal plants

scholarly journals Protective Effects of an Ancient Chinese Kidney-Tonifying Formula against H2O2-Induced Oxidative Damage to MES23.5 Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-9
Author(s):  
Yihui Xu ◽  
Wei Lin ◽  
Shuifen Ye ◽  
Huajin Wang ◽  
Tingting Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Critical Role ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Transmission Electron ◽  
Potential Strategy

Oxidative damage plays a critical role in the etiology of neurodegenerative disorders including Parkinson’s disease (PD). In our study, an ancient Chinese kidney-tonifying formula, which consists ofCistanche,Epimedii,andPolygonatum cirrhifolium, was investigated to protect MES23.5 dopaminergic neurons against hydrogen peroxide- (H2O2-) induced oxidative damage. The damage effects of H2O2on MES23.5 cells and the protective effects of KTF against oxidative stress were evaluated using MTT assay, transmission electron microscopy (TEM), immunocytochemistry (ICC), enzyme-linked immunosorbent assay (ELISA), and immunoblotting. The results showed that cell viability was dramatically decreased after a 12 h exposure to 150 μM H2O2. TEM observation found that the H2O2-treated MES23.5 cells presented cellular organelle damage. However, when cells were incubated with KTF (3.125, 6.25, and 12.5 μg/ml) for 24 h after H2O2exposure, a significant protective effect against H2O2-induced damage was observed in MES23.5 cells. Using ICC, we found that KTF inhibited the reduction of the tyrosine hydroxylase (TH) induced by H2O2, upregulated the mRNA and protein expression of HO-1, CAT, and GPx-1, and downregulated the expression of caspase 3. These results indicated that KTF may provide neuron protection against H2O2-induced cell damage through ameliorating oxidative stress, and our findings provide a new potential strategy for the prevention and treatment of Parkinson’s disease.

scholarly journals Mitophagy of damaged mitochondria occurs locally in distal neuronal axons and requires PINK1 and Parkin

2014 ◽  
Vol 206 (5) ◽  
pp. 655-670 ◽  
Author(s):  
Ghazaleh Ashrafi ◽  
Julia S. Schlehe ◽  
Matthew J. LaVoie ◽  
Thomas L. Schwarz
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Retrograde Transport ◽  
Mitochondrial Damage ◽  
Lysosomal Degradation ◽  
Associated Proteins

To minimize oxidative damage to the cell, malfunctioning mitochondria need to be removed by mitophagy. In neuronal axons, mitochondrial damage may occur in distal regions, far from the soma where most lysosomal degradation is thought to occur. In this paper, we report that PINK1 and Parkin, two Parkinson’s disease–associated proteins, mediate local mitophagy of dysfunctional mitochondria in neuronal axons. To reduce cytotoxicity and mimic physiological levels of mitochondrial damage, we selectively damaged a subset of mitochondria in hippocampal axons. Parkin was rapidly recruited to damaged mitochondria in axons followed by formation of LC3-positive autophagosomes and LAMP1-positive lysosomes. In PINK1−/− axons, damaged mitochondria did not accumulate Parkin and failed to be engulfed in autophagosomes. Similarly, initiation of mitophagy was blocked in Parkin−/− axons. Our findings demonstrate that the PINK1–Parkin-mediated pathway is required for local mitophagy in distal axons in response to focal damage. Local mitophagy likely provides rapid neuroprotection against oxidative stress without a requirement for retrograde transport to the soma.

Iron-Melanin Interaction and Parkinson's Disease

Physiology ◽  
1993 ◽  
Vol 8 (1) ◽  
pp. 45-49 ◽  
Author(s):  
MBH Youdim ◽  
D Ben-Shachar ◽  
P Riederer
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Free Radicals ◽  
Substantia Nigra ◽  
Oxygen Free Radicals

There now is evidence for oxidative stress in the substantia nigra in brains of patients with Parkinson's disease that may be initiated either by an excessive generation of oxygen free radicals and/or a diminution of scavenging radicals. Evidence for participation of iron and melanin in these processes is described.

Mitochondria as an Easy Target to Oxidative Stress Events in Parkinson's Disease

2012 ◽  
Vol 11 (4) ◽  
pp. 430-438 ◽  
Author(s):  
Marcella Reale ◽  
Mirko Pesce ◽  
Medha Priyadarshini ◽  
Mohammad A Kamal ◽  
Antonia Patruno
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease

scholarly journals The Contribution of Microglia to Neuroinflammation in Parkinson’s Disease

2021 ◽  
Vol 22 (9) ◽  
pp. 4676
Author(s):  
Katja Badanjak ◽  
Sonja Fixemer ◽  
Semra Smajić ◽  
Alexander Skupin ◽  
Anne Grünewald
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Cytokine ◽  
Population Ageing ◽  
Future Research ◽  
Cytokine Release ◽  
Vicious Cycle ◽  
Inflammatory Processes ◽  
Great Evidence

With the world’s population ageing, the incidence of Parkinson’s disease (PD) is on the rise. In recent years, inflammatory processes have emerged as prominent contributors to the pathology of PD. There is great evidence that microglia have a significant neuroprotective role, and that impaired and over activated microglial phenotypes are present in brains of PD patients. Thereby, PD progression is potentially driven by a vicious cycle between dying neurons and microglia through the instigation of oxidative stress, mitophagy and autophagy dysfunctions, a-synuclein accumulation, and pro-inflammatory cytokine release. Hence, investigating the involvement of microglia is of great importance for future research and treatment of PD. The purpose of this review is to highlight recent findings concerning the microglia-neuronal interplay in PD with a focus on human postmortem immunohistochemistry and single-cell studies, their relation to animal and iPSC-derived models, newly emerging technologies, and the resulting potential of new anti-inflammatory therapies for PD.

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