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Impact of Amyloid β 25-35 on Membrane Stability, Energy Metabolism, and Antioxidant Enzymes in Erythrocytes

2014; SAGE Publishing; Volume: 29; Issue: 8 Linguagem: Inglês

10.1177/1533317514534757

1938-2731

Lyudmila Tikhonova, Yury G. Kaminsky, V. Prakash Reddy, Yi Li, Ilya Solomadin, Еlena Kosenko, Gjumrakch Aliev,

Drug Transport and Resistance Mechanisms

Amyloid β 25-35 (Aβ 25-35 ) represents a neurotoxic fragment of Aβ 1 - 40 or Aβ 1 - 42 , and is implicated in the progressive neurodegeneration in cases of the Alzheimer disease (AD). Amyloid β 25-35 was shown to lyse rat erythrocytes (RBCs) of all ages, and the extent of the RBC toxicity is directly correlated with Aβ 25-35 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, Aβ 25-35 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 Aβ 25-35 toxicity may contribute to the ultimate death of the RBCs in patients with AD.