Independent thesis Advanced level (degree of Master (Two Years)), 20 credits / 30 HE credits
Background: Ketamine, a widely used anaesthetic, has raised concerns about its potential neurotoxic effects, especially in paediatric populations. Previous studies suggest ketamine may induce oxidative stress and neuroapoptosis. Oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) and antioxidant defences, can disrupt neuronal development. This study aimed to investigate whether ketamine changes gene expression of antioxidant enzymes (CAT, SOD1, SOD2, GPX1, TRX1) during neuronal differentiation.
Methods: SH-SY5Y cells, a human neuroblastoma cell line, were differentiated into neuron-like cells and simultaneously exposed to ketamine (0.1, 1, 10, 100 µM and 1 mM) or a saline control for 7 days. Gene expressions of CAT, SOD1 and GPX1 were analysed using quantitative real-time PCR (q-PCR), with GAPDH as the reference gene. SOD2 and TRX1 were not analysed due to unsatisfactory primer efficiency. Statistical analysis was performed using one-way ANOVA.
Results: Exposure to 1 mM ketamine resulted in complete cell death by day 7. At the tested concentrations of 0.1-100 µM, q-PCR analysis showed no statistically significant difference (p>0.05) in gene expression for CAT, SOD1, or GPX1 between the ketamine-treated groups and the control.
Conclusion: This study found no significant transcriptional changes in the expression of CAT, SOD1 or GPX1 in differentiating SH-SY5Y cells after ketamine exposure. These results are consistent with some previous results. Limitations include lack of functional NMDA receptors in undifferentiated SH-SY5Y cells. Further research is needed to clarify ketamine’s effects on oxidative stress and neuronal development.
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