title: beta Amyloid does not activate the antioxidant pentose phosphate pathway within the B12 neural cell line.
abstract: 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.
authors.affiliation: Renal Division, Beth Israel Deaconess Medical Center, Joslin Diabetes Center,Boston, MA 02215, USA.
authors.forename: A
authors.initials: A
authors.lastname: Kopp
authors.forename: R C
authors.initials: RC
authors.lastname: Stanton
mesh_terms: 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
chemical_list: D016229:Amyloid beta-Peptides; D000975:Antioxidants; D002374:Catalase