Salvi 2016 Oxid Med Cell Longev
Β» [[Has info::Open Access]]
Was written by::Salvi A, Was written by::Patki G, Was written by::Khan E, Was written by::Asghar M, Was written by::Salim S (Was published in year::2016) Was published in journal::Oxid Med Cell Longev
Abstract: [[has abstract::Using a simulated oxidative stress model of hippocampus-derived immortalized cell line (HT22), we report that pro-oxidant buthionine sulfoximine (BSO, 1mM, 14h) without adversely affecting cell viability or morphology, induced oxidative stress by inhibiting glutathione synthesis. BSO treatment also significantly reduced superoxide dismutase (SOD) activity (p<0.05) and significantly lowered total antioxidant capacity (p<0.001) in HT22 cells when compared to vehicle treated control cells. Antioxidant tempol, a piperidine nitroxide considered a SOD mimetic, reversed BSO-induced decline in SOD activity (p<0.01) and also increased BSO-induced decline in total antioxidant capacity (p<0.05). Interestingly, BSO treatment significantly reduced mitochondrial oxygen consumption (p<0.05), decreased mitochondrial membrane potential (p<0.05), and lowered ATP production (p<0.05) when compared to vehicle treated control cells, collectively indicative of mitochondrial impairment. Antioxidant tempol treatment mitigated all three indicators of mitochondrial impairment. We postulate that BSO-induced oxidative stress in HT22 cells caused mitochondrial impairment, and tempol by increasing SOD activity and improving antioxidant capacity presumably protected the cells from BSO-induced mitochondrial impairment. In conclusion, present study provides an interesting simulation of oxidative stress in hippocampal cells, which will serve as an excellent model to study mitochondrial functions.]] β’ Keywords: has publicationkeywords::Tempol, has publicationkeywords::Buthionine sulfoximine, has publicationkeywords::Oxidative stress, has publicationkeywords::Mitochondria, has publicationkeywords::Mouse hippocampal HT22 cells
Labels: MiParea: MiP area::Respiration, MiP area::Pharmacology;toxicology
Stress:Injury and adaptation::Oxidative stress;RONS Organism: Organism::Mouse Tissue;cell: tissue and cell::Nervous system Preparation: Preparation::Intact cells
Regulation: Topic::ATP production Coupling state: Coupling states::ROUTINE