ArticleNeurochemical research2016
SOD3 Ameliorates H2O2-Induced Oxidative Damage in SH-SY5Y Cells by Inhibiting the Mitochondrial Pathway.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Less Is More: A Physiological Dose of Vitamin B12 Enhances Neural Recovery Compared to a High Dose in an H₂O₂-Stressed SH-SY5Y Neural-Like Cell Model.Molecular neurobiology · 2026Article
- Overexpression of Extracellular Superoxide Dismutase 3 Inhibits Cancer Cell Growth and Migration in Colorectal Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024Article
- Use of Electron Paramagnetic Resonance (EPR) to Evaluate Redox Status in a Preclinical Model of Acute Lung Injury.Molecular imaging and biology · 2024Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Extracellular superoxide dismutase (EC-SOD) R213G variant reduces mitochondrial ROS and preserves mitochondrial function in bleomycin-induced lung injury: EC-SOD R213G variant and intracellular redox regulation.Advances in redox research · 2022Article
- The NRF2-Dependent Transcriptional Regulation of Antioxidant Defense Pathways: Relevance for Cell Type-Specific Vulnerability to Neurodegeneration and Therapeutic Intervention.Antioxidants (Basel, Switzerland) · 2021Review
- Evaluation of the Antioxidant Activity of the Marine Pyrroloiminoquinone Makaluvamines.Marine drugs · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study was designed to investigate the protective effects of extracellular superoxide dismutase (SOD3) against hydrogen peroxide (H2O2) induced damage in human neuroblastoma SH-SY5Y cells and to elucidate the mechanisms responsible for this beneficial effect. SOD3-overexpressing SH-SY5Y cells were generated by adenoviral vector-mediated infection, and H2O2 was then added into the cell culture system to establish an in vitro model of oxidative stress. Cell viability, the generation of intracellular reactive oxygen species (ROS), the expression and activity of antioxidant enzymes, the levels of lipid peroxidation malondialdehyde (MDA), the expression of mitochondrial apoptosis-related genes, and calcium imaging were examined. Following H2O2 exposure, the over-expression of SOD3 promoted the survival of SH-SY5Y cells; decreased the production of ROS, MDA levels, cytochrome C, caspase-3, caspase-9, and Bax gene expression, and calcium levels; and increased the expression and activity of antioxidant enzyme genes and the expression level of Bcl-2. Together, our data demonstrate that SOD3 ameliorates H2O2-induced oxidative damage in neuroblastoma SH-SY5Y cells by inhibiting the mitochondrial pathway and provide new insights into the functional actions of SOD3 on oxidative stress-induced cell damage.
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