composite(a(CHEBI:"L-ascorbic acid"), a(CHEBI:Trolox), a(CHEBI:glutathione)) decreases p(RGD:Mapt, pmod(Ph, Ser, 262))

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PubMed:23722080

Primary cortical neurons exposed to the mitochondrial toxin NaN3 (0.1-3 mM) were submitted to oxidative stress with H2O2 (30-150 μM), to mimic conditions observed in neurodegenerative disorders. The effects of such treatment on a series of parameters useful in characterizing neuronal damage were investigated: (i) the basal release of glutamate, evaluated as (3)H-d-Aspartate efflux, was sharply, concentration-dependently, increased; (ii) the phosphorylation status of intracellular markers known to be involved in the neurodegenerative processes, in particular in Alzheimer disease: tau and GSK3β were increased, as well as the protein level of β-secretase (BACE1) and p35/25 evaluated by Western blotting, while (iii) the cell metabolic activity, measured with the MTT method, was reduced, in a concentration- and time-dependent manner. The latter effect, as well as tau hyperphosphorylation, was prevented both by a mixture of antioxidant drugs (100 μM ascorbic acid, 10 μM trolox, 100 μM glutathione) and by the anti-Alzheimer drug, memantine, 20 μM.

Related Edges 19

• a(CHEBI:"hydrogen peroxide") increases bp(MESH:"Oxidative Stress")
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• composite(a(CHEBI:"L-ascorbic acid"), a(CHEBI:Trolox), a(CHEBI:glutathione)) decreases p(RGD:Mapt, pmod(Ph, Ser, 404))
• composite(a(CHEBI:"L-ascorbic acid"), a(CHEBI:Trolox), a(CHEBI:glutathione)) increases bp(GO:"cellular metabolic process")
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• composite(a(CHEBI:"hydrogen peroxide"), a(CHEBI:"sodium azide")) increases p(RGD:Mapt, pmod(Ph, Ser, 404))
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Uberon

cerebral cortex

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