Oxytocin administration improves DNA damage and total oxidative stress parameters in vincristine and cisplatin-induced cortical neuron toxicity Oksitosin uygulaması vinkristin ve sisplatin kaynaklı kortikal nöron toksisitesinde DNA hasarını ve toplam oksidatif stres parametrelerini iyileştirir

Objective: Oxytocin (OXT) has been reported to have promising therapeutic potential due to its antioxidant properties in vincristine (VCR) and cisplatin (CP) induced peripheral neuropathy in both in vivo and in vitro studies. The cerebral cortex is responsible for sense, perception, and memory. Damage to these parts of the brain can lead to impairment of central nervous system functions. However, the effectiveness of OXT in toxicity caused by vincristine and cisplatin in cortical neurons has not been reported. In this study,we aimed to investigate the effects of OXT in VCR and CP-induced cortical neuron cell culture toxicity via biochemically measuring TAS-TOS levels and immunohistochemically determining 8-OHDG expression. Methods: Cortical neuronal cells were exposed to different concentrations of VCR and CP, and also after the neuronal cells were exposed to OXT (1 μM) for 5 minutes, VCR and CP concentrations were applied to the cells. Cell viability was determined using the MTT method. TAC and TOS were measured for antioxidant/oxidant activity. The expression of 8-OHdG was investigated as an indicator of oxidative DNA damage. Results: Administration of OXT before CP and VCR exposure was able to protect against neuronal cytotoxicity. TAS levels increased positively correlated with in cells exposed to OXT+ VCR and OXT+ CP, while TOS levels and DNA damage (8-OHdG levels) negatively correlated. Conclusion: OXT alleviated the toxic effects of VCR and CP-induced cortical neuron toxicity by increasing the TAS levels, while decreasing TOS levels and DNA damages. According to the results of this study, OXT has the potential to be used protective agent for anticancer agents induced toxicity. However, further studies are needed to clarify mechanisms of action of OXT.