Salvi 2016 Oxid Med Cell Longev: Difference between revisions
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{{Labeling | {{Labeling | ||
|area=Respiration, Pharmacology;toxicology | |area=Respiration, Pharmacology;toxicology | ||
|injuries=Oxidative stress;RONS | |||
|organism=Mouse | |organism=Mouse | ||
|tissues=Nervous system | |tissues=Nervous system, Other cell lines | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|topics=ATP production | |topics=ATP production | ||
|couplingstates=ROUTINE | |couplingstates=ROUTINE |
Latest revision as of 15:06, 9 November 2016
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. |
ยป 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. โข 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