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Induced oxidative stress and apoptosis by 1-bromopropane in SH-SY5Y cells correlates with inhibition of Nrf2 function
Guangtao Yang1, Wei Zhou1, Minhong Zhang1
1Institute of Occupational Hazard Assessment, Shenzhen Prevention and Treatment Center for Occupational Diseases, Shenzhen, Guangdong, China.
Abstract:
In this study, we established SH-SY5Y human neuroblastoma cells as an in vitro model to investigate whether oxidative stress and the nuclear erythroid-2 related factor 2 (Nrf2) signaling pathway are associated with 1-bromopropane (1-BP) -induced nerve cell injury. We identified that 1-BP exhibited neurotoxicity mainly through oxidant-based processes in SH-SY5Y cells, as reactive oxygen species, malondialdehyde levels, and 8-hydroxy-2' -deoxyguanosine significantly increased, while superoxide dismutase activity decreased. Furthermore, Nrf2 translocation from the cytosol to the nucleus was inhibited, as was downstream protein expression of the Nrf2-regulated genes HO-1 and Bcl-2. Activation of caspase-9 and -3 increased, and apoptosis was observed. Vitamin C alleviated 1-BP-induced apoptosis by decreasing oxidative stress and activating the Nrf2 signaling pathway. Knockdown of Nrf2 in SH-SY5Y cells increased 1-BP-induced reactive oxygen species production and cell apoptosis, and inhibited HO-1 and Bcl-2 protein expression, while overexpression of Nrf2 alleviated these processes. These findings suggest that 1-BP-induced oxidative stress and apoptosis in SH-SY5Y cells are associated with Nrf2 function inhibition.
Insights
1-bromopropane causes nerve cell damage by increasing oxidative stress and inhibiting the Nrf2 pathway. Vitamin C and Nrf2 activation protect against this neurotoxicity.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- 1-bromopropane (1-BP) is a solvent with potential neurotoxic effects.
- Oxidative stress and the Nrf2 signaling pathway are critical in cellular defense mechanisms.
- The specific mechanisms linking 1-BP neurotoxicity to oxidative stress and Nrf2 pathway dysfunction require elucidation.
Purpose of the Study:
- To investigate the association between oxidative stress, Nrf2 signaling, and 1-BP-induced neurotoxicity.
- To establish an in vitro model using SH-SY5Y human neuroblastoma cells for studying 1-BP neurotoxicity.
Main Methods:
- SH-SY5Y cells were exposed to 1-BP to assess neurotoxicity markers.
- Measurements included reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) activity.
- Nrf2 pathway activation, caspase activity, and apoptosis were evaluated; Nrf2 knockdown and overexpression were performed.
Main Results:
- 1-BP exposure increased oxidative stress markers (ROS, MDA) and decreased antioxidant enzyme activity (SOD).
- 1-BP inhibited Nrf2 translocation, reduced Nrf2-regulated gene expression (HO-1, Bcl-2), and induced apoptosis.
- Vitamin C mitigated 1-BP effects; Nrf2 knockdown exacerbated toxicity, while Nrf2 overexpression offered protection.
Conclusions:
- 1-BP induces neurotoxicity in SH-SY5Y cells primarily through oxidative stress.
- Inhibition of the Nrf2 signaling pathway is a key mechanism in 1-BP-induced neurotoxicity and apoptosis.
- Targeting the Nrf2 pathway may offer therapeutic strategies against 1-BP nerve cell injury.
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