Role of glycolysis and antioxidant enzymes in the toxicity of amyloid beta peptide Abeta25-35 to erythrocytes

• Published in: Bioorganicheskaia khimiia Vol. 34; no. 5; p. 654
• Main Authors: Kosenko, E A, Solomadin, I N, Marov, N V, Venediktova, N I, Pogosian, A S, Kaminskiĭ, Iu G
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01-09-2008
• Subjects: Amyloid beta-Peptides - physiology; Amyloid beta-Peptides - toxicity; Animals; Antioxidants - metabolism; Catalase - antagonists & inhibitors; Culture Media; Erythrocytes - cytology; Erythrocytes - drug effects; Erythrocytes - enzymology; Fullerenes - pharmacology; Glucose - metabolism; Glutathione Peroxidase - antagonists & inhibitors; Glycolysis; Humans; In Vitro Techniques; Ouabain - pharmacology; Peptide Fragments - physiology; Peptide Fragments - toxicity; Potassium Cyanide - pharmacology; Rats; Sodium Azide - pharmacology; Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors; Species Specificity; Superoxide Dismutase - antagonists & inhibitors; Thiomalates - pharmacology; Young Adult
• ISSN: 0132-3423

The role of glycolysis and antioxidant enzymes in amyloid beta peptide Abeta(25-35) toxicity to human and rat erythrocytes was studied. The erythrotoxicity of Abeta(25-35) was shown to increase two- to fourfold both in the absence of glucose in the incubation medium and upon the addition of sodium fluoride, an enolase inhibitor. Potassium cyanide, a Cu,Zn-superoxide dismutase inhibitor, abolishes the toxic effect of Abeta(25-35) to erythrocytes, whereas mercaptosuccinate, a glutathione peroxidase inhibitor, and ouabain, a Na+,K+-ATPase inhibitor, promote it. Sodium azide, a catalase inhibitor, did not affect the cell lysis under the action of Abeta(25-35) . The results support the hypothesis that H2O2, Cu,Zn superoxide dismutase, and glutathione peroxidase are involved in the toxicity mechanism rather than superoxide radical. Glycolysis and Na+,K+-ATPase play a substantial protective role. Fullerene C(60) nanoparticles are toxic to erythrocytes of both types; their toxicity is not related to enhanced oxidative stress and the mechanism of toxicity differs from that of Abeta(25-35) .