ArticleOxidative medicine and cellular longevity2016
Protective Effect of Tempol on Buthionine Sulfoximine-Induced Mitochondrial Impairment in Hippocampal Derived HT22 Cells.
Article in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Genistein Protects Against Lead-Induced Cognitive Impairment Through a Glutathione-Dependent Redox-Mitochondrial Apoptosis Axis.Molecules (Basel, Switzerland) · 2026Article
- Mechanism of L-Buthionine-(S,R)-sulfoximine-induced ferroptotic cell death in mouse hippocampal neuronal cells.Cell communication and signaling : CCS · 2026Article
- TEMPOL Enhances Polyethylene Glycol Axon Fusion Following Sciatic Nerve Transection in Adult Rats.ACS chemical neuroscience · 2026Article
- 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol) alleviates lung injury by inhibiting SIRT6-HIF-1α signaling pathway activation through the upregulation of miR-212-5p expression.Molecular biology reports · 2024Article
- Effect of Low Concentration of Nitroxides on SH-SY5Y Cells Transfected with the Tau Protein.International journal of molecular sciences · 2023Article
- Ginkgo Biloba and Long COVID: In Vivo and In Vitro Models for the Evaluation of Nanotherapeutic Efficacy.Pharmaceutics · 2023Review
- The Role of ROS as a Double-Edged Sword in (In)Fertility: The Impact of Cancer Treatment.Cancers · 2022Review
- The heterocyclic compound Tempol inhibits the growth of cancer cells by interfering with glutamine metabolism.Cell death & disease · 2020Article
- Renal Dopamine Oxidation and Inflammation in High Salt Fed Rats.Journal of the American Heart Association · 2020Article
- Design, Synthesis, and In Vitro Evaluation of a Novel Probucol Derivative: Protective Activity in Neuronal Cells Through GPx Upregulation.Molecular neurobiology · 2018Article
- Modulating Oxidative Stress Relieves Stress-Induced Behavioral and Cognitive Impairments in Rats.The international journal of neuropsychopharmacology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
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.
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