SOD3 Ameliorates H2O2-Induced Oxidative Damage in SH-SY5Y Cells by Inhibiting the Mitochondrial Pathway

• Published in: Neurochemical research Vol. 41; no. 7; pp. 1818 - 1830
• Main Authors: Yang, Rong, Wei, Li, Fu, Qing-Qing, Wang, Hua, You, Hua, Yu, Hua-Rong
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.07.2016; Springer Nature B.V
• Subjects: Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell Line, Tumor; Cell Survival - drug effects; Cell Survival - physiology; Humans; Hydrogen Peroxide - toxicity; Mitochondria - drug effects; Mitochondria - metabolism; Neurochemistry; Neurology; Neurosciences; Original Paper; Oxidative Stress - drug effects; Oxidative Stress - physiology; Signal Transduction - drug effects; Signal Transduction - physiology; Superoxide Dismutase - biosynthesis; Oxidative stress; Reactive oxygen species; Extracellular superoxide dismutase; Mitochondrial pathway; Antioxidant enzymes
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-016-1897-x

This study was designed to investigate the protective effects of extracellular superoxide dismutase (SOD3) against hydrogen peroxide (H 2 O 2 ) 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 H 2 O 2 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 H 2 O 2 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 H 2 O 2 -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.