Oxidative damage and cytogenetic analysis in leukocytes of Parkinson’s disease patients

Migliore, Lucia; Petrozzi, Lucia; Lucetti, Claudio; Gambaccini, G; Bernardini, Silvia; Scarpato, Roberto; Trippi, F.; Barale, Roberto; Frenzilli, Giada; Rodilla, Vicente; Bonuccelli, Ubaldo

doi:10.1212/wnl.58.12.1809

Cited by 139 publications

(76 citation statements)

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“…There is a plethora of clinical and experimental data indicating that oxidative cell damage attributable to either ROS or NOderived reactive species is central to PD and other neurodegenerative diseases (Perry and Yong, 1986;Dexter et al, 1987;Sofic et al, 1991;Alam et al, 1997;Pearce et al, 1997;Knott et al, 2000;Migliore et al, 2002;Kunikowska and Jenner, 2003). In recent years, several genetically engineered mouse lines have been examined for their ability to model the pathology of PD.…”

Section: Discussionmentioning

confidence: 99%

“…Selective decreases in reduced glutathione (GSH) (Perry and Yong, 1986;Pearce et al, 1997), mitochondrial complex I activity (Parker et al, 1989;Schapira et al, 1990;Tieu et al, 2004) and reactive oxygen species (ROS)-destroying enzymes (Kunikowska and Jenner, 2003) or elevated concentrations of iron, which can act as a catalyst for detrimental oxidative reactions (Dexter et al, 1987;Sofic et al, 1991), have been reported within the parkinsonian SN. In addition, there is evidence of oxidative damage to lipids, proteins, and DNA in the brains and leukocytes of PD patients (Alam et al, 1997;Migliore et al, 2002). Inflammatory-related events, such as nitric oxide (NO)-derived reactive species produced by glial inducible NO synthase (iNOS), appear also to participate in SN dopaminergic degeneration (Liberatore et al, 1999;Chung et al, 2004;Yao et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotection by Transgenic Expression of Glucose-6-Phosphate Dehydrogenase in Dopaminergic Nigrostriatal Neurons of Mice

Mejı́as¹,

Villadiego²,

Pintado³

et al. 2006

J. Neurosci.

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Oxidative damage to dopaminergic nigrostriatal (DNS) neurons plays a central role in the pathogenesis of Parkinson's disease (PD).Glucose-6-phosphate dehydrogenase (G6PD) is a key cytoprotective enzyme that provides NADPH, the major source of the reducing equivalents of a cell. Mutations of this enzyme are the most common enzymopathies worldwide. We have studied in vivo the role of G6PD overexpressed specifically in the DNS pathway and show that the increase of G6PD activity in the soma and axon terminals of DNS neurons, separately from other neurons or glial cells, protects them from parkinsonism. Analysis of DNS neurons by histological, neurochemical, and functional methods showed that even a moderate increase of G6PD activity rendered transgenic mice more resistant than control littermates to the toxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The neuroprotective action of G6PD was also observed in aged animals despite that they had a greater susceptibility to MPTP. Therefore, overexpression of G6PD in dopaminergic neurons or pharmacological activation of the native enzyme should be considered as potential therapeutic strategies to PD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuroprotection by Transgenic Expression of Glucose-6-Phosphate Dehydrogenase in Dopaminergic Nigrostriatal Neurons of Mice

Mejı́as¹,

Villadiego²,

Pintado³

et al. 2006

J. Neurosci.

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“…An increase in oxidative damage to DNA was also reported in leukocytes, serum, and CSF of PD patients Migliore et al, 2002). An increase in 3-nitrotyrosine immunoreactivity was reported in Lewy bodies in PD .…”

Section: Oxidative Damage In Pdmentioning

confidence: 82%

Perioperative Neuroprotection Symposium

Fiskum¹

2004

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Public reporting burden for this collection of information is estimated to average 1 hour par the data needed, and completing and reviewing this collection of information. Send conranls reducing this burden to Washington Headquarters Services. Directorate for Information Operations Management and Budget, Paperwork Reduction Protect (0704-01681. Washington, DC 20803Indudkig the «ma for reviewing instructions, searching existing data sources, gathering and maintaining tMs burden estimate or any other aspect of this ooHecMon of information, including suggestions for 1218 Jefferson Davis Highway, Suite 1204, Arttngton, VA 22202-4302, and to the Office of AGENCY USE ONLY (Leave blank) REPORT DATE June 2004 REPORT TYPE AND DATES COVERED Final Proceedings (13 Sep 03-22 May 04) TITLE AND SUBTITLE Perioperative Neuroprotection Symposium AUTHOR(S)Gary Fiskum, Ph.D. S. FUNDING NUMBERS DAMD17-03-1-0500 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)University of Maryland, Baltimore Baltimore, MD 21201 E-Mail: gfisk001@umaryland.edu PERFORMING ORGANIZATION REPORT NUMBER SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSORING / MONITORING AGENCY REPORT NUMBER SUPPLEMENTARY NOTESOriginal contains color plates: ALL DTIC reproductions will be in black and white 12a. DISTRIBUTION / AVAILABILITY STATEMENT Approved for Public Release; Distribution Unlimited 12b. DISTRIBUTION CODE A-TRACT IMaiiliwyiH 200 VVwW)The Perioperative Neuroprotection Symposium was held on April 16-19 in Ft. Lauderdale, Fl. The meeting was attended by approximately 140 registrant». Twenty four invited speakers made presentations in five sessions. An additional 40 poster presentations were^available for discussion throughout the meeting. Each participant received a symposium abstract book that included mini-reviews from each of the speakers and the short abstracts from the posters. The speakers also submitted formal manuscripts for peer-reviewed publication.Five of the poster presenters were also invited to submit short research manuscripts. Mitochondria and Neuroprotection Symposium April [16][17][18][19] 2004 Albert Lester Lehninger February 17,1917-March4,1986 Albert Lehninger was born in Bridgeport, Connecticut and received a B.A. in English from Wesleyan University in 1939. He received his Ph.D. in Physiological Chemistry from the University of Wisconsin in 1942. Lehninger stayed on at the Univ. of Wisconsin as an Instructor until 1945, when he was appointed Assistant Professor of Biochemistry and Surgery at the University of Chicago. At this juncture he had published 11 research articles. From 1945From -1952, he published an additional 33 articles. These studies included the discovery that fatty acid oxidation, ketone body metabolism, and the TCA cycle occur in the mitochondrion, some of the first investigations employing isolation of this organelle (see e.g., JBC1949 and 1950). Thus, while Lehninger was a chemist at heart, he was one of the founding father...

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“…Moreover, the accelerated metabolism of dopamine by monoamine-oxidase-B may induce an excessive formation of hydrogen peroxide, superoxide anions, and hydroxyl radicals, which not only maintain the oxidative stress level, but also initiate/propagate apoptosis of the dopaminergic neurons [76]. According to the reports in the pertinent literature, Parkinson's disease is associated with increased oxidative damage to DNA [77], proteins [78] and lipids [79].…”

Section: Parkinson's Diseasementioning

confidence: 99%

Review Article: Oxidative Stress Versus Antioxidants

Al-Dalaen¹

2014

BIO

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Abstract:Oxidative stress is a phenomenon that reflects an imbalance between the production of reactive oxygen species and so-called oxidants, and their elimination by protective mechanisms. These are referred to as antioxidative systems which can detoxify the reactive intermediates, or repair the resulting damage causing toxic effects through the production of peroxides and free radicals that damage all cell components. Further, some reactive oxidative species act as cellular messengers in redox signaling that can cause disruptions in normal cellular signaling mechanisms. In humans, oxidative stress is thought to be involved in the development of atherosclerosis, neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, cancer, diabetes mellitus, inflammatory diseases, as well as psychological diseases or aging processes. It is presently accepted that the reactive oxygen species can be beneficial. Depending on the type of oxidants, intensity and time of redox imbalance, as well as on the type of cells, oxidative stress can play a role in the regulation of other important processes. This is achieved through modulation of signal pathways, influencing synthesis of antioxidant enzymes, repair processes, inflammation, or via the immune system, as a way to attack and kill pathogens. This limits the potential for apoptosis and cell proliferation, and thus affects malignant processes. Imprudent administration of antioxidants may therefore have a negative impact on the organism.

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Oxidative damage and cytogenetic analysis in leukocytes of Parkinson’s disease patients

Abstract: There is chromosomal, primary DNA damage and oxidative DNA damage demonstrable in lymphocytes of patients with untreated PD.

Cited by 139 publications

References 56 publications

Neuroprotection by Transgenic Expression of Glucose-6-Phosphate Dehydrogenase in Dopaminergic Nigrostriatal Neurons of Mice

Neuroprotection by Transgenic Expression of Glucose-6-Phosphate Dehydrogenase in Dopaminergic Nigrostriatal Neurons of Mice

Perioperative Neuroprotection Symposium

Review Article: Oxidative Stress Versus Antioxidants

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