Elevated levels of oxidative DNA damage in lymphocytes from patients with Alzheimer's disease

M Morocz, J Kalman, A Juhasz, I Sinko, AP McGlynn, Stephen Downes, Z Janka, I Rasko

Research output: Contribution to journalArticle

102 Citations (Scopus)

Abstract

Previous studies have provided evidence of the involvement of oxidative damage in the pathogenesis of Alzheimer's disease (AD). Although the role of oxidative stress in the aetiology of the disease is still not clear, the detection of an increased damage status in the cells of patients could have important therapeutic implications. The level of oxidative damage and repair capacity in peripheral lymphocytes of AD patients and of age-matched controls was determined by the Comet assay applied to freshly isolated blood samples with oxidative lesion-specific DNA repair endonucleases. This is less prone to errors arising from oxidative artifacts than chemical analytical methods; and is therefore a relatively reliable, as well as rapid method for assay of oxidative DNA damage in cells. Statistically significant elevations (P < 0.05) of oxidized purines were observed in nuclear DNA of peripheral lymphocytes from AD patients, compared. to age matched control subjects, both at basal level and after oxidative stress induced by H2O2. AD patients also showed a diminished repair of H2O2 -induced oxidized purines. (C) 2002 Elsevier Science Inc. All rights reserved.
LanguageEnglish
Pages47-53
JournalNeurobiology of Aging
Volume23
Issue number1
Publication statusPublished - Jan 2002

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DNA Damage
Alzheimer Disease
Lymphocytes
Purines
Oxidative Stress
Comet Assay
Deoxyribonuclease I
DNA Repair
Artifacts
DNA
Therapeutics

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Morocz, M., Kalman, J., Juhasz, A., Sinko, I., McGlynn, AP., Downes, S., ... Rasko, I. (2002). Elevated levels of oxidative DNA damage in lymphocytes from patients with Alzheimer's disease. Neurobiology of Aging, 23(1), 47-53.
Morocz, M ; Kalman, J ; Juhasz, A ; Sinko, I ; McGlynn, AP ; Downes, Stephen ; Janka, Z ; Rasko, I. / Elevated levels of oxidative DNA damage in lymphocytes from patients with Alzheimer's disease. In: Neurobiology of Aging. 2002 ; Vol. 23, No. 1. pp. 47-53.
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Morocz, M, Kalman, J, Juhasz, A, Sinko, I, McGlynn, AP, Downes, S, Janka, Z & Rasko, I 2002, 'Elevated levels of oxidative DNA damage in lymphocytes from patients with Alzheimer's disease', Neurobiology of Aging, vol. 23, no. 1, pp. 47-53.

Elevated levels of oxidative DNA damage in lymphocytes from patients with Alzheimer's disease. / Morocz, M; Kalman, J; Juhasz, A; Sinko, I; McGlynn, AP; Downes, Stephen; Janka, Z; Rasko, I.

In: Neurobiology of Aging, Vol. 23, No. 1, 01.2002, p. 47-53.

Research output: Contribution to journalArticle

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AB - Previous studies have provided evidence of the involvement of oxidative damage in the pathogenesis of Alzheimer's disease (AD). Although the role of oxidative stress in the aetiology of the disease is still not clear, the detection of an increased damage status in the cells of patients could have important therapeutic implications. The level of oxidative damage and repair capacity in peripheral lymphocytes of AD patients and of age-matched controls was determined by the Comet assay applied to freshly isolated blood samples with oxidative lesion-specific DNA repair endonucleases. This is less prone to errors arising from oxidative artifacts than chemical analytical methods; and is therefore a relatively reliable, as well as rapid method for assay of oxidative DNA damage in cells. Statistically significant elevations (P < 0.05) of oxidized purines were observed in nuclear DNA of peripheral lymphocytes from AD patients, compared. to age matched control subjects, both at basal level and after oxidative stress induced by H2O2. AD patients also showed a diminished repair of H2O2 -induced oxidized purines. (C) 2002 Elsevier Science Inc. All rights reserved.

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Morocz M, Kalman J, Juhasz A, Sinko I, McGlynn AP, Downes S et al. Elevated levels of oxidative DNA damage in lymphocytes from patients with Alzheimer's disease. Neurobiology of Aging. 2002 Jan;23(1):47-53.