Abstract
Subject age and brain oxidative stress play pivotal roles in Alzheimer disease (AD) pathology. Erythrocytes (red blood cells: RBC) are considered as passive “reporter cells” for the oxidative status of the whole organism, not active participants in mechanisms of AD pathogenesis and are not well studied in AD. The aim of this work is to assess whether the antioxidant status and energy state of RBC from elderly people change in AD. We measured levels of key products and enzymes of oxidative metabolism in RBC from AD (n = 12) and non-Alzheimer dementia (NA, n = 13) patients, as well as in cells from age-matched controls (AC, n = 14) and younger adult controls (YC, n = 14). Parameters of the adenylate system served to evaluate the energy state of RBC. In both aging and dementia, oxidative stress in RBC increased and exhibited elevated concentrations of H2O2 and organic hydroperoxides, decreased the GSH/GSSG ratio and glutathione-S-transferase activity. Reductions in the ATP levels, adenine nucleotide pool size (AN) and adenylate energy charge accompanied these oxidative disturbances. The patterns of changes in these indices between groups strongly correlated with each other, Spearman rank correlation coefficients being rs = 1.0 or -1.0 (p<0.01). Alterations of the RBC parameters of oxidative stress and adenylate metabolism were nonspecific and interpreted as age-related abnormalities. Decreased glutathione peroxidase activity in RBC may be considered as a new peripheral marker for AD.
Keywords: Alzheimer disease, aging, erythrocyte (red blood cells), oxidative stress, antioxidants, AD pathogenesis, adenylate system, glutathione-S-transferase, adenine nucleotide, peripheral marker
CNS & Neurological Disorders - Drug Targets
Title:Antioxidant Status and Energy State of Erythrocytes in Alzheimer Dementia: Probing for Markers
Volume: 11 Issue: 7
Author(s): Elena A. Kosenko, Gjumrakch Aliev, Lyudmila A. Tikhonova, Yi Li, Armenuhi C. Poghosyan and Yury G. Kaminsky
Affiliation:
Keywords: Alzheimer disease, aging, erythrocyte (red blood cells), oxidative stress, antioxidants, AD pathogenesis, adenylate system, glutathione-S-transferase, adenine nucleotide, peripheral marker
Abstract: Subject age and brain oxidative stress play pivotal roles in Alzheimer disease (AD) pathology. Erythrocytes (red blood cells: RBC) are considered as passive “reporter cells” for the oxidative status of the whole organism, not active participants in mechanisms of AD pathogenesis and are not well studied in AD. The aim of this work is to assess whether the antioxidant status and energy state of RBC from elderly people change in AD. We measured levels of key products and enzymes of oxidative metabolism in RBC from AD (n = 12) and non-Alzheimer dementia (NA, n = 13) patients, as well as in cells from age-matched controls (AC, n = 14) and younger adult controls (YC, n = 14). Parameters of the adenylate system served to evaluate the energy state of RBC. In both aging and dementia, oxidative stress in RBC increased and exhibited elevated concentrations of H2O2 and organic hydroperoxides, decreased the GSH/GSSG ratio and glutathione-S-transferase activity. Reductions in the ATP levels, adenine nucleotide pool size (AN) and adenylate energy charge accompanied these oxidative disturbances. The patterns of changes in these indices between groups strongly correlated with each other, Spearman rank correlation coefficients being rs = 1.0 or -1.0 (p<0.01). Alterations of the RBC parameters of oxidative stress and adenylate metabolism were nonspecific and interpreted as age-related abnormalities. Decreased glutathione peroxidase activity in RBC may be considered as a new peripheral marker for AD.
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Cite this article as:
A. Kosenko Elena, Aliev Gjumrakch, A. Tikhonova Lyudmila, Li Yi, C. Poghosyan Armenuhi and G. Kaminsky Yury, Antioxidant Status and Energy State of Erythrocytes in Alzheimer Dementia: Probing for Markers, CNS & Neurological Disorders - Drug Targets 2012; 11 (7) . https://dx.doi.org/10.2174/1871527311201070926
DOI https://dx.doi.org/10.2174/1871527311201070926 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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