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Salvi 2016 Oxid Med Cell Longev

From Bioblast
Publications in the MiPMap
Salvi A, Patki G, Khan E, Asghar M, Salim S (2016) Protective effect of tempol on buthionine sulfoximine (BSO)-induced mitochondrial impairment in hippocampal derived HT22 cells. Oxid Med Cell Longev 2016:5059043.

Β» Open Access

Salvi A, Patki G, Khan E, Asghar M, Salim S (2016) Oxid Med Cell Longev

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: Tempol, Buthionine sulfoximine, Oxidative stress, Mitochondria, Mouse hippocampal HT22 cells


Labels: MiParea: Respiration, Pharmacology;toxicology 

Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Nervous system, Other cell lines  Preparation: Intact cells 

Regulation: ATP production  Coupling state: ROUTINE 

HRR: Oxygraph-2k 

2016-03