Aim: Acetamiprid (ACE) is one of the most widely used neonicotinoids used globally to protect crops from insects. In this study, it was aimed to evaluate the potential neutotoxicity effect of acetamiprid on human neuroblastoma cell line SH-SY5Y cells.
Materials and Methods: MTT and MUSE analysis were performed to examine the effect on cell viability. Increasing doses of ACE were administered for 24 hours in SHSY5 neuroblastoma cell lines. To evaluate the efficacy of ACE on oxidative stress in neuroblastoma cell lines, NOS1, NOS2, NOS3; caspase-3 for assessment of apoptosis; Ki67 immunocytochemical staining was performed to evaluate proliferation and relative mRNA values of these markers were measured by qRT-PCR analysis method.
Results: The IC50 value for ACE 24 hours was found to be 21.35 mM. In SHSY5 cells, the immunoreactivity of NOS1, NOS3 and caspase-3 markers in the ACE applied group increased statistically significantly compared to the control group; Ki67 immunoreactivity was also found to be decreased (p< 0.05). qRT-PCR results were consistent with immunocytochemical findings and relative mRNA values were found to be increased in ACE groups compared to the control group. Ki67 relative mRNA values were found to be decreased compared to the control group.
Conclusion: In our study, it was found that ACE suppressed proliferation in SH-SY5Y cells, induced apoptosis, and caused cell toxicity by increasing oxidative stress.
Key words: Acetamiprid; apoptosis; human neuroblastoma cells; oxidative stress; neurotoxicity
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