Differential effects of antioxidants on amyloid β‐ and H2O2‐induced cell death in the SHSY‐5Y neuronal cell‐line

Abstract

Introduction: Amyloid β (Aβ) protein, a 38–42 amino acid peptide is the major component of senile plaques in Alzheimer's disease and has been suggested to exert its toxic effects via the direct and indirect production of reactive oxygen species.Materials and methods: We have investigated the role of reactive oxygen species in the toxic actions of Aβ on a human neuronal cell line SHSY‐5Y, using the MTT assay for cellular viability and comparing the toxicity of Aβ with that of H2O2.Results: The neurotoxic fragment of Aβ protein, Aβ25–35, had clear concentration‐ and time‐dependent toxic effects on SHSY‐5Y cells. The ability of antioxidants to reverse these toxic effects of 10 µm Aβ25–35 or 200 µm H2O2 were tested. Vitamin E (10–100 µm) did not affect either Aβ or H2O2. Trolox, a vitamin E analogue (5–200 µm) had protective effects on H2O2‐induced cell death but was ineffective in preventing the cell death induced by Aβ. Vitamin C (10–1000 µm) partially reversed H2O2‐induced toxicity but had no protective action when cells were exposed to Aβ.Discussion: These results indicate that the mechanisms by which Aβ and H2O2 exert their toxic effects are different and suggest that in this experimental system, formation of reactive oxygen species do not have major role in Aβ‐induced cell death.