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Nanomolar Amyloid β Protein‐Induced Inhibition of Cellular Redox Activity in Cultured Astrocytes
Author(s) -
Kato Mayumi,
Saito Hiroshi,
Abe Kazuho
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.68051889.x
Subject(s) - astrocytosis , reactive oxygen species , neurotoxicity , redox , oxidative stress , chemistry , beta (programming language) , amyloid beta , astrocyte , biochemistry , biophysics , microbiology and biotechnology , biology , endocrinology , toxicity , central nervous system , organic chemistry , peptide , computer science , programming language
It has been previously reported that Alzheimer's amyloid β protein (Aβ) induces reactive astrocytosis in culture. In the present study, we found that Aβ potently inhibits cellular redox activity of cultured astrocytes, as determined by the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide reduction assay. The following comparative studies revealed several differences between these two actions of Aβ on astrocytes. First, Aβ‐induced reactive morphological change was suppressed by the presence of serum or thrombin, and Aβ inhibition of cellular redox activity was observed in either the presence or the absence of serum. Second, micromolar concentrations (10 µ M or more) were required for Aβ to induce reactive astrocytosis, whereas nanomolar concentrations (0.1–100 n M ) were sufficient to inhibit cellular redox activity. Third, the effect of micromolar Aβ was virtually irreversible, but nanomolar Aβ‐induced inhibition of cellular redox activity was reversed by washing out Aβ. Furthermore, as it has been reported that Aβ neurotoxicity is mediated by reactive oxygen species, we also examined if similar mechanisms are involved in astrocytic response to Aβ. However, neither Aβ‐induced morphological change nor inhibition of redox activity was blocked by antioxidants, suggesting that these effects are not caused by oxidative stress.