Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells
Using a simulated oxidative stress model of hippocampus-derived immortalized cell line (HT22), we report that prooxidant buthionine sulfoximine (BSO, 1 mM, 14 h), without adversely affecting cell viability or morphology, induced oxidative stress by inhibiting glutathione synthesis. BSO treatment als...
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Online Access: | http://dx.doi.org/10.1155/2016/5059043 |
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doaj-867754036c2143c5818fe9166bac55ec2020-11-24T23:24:05ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942016-01-01201610.1155/2016/50590435059043Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 CellsAnkita Salvi0Gaurav Patki1Eisha Khan2Mohammad Asghar3Samina Salim4Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USADepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USADepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USADepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USADepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, USAUsing a simulated oxidative stress model of hippocampus-derived immortalized cell line (HT22), we report that prooxidant buthionine sulfoximine (BSO, 1 mM, 14 h), 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.http://dx.doi.org/10.1155/2016/5059043 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ankita Salvi Gaurav Patki Eisha Khan Mohammad Asghar Samina Salim |
spellingShingle |
Ankita Salvi Gaurav Patki Eisha Khan Mohammad Asghar Samina Salim Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells Oxidative Medicine and Cellular Longevity |
author_facet |
Ankita Salvi Gaurav Patki Eisha Khan Mohammad Asghar Samina Salim |
author_sort |
Ankita Salvi |
title |
Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells |
title_short |
Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells |
title_full |
Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells |
title_fullStr |
Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells |
title_full_unstemmed |
Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells |
title_sort |
protective effect of tempol on buthionine sulfoximine-induced mitochondrial impairment in hippocampal derived ht22 cells |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2016-01-01 |
description |
Using a simulated oxidative stress model of hippocampus-derived immortalized cell line (HT22), we report that prooxidant buthionine sulfoximine (BSO, 1 mM, 14 h), 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. |
url |
http://dx.doi.org/10.1155/2016/5059043 |
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