beta Amyloid does not activate the antioxidant pentose phosphate pathway within the B12 neural cell line.
The aim of this study was to determine whether neural cells exposed to beta amyloid (A beta) activate the pentose phosphate pathway (PPP), a critical oxidative stress defense mechanism. A beta stimulated H2O2 production in neural (B12) and non-neural (HepG2) cells and stimulated PPP activity, the source of the main intracellular reductant NADPH, in HepG2 cells (67% increase). Catalase blocked the A beta-induced increase in PPP, demonstrating that H2O2 mediated the increase in PPP activity. B12 cells showed no increase in PPP following A beta exposure. Fifty-five per cent of HepG2 cells but only 11.1% of B12 cells remained viable after A beta exposure. Lack of PPP activation may contribute to A beta cytotoxicity in neural calls and may lead to differences in survival between neural and non-neural cells.
Kopp
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Renal Division, Beth Israel Deaconess Medical Center, Joslin Diabetes Center,Boston, MA 02215, USA.
Stanton
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D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000704:Analysis of Variance; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D006801:Humans; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010427:Pentose Phosphate Pathway / Q000187:drug effects*; D051381:Rats; D014407:Tumor Cells, Cultured
D016229:Amyloid beta-Peptides; D000975:Antioxidants; D002374:Catalase