Impact of Amyloid ß25-35 on Membrane Stability, Energy Metabolism, and Antioxidant Enzymes in Erythrocytes
Amyloid ß25-35 (Aß25-35) represents a neurotoxic fragment of Aß1-40 or Aß1-42, and is implicated in the progressive neurodegeneration in cases of the Alzheimer disease (AD). Amyloid ß25-35 was shown to lyse rat erythrocytes (RBCs) of all ages, and the extent of the RBC toxicity is directly correlated with Aß25-35 concentration and cell age. Activities of glycolytic, antioxidant, and Na+/K+-adenosine triphosphatase (ATPase) enzymes, in vivo, are significantly decreased in older RBCs as compared to the young RBCs. In vitro, Aß25-35 reduced activities of hexokinase, phosphofructokinase, pyruvate kinase, glutathione peroxidase, and glutathione transferase and increased Na+/K+-ATPase activity; these effects are significantly greater in aged RBCs as compared to those of the younger cells. The diminution in activity of certain enzymes may determine the life span of the RBCs in vivo and may be relevant to the human AD; higher sensitivity of older RBCs to Aß25-35 toxicity may contribute to the ultimate death of the RBCs in patients with AD.
L. A. Tikhonova et al., "Impact of Amyloid ß25-35 on Membrane Stability, Energy Metabolism, and Antioxidant Enzymes in Erythrocytes," American Journal of Alzheimer's Disease and other Dementias, vol. 29, no. 8, pp. 685-695, SAGE Publications Inc., Dec 2014.
The definitive version is available at http://dx.doi.org/10.1177/1533317514534757
Keywords and Phrases
Alzheimer Disease; Antioxidant Enzymes; Energy Metabolism; Erythrocytes; Membrane Stability
International Standard Serial Number (ISSN)
Article - Journal
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