Peripheral Blood Markers of Oxidative Stress in Parkinson’s Disease

Younes-Mhenni, S.; Frih-Ayed, M.; Kerkeni, Abdelhamid; Bost, M.; Carrault, Guy

doi:10.1159/000103641

Cited by 90 publications

(69 citation statements)

References 70 publications

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“…Altered redox status in PD has been demonstrated in studies of two potent antioxidants, coenzyme Q10 in blood 35,36 and CSF 37 and glutathione in plasma samples. 38 Oxidative damage to DNA has been demonstrated in PD by detection of elevated levels of 8-hydroxy-2-deoxyguanosine, …”

Section: Markers Of Oxidative Stress and Mitochondrial Dysfunctionmentioning

confidence: 99%

“…39,40 Markers of oxidative damage to lipids are similarly elevated. Malondialdehyde, formed as reactive oxygen species degrade polyunsaturated lipids, was found to be significantly increased in plasma levels in PD, 38,41 and plasma F(2)-isoprostanes (a fatty acid peroxidation product) and cholesterol oxidation products have been found to be elevated in PD. 42 Urate is included in this section since it is a potent antioxidant, as well as a metal chelator capable of binding iron.…”

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confidence: 96%

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Blood and cerebrospinal fluid markers in Parkinson's disease: current biomarker findings

Henchcliffe

2014

CBF

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Abstract:Parkinson's disease (PD) is a common, progressive, and disabling neurodegenerative movement disorder. Signs and symptoms begin insidiously and overlap with other neurodegenerative conditions, making diagnosis challenging in early disease. Moreover, there are as yet no established biomarkers that will objectively measure disease progression, and this hampers efforts to obtain neuroprotective therapies. At present, diagnosis, measurement of progression, and response to therapeutic intervention rely almost exclusively upon clinical observation. There remains, therefore, a critical need for validated biomarkers. Recent advances in understanding the underlying pathophysiology of PD have aided in identifying strong candidate markers to assist in diagnosis and evaluate progression. Pathways that are disrupted in PD include protein misfolding, mitochondrial dysfunction and increased oxidative stress, dysregulated inflammatory processes, and altered gene expression. For example, α-synuclein is a key contributor to PD pathology, in which misfolded and damaged α-synuclein accumulates in neurons; this is now a leading candidate as a PD biomarker in cerebrospinal fluid. There is also recent evidence that markers of Alzheimer's disease may be "repurposed" to provide information on PD diagnosis, prognosis, and nonmotor symptoms, including cognitive dysfunction. At the same time, increasingly sophisticated bioinformatics technology allows an unbiased approach to biomarker identification, for example, using proteomic, transcriptomic, and metabolomic analysis. Such generally accessible blood or cerebrospinal fluid tests, if successful, will likely lead to significant improvements in PD diagnosis, management, and research.

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Section: Markers Of Oxidative Stress and Mitochondrial Dysfunctionmentioning

confidence: 99%

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confidence: 96%

Blood and cerebrospinal fluid markers in Parkinson's disease: current biomarker findings

Henchcliffe

2014

CBF

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“…Specifically, we (10,11) and others (12)(13)(14)(15)(16) have used lymphocytes to understand the relationship between OS phenomena and PD. Previous studies have shown that ROT induced apoptosis in lymphocytes in a concentration-and time-dependent manner by a molecular signaling mechanism under standard G condition (i.e., 11 mM G, hereafter 11 G) (17).…”

Section: Introductionmentioning

confidence: 99%

Glucose promotes resistance in lymphocytes against oxidative stress-induced apoptosis through signaling and metabolic pathways. Implications for Parkinson’s disease

Bonilla-Rairez

Jiménez-Del-Río

Vélez-Pardo

2017

iatreia

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SUMMARYIntroduction: Parkinson's disease (PD) is a neurological disorder associated with the selective loss of dopaminergic (DAergic) neurons. Clinical data suggest that oxidative stress (OS) and dysregulation of glucose (G) metabolism are early events in PD. However, no data are available to explain the molecular connection between glucose metabolism, OS, and neuronal demise in PD. Human lymphocytes share a similar dopaminergic signaling mechanism with DAergic neurons. Further, rotenone (ROT) is a mitochondrial complex I inhibitor that selectively induces apoptosis through OS in dopaminergic neurons and lymphocytes. Thus, to test the hypothesis that G metabolism and OS are linked in dopaminergic system toxicity and PD, human lymphocytes were cultured with ROT in the presence or absence of various concentrations of glucose.

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“…Environmental toxins and genetic disorders associated with apoptosis and protein breakdown may also play a role [2,3]. Oxidative stress leads to the damage of extremely sensitive neurons and is an important factor in both the initiation and progression of PD.…”

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confidence: 99%

“…The listed properties of propofol suggest that it may have protective effects that are relevant to neurodegenerative disease. Accounting for the special role of oxidative stress in the pathogenesis of PD, it has been suggested that future treatments will include antioxidant therapy [3,6]. The present study aimed to evaluate selected parameters of the liver oxidativeantioxidative system in a Wistar rat model of Parkinson's disease treated with propofol.…”

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confidence: 99%

Effects of Propofol on the Liver Oxidative-Antioxidant Balance in a Rat Model of Parkinson’s Disease

Romuk¹,

Szczurek²,

Nowak³

et al. 2016

Adv Clin Exp Med

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ing potentiation of lipid peroxidation, reduction in the concentrations of reduced glutathione and antioxidant enzyme activity, increased malondialdehyde concentration, and disruption of iron metabolism. Environmental toxins and genetic disorders associated with apoptosis and protein breakdown may also play a role [2,3]. Oxidative stress leads to the damage of extremely sensitive neurons and is an important factor in both the initiation and progression of PD. This damage is revealed by increases in either the oxidation or reduction activity of enzymes with antioxidant activity. These changes to the oxidation-antioxidant system may also simultaneously affect both oxidation and reduction Parkinson's disease (PD) is a chronic, progressive neurodegenerative disorder affecting 1% of the population over the age of 55, and the risk of PD is significantly increased in the elderly [1]. As PD progresses, dopaminergic neurons in the substantia nigra of the midbrain are lost as a result of the progressive degenerative process revealed by a reduction in dopamine levels in this structure [2]. Despite years of research, the pathogenesis of PD is not fully understood, although many factors are thought to be involved. One hypothesis is that PD is caused by increased oxidative stress. Roles for the oxidation-oxidant system in other disorders have been confirmed by numerous studies demonstrat- Objectives. The present study aimed to evaluate selected parameters of the liver oxidative-antioxidative system in a Wistar rat model with Parkinson's disease treated with propofol. Material and Methods. Experiments were performed on 32 rats divided into 4 groups: 1 -control, 2 -Parkinson's disease, 3 -control with propofol, 4 -Parkinson's disease with propofol. The rats were decapitated at 8 weeks of age and their livers were collected. In the liver, the activities of catalase (CAT), glutathione peroxidase (GPx), glutathione transferase (GST), glutathione reductase (GR) and the concentrations of: Malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS) were assessed. Results. The study demonstrated a decrease in CAT activity and an increase in MDA, TOS concentrations in group 2 compared to that of group 1. Administration of propofol in rats of group 4 caused an increase in CAT activity and a decrease in MDA concentration compared to that of group 2 and an increase in TAC, CAT, GR levels, decrease in MDA levels compared to that of group 1. There was also an increase in GR and TAC in group 3 compared to that of group 1. Conclusions. Propofol in Parkinson's disease stimulates the production of antioxidant enzymes in the liver, simultaneously decreasing oxidative stress, which has a beneficial effect on the oxidative-antioxidative balance (Adv Clin Exp Med 2016, 25, 5, 815-820).

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Peripheral Blood Markers of Oxidative Stress in Parkinson’s Disease

Cited by 90 publications

References 70 publications

Blood and cerebrospinal fluid markers in Parkinson's disease: current biomarker findings

Blood and cerebrospinal fluid markers in Parkinson's disease: current biomarker findings

Glucose promotes resistance in lymphocytes against oxidative stress-induced apoptosis through signaling and metabolic pathways. Implications for Parkinson’s disease

Effects of Propofol on the Liver Oxidative-Antioxidant Balance in a Rat Model of Parkinson’s Disease

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Peripheral Blood Markers of Oxidative Stress in Parkinson’s Disease

Cited by 90 publications

References 70 publications

Blood and cerebrospinal fluid markers in Parkinson&#39;s disease: current biomarker findings

Blood and cerebrospinal fluid markers in Parkinson&#39;s disease: current biomarker findings

Glucose promotes resistance in lymphocytes against oxidative stress-induced apoptosis through signaling and metabolic pathways. Implications for Parkinson’s disease

Effects of Propofol on the Liver Oxidative-Antioxidant Balance in a Rat Model of Parkinson’s Disease

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Blood and cerebrospinal fluid markers in Parkinson's disease: current biomarker findings

Blood and cerebrospinal fluid markers in Parkinson's disease: current biomarker findings