Increased erythrocyte susceptibility to lipid peroxidation in human Parkinson's disease

Kilinç, Ahmet; Yalçın, A. Süha; Yalcin, Destina; Taga, Yavuz; Emerk, Kaya

doi:10.1016/0304-3940(88)90467-3

Cited by 51 publications

(18 citation statements)

References 11 publications

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“…Results of peripheral studies have been contradictory. Several studies support our findings with increased levels in CSF [25], plasma [37] and blood [25, 27] of PD patients. However, some studies have shown no differences in serum [42, 43] or erythrocyte [44] MDA levels between PD patients and controls.…”

Section: Discussionsupporting

confidence: 80%

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Peripheral Blood Markers of Oxidative Stress in Parkinson’s Disease

et al. 2007

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Oxidative stress and generation of reactive oxygen species are believed to be implicated in Parkinson’s disease (PD). Erythrocyte activity of superoxide dismutase (SOD) and catalase, the blood glutathione system, and plasma levels of thiobarbituric-acid-reactive substances (TBARS) were measured in 80 PD patients. These biochemical parameters were also measured in 29 age-matched controls. Patients with PD had significantly higher red blood corpuscle (RBC) activity of SOD. The mean RBC activity of catalase in PD patients did not differ significantly from those of controls. RBC catalase activity was significantly lower in advanced cases of PD compared to early cases. Oxidized glutathione was significantly higher in RBCs of PD patients, although there were no changes in total glutathione and reduced glutathione compared to controls. TBARS content was increased in patients with PD. Levodopa therapy, age and duration of illness did not significantly influence the measured parameters. Our study supports the previous hypothesis that oxidative stress is implicated in the pathogenesis of PD. Perspectives for treatment of PD in the future could include antioxidant therapy.

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Section: Discussionsupporting

confidence: 80%

“…Kilinc et al [37] and Sudha et al [32] indicated no significant change in erythrocyte catalase activity of PD patients compared to controls. Catalase in peripheral blood leukocytes appeared to be unaltered in the study of Marttila et al [33].…”

Section: Discussionmentioning

confidence: 99%

Peripheral Blood Markers of Oxidative Stress in Parkinson’s Disease

et al. 2007

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“…The interaction of this systemic defect with the usual dopamine-generated oxidant stress within the substantia nigra could result in degeneration of this nucleus and, consequently, Parkinson's disease. As evidence, Kilinc et al (15) and Kalra et al (16) reported elevated concentrations of malondialdehyde in the circulation of patients with Parkinson's disease. Malondialdehyde is a product of peroxidative attack of oxygen free radicals on lipid membranes.…”

Section: Discussionmentioning

confidence: 95%

No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease

et al. 1995

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Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemical abnormalities extending beyond the central nervous system have been identified in patients with this condition. Previous investigators have found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Parkinson's disease. We attempted to replicate these findings but controlled for other factors that could influence malondialdehyde levels. We detected no significant elevations in mean serum malondialdehyde concentrations in either levodopa-treated or untreated patients with Parkinson's disease, compared to normal controls; similarly, no elevation was found in a group of patients with dementia of Alzheimer's type. On the other hand, a group of subjects with diabetes mellitus but no neurodegenerative disease had significantly elevated mean serum malondialdehyde levels, consistent with previous studies of diabetic patients. Autoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxidation product of dopa, 5-S-cysteinyl-dopa, in the plasma of these same groups of patients with neurodegenerative disease and normal controls; no significant differences were identified. Serum concentrations of two other antioxidant substances, alpha-tocopherol and uric acid, were also statistically similar in these groups. In conclusion, analysis of several blood products relevant to oxidant stress, including malondialdehyde, 5-S-cysteinyl-dopa, alpha-tocopherol, and uric acid, failed to distinguish patients with Parkinson's disease or dementia of Alzheimer's type from controls.

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“…In substantia nigra, increased iron levels (Sofic et al, 1988;Dexter et al, 1989;Riederer et a!., 1989), decreased levels of GSH (Perry and Young, 1986;Sofic et al, 1992;Sian et al, 1994), increased activity of superoxide dismutase (Saggu et al, 1989), decreased activity of complex I of the mitochondrial respiratory chain (Schapira et al, 1990a ,b), and elevated concentrations of the lipid peroxidation product malondialdehyde (MDA) have been observed. There are also claims that plasma (Kilinc et al, 1988) and serum (Kalra et al, 1992) MDA are increased in PD patients, but Ahlskog et al…”

mentioning

confidence: 99%

Oxidative DNA Damage in the Parkinsonian Brain: An Apparent Selective Increase in 8‐Hydroxyguanine Levels in Substantia Nigra

Alam

Jenner

Daniel

et al. 1997

Journal of Neurochemistry

764

460

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Abstract:Oxidative damage has been implicated in the pathology of Parkinson's disease (PD), eg., rises in the level of the DNA damage product, 8-hydroxy-2 '-deoxyguanosine, have been reported. However, many other products result from oxidative DNA damage, and the pattern of products can be diagnostic of the oxidizing species. Gas chromatography/mass spectrometry was used to examine products of oxidation and deamination of all four DNA bases in control and PD brains. Products were detected in all brain regions examined, both normal and PD. Analysis showed that levels of 8-hydroxyguanine (8-OHG) tended to be elevated and levels of 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FAPy guanine) tended to be decreased in PD. The most striking difference was a rise in 8-OHG in PD substantia nigra (p = 0.0002); rises in other base oxidation/deamination products were not evident, showing that elevation in 8-OHG is unlikely to be due to peroxynitrite (0N00) or hydroxyl radicals (0H), or to be a prooxidant effect of treatment with L-Dopa. However, some or all of the rise in 8-OHG could be due to a change in 8-OHG/FAPy guanine ratios rather than to an increase in total oxidative guanine damage. Key Words: Parkinson's diseaseOxidative damage-8-Hydroxyguanosine-Substantia nigra.

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Increased erythrocyte susceptibility to lipid peroxidation in human Parkinson's disease

Cited by 51 publications

References 11 publications

Peripheral Blood Markers of Oxidative Stress in Parkinson’s Disease

Peripheral Blood Markers of Oxidative Stress in Parkinson’s Disease

No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease

Oxidative DNA Damage in the Parkinsonian Brain: An Apparent Selective Increase in 8‐Hydroxyguanine Levels in Substantia Nigra

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