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- W2019671362 abstract "We examined neurotoxic effects of Aβ(25–35), an active fragment of β-amyloid (Aβ), and compared the effect with H2O2 neurotoxicity in PC12 cells. Aβ(25–35) induced the loss of mitochondria function as detected using a tetrazolium salt (WST-1) reduction assay and decreased the number of cells adhering to collagen type 1-coated plates. Aβ(25–35) did not induce cell death, as detected by Hoechst 33342/propidium iodide staining. The caspase tetrapeptide inhibitor z-IETD-fluoromethylketone (FMK) and z-LEHD-FMK inhibited the attenuation of WST-1 reduction induced by Aβ(25–35) and H2O2, while the caspase-3 inhibitor z-DEVD-FMK afforded protection only against H2O2 neurotoxicity. Caspase-3 protease activity was increased by treatment of H2O2 but not Aβ(25–35). Thus, Aβ(25–35) induces early neurotoxic events by activating caspases other than caspase-3. H2O2-induced oxidative stress may not be implicated in Aβ-induced neurotoxic pathways." @default.
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- W2019671362 title "β-amyloid induces caspase-dependent early neurotoxic change in PC12 cells: correlation with H2O2 neurotoxicity" @default.
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- W2019671362 doi "https://doi.org/10.1016/s0304-3940(01)01808-0" @default.
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