Circulating plasma factors in Parkinson’s disease enhance nitric oxide release of normal human neutrophils

Gatto, Emilia; Riobó, Natalia A.; Carreras, Marı́a Cecilia; Schöpfer, Francisco J.; Pargament, Griselda A.; Poderoso, Juan José

doi:10.1016/s0022-510x(99)00079-9

Cited by 10 publications

(6 citation statements)

References 20 publications

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“…However, NO may act as a neurotoxin and cause neuronal injury and death when inappropriate/excessive NO is produced in the brain [36], [38]–[40]. Moreover, there is increasing evidence that NO is involved in the pathogenesis of neurodegenerative diseases, including PD [41]–[43]. To date, NOS has four known isoforms: nNOS, iNOS, eNOS, and mitochondrial nitric oxide synthase [37], [44].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Tetrahydroxystilbene Glucoside on 6-OHDA-Induced Apoptosis in PC12 Cells through the ROS-NO Pathway

Tao

Zhang

et al. 2011

PLoS ONE

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Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson's disease. The molecule, 2,3,5,4′-tetrahydr- oxystilbene-2-O-β-D-glucoside (TSG), is a potent antioxidant derived from the Chinese herb, Polygonum multiflorum Thunb. In this study, we investigated the protective effect of TSG against 6-hydroxydopamine-induced apoptosis in rat adrenal pheochromocytoma PC12 cells and the possible mechanisms. Our data demonstrated that TSG significantly reversed the 6-hydroxydopamine-induced decrease in cell viability, prevented 6-hydroxydopamine-induced changes in condensed nuclei and decreased the percentage of apoptotic cells in a dose-dependent manner. In addition, TSG slowed the accumulation of intracellular reactive oxygen species and nitric oxide, counteracted the overexpression of inducible nitric oxide syntheses as well as neuronal nitric oxide syntheses, and also reduced the level of protein-bound 3-nitrotyrosine. These results demonstrate that the protective effects of TSG on rat adrenal pheochromocytoma PC12 cells are mediated, at least in part, by the ROS-NO pathway. Our results indicate that TSG may be effective in providing protection against neurodegenerative diseases associated with oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Tetrahydroxystilbene Glucoside on 6-OHDA-Induced Apoptosis in PC12 Cells through the ROS-NO Pathway

Tao

Zhang

et al. 2011

PLoS ONE

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“…It has been reported that PD patients have elevated RNS as indicated from increased levels of nitrite/nitrate in cerebral spinal fluid 5 and blood 6 . More specifically, in PD it has been reported that white blood cell-neutrophils have higher expression of nNOS and an increased ability to produce excess NO 7 . In fact, Kouti et al reported that serum levels of nitric oxide positively correlated with increased UPDRS scores (Universal Parkinson's disease rating scale) and duration of disease regardless of sex or age 6 ; however, these findings are contentious 8,9 .…”

mentioning

confidence: 99%

Nitrosative stress in Parkinson’s disease

Stykel

Ryan

2022

npj Parkinsons Dis.

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Parkinson’s Disease (PD) is a neurodegenerative disorder characterized, in part, by the loss of dopaminergic neurons within the nigral-striatal pathway. Multiple lines of evidence support a role for reactive nitrogen species (RNS) in degeneration of this pathway, specifically nitric oxide (NO). This review will focus on how RNS leads to loss of dopaminergic neurons in PD and whether RNS accumulation represents a central signal in the degenerative cascade. Herein, we provide an overview of how RNS accumulates in PD by considering the various cellular sources of RNS including nNOS, iNOS, nitrate, and nitrite reduction and describe evidence that these sources are upregulating RNS in PD. We document that over 1/3 of the proteins that deposit in Lewy Bodies, are post-translationally modified (S-nitrosylated) by RNS and provide a broad description of how this elicits deleterious effects in neurons. In doing so, we identify specific proteins that are modified by RNS in neurons which are implicated in PD pathogenesis, with an emphasis on exacerbation of synucleinopathy. How nitration of alpha-synuclein (aSyn) leads to aSyn misfolding and toxicity in PD models is outlined. Furthermore, we delineate how RNS modulates known PD-related phenotypes including axo-dendritic-, mitochondrial-, and dopamine-dysfunctions. Finally, we discuss successful outcomes of therapeutics that target S-nitrosylation of proteins in Parkinson’s Disease related clinical trials. In conclusion, we argue that targeting RNS may be of therapeutic benefit for people in early clinical stages of PD.

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“…A 50 % increase in NO production by polymorphonuclear leucocytes was reported in treated (L-DOPA) and untreated PD patients (32). In a follow-up study, neutrophils from healthy subjects were treated with plasma from PD patients, and a similar increase in NO production was observed (33). These studies point to the importance of plasma circulating factors in PD that may contribute and/or underlie pathophysiological changes.…”

Section: Discussionmentioning

confidence: 70%

Involvement of nitric oxide in Parkinson's disease: Emphasis on sex difference in prevalence

Taşkıran

Nazlıel

İrkeç

et al. 2003

Neuroscience Res Communica

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Parkinson's disease (PD) is characterized by severe movement disorders. Excessive production of reactive oxygen species has been implicated as a possible mediator of neurodegenerative changes in nigrostriatal neurons in PD. Nitric oxide (NO) has received substantial attention among pathophysiological factors underlying glutamate neurotoxicity in neurodgenerative disorders including PD. PD is more prevalent in men than in women by an approximate 3:2 ratio; the nitrergic systems are also more active in males than females. In this study, NOZ-+NOJ-(stable metabolites of NO) levels were determined in sera of PD patients (n=20) and control subjects (n=I6). NOz-+NOj-Levels were higher in PD patients compared to controls, and in males compared to females. Furthermore, there was a correlation between age and NO metabolites in females but not in males. These data support a role for NO in PD and provide further evidence for sex differences in NO activity that may underlie neurodegenerative disorders.

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Circulating plasma factors in Parkinson’s disease enhance nitric oxide release of normal human neutrophils

Cited by 10 publications

References 20 publications

Protective Effect of Tetrahydroxystilbene Glucoside on 6-OHDA-Induced Apoptosis in PC12 Cells through the ROS-NO Pathway

Protective Effect of Tetrahydroxystilbene Glucoside on 6-OHDA-Induced Apoptosis in PC12 Cells through the ROS-NO Pathway

Nitrosative stress in Parkinson’s disease

Involvement of nitric oxide in Parkinson's disease: Emphasis on sex difference in prevalence

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