Oxidative stress in a clonal cell line of neuronal origin: effects of antioxidant enzyme modulation.

摘要: The effects of intracellularly generated H2O2 on cell viability, morphology, and biochemical markers injury have been investigated in a clonal line neuronal origin (140-3, mouse neuroblastoma X rat glioma) as culture model for the role oxidative stress long-term loss neurons brain. was from redox cycling menadione, or by oxidation serotonin catalyzed monoamine oxidase, to simulate effect amine neurotransmitter turnover. Incubation with menadione at concentrations low 10 microM several hours resulted significant losses viability altered morphology. Similar were evident presence only after incubation overnight > 1 mM. cytotoxicity either agent potentiated preincubation specific inhibitors two enzymes important cellular antioxidant defenses, 3-amino-1,2,4-triazole catalase 1,3-bis(chloromethyl)-1-nitrosourea glutathione reductase. Activity another enzyme particular importance defenses brain, selenoprotein peroxidase, stimulated fourfold growth cultures sodium selenite source active-site Se enzyme. other functionally coupled decrease activity superoxide dismutase 200 nM. substantially protected cells against induced combinations 3-amino-1,2,4-triazole, 1,3-bis(chloromethyl)-1-nitrosourea, but marginally effective stress. oxidase inhibitor pargyline increased survival serotonin, demonstrating this its cytotoxicity. DNA damage (single strand breaks), not lipid peroxidation, correlated cytotoxic menadione.