Salvi 2016 Oxid Med Cell Longev: Difference between revisions
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{{Publication | {{Publication | ||
|title=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. | |title=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. | ||
|info=[http://www.hindawi.com/journals/omcl/2016/5059043/] | |info=[http://www.hindawi.com/journals/omcl/2016/5059043/ Open Access] | ||
|authors=Salvi A, Patki G, Khan E, Asghar M, Salim S | |authors=Salvi A, Patki G, Khan E, Asghar M, Salim S | ||
|year=2016 | |year=2016 | ||
|journal=Oxid Med Cell Longev | |journal=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. | |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. | ||
|keywords=Tempol, Buthionine sulfoximine, Oxidative stress, Mitochondria, Mouse hippocampal HT22 cells | |||
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|couplingstates=ROUTINE | |couplingstates=ROUTINE | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional= | |additional=2016-03 | ||
}} | }} | ||
Revision as of 13:48, 22 March 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. |
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. • 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 Preparation: Intact cells
Regulation: ATP production Coupling state: ROUTINE
HRR: Oxygraph-2k
2016-03
