Potential effects of Amygdalin on cytotoxicity, apoptosis, oxidative damage, and cell cycle related genes expressions in H1650 lung adenocarcinoma cells

Purpose: The aim of this study is to determine the anticancer effects of the active ingredient amygdalin on H1650 lung cancer cells.Materials and Methods: The antiproliferative effect of amygdalin on H1650 lung cancer cells was evaluated using the MTT assay. Its effect on oxidative damage was determined using 8-OHdG and total antioxidant status (TAS), total oxidant status (TOS), and by calculating the oxidative stress index (OSI). Its effect on apoptosis was demonstrated using the caspase-3 ELISA method. Changes in mRNA expression of the CDK1, CDK2, CDK4, CDK6, Cyclin D1, Cyclin B1, and Cyclin E genes were assessed by RT-PCR.Results: The IC50 dose of amygdalin in H1650 cells was determined to be 443.8 μM at 24 h. A significant decrease in the expression of CDK1 (0.48-fold), CDK2 (0.31-fold,), CDK6 (0.16-fold), Cyclin D1 (0.24-fold,), Cyclin B1 (0.07-fold), and Cyclin E (0.05-fold) genes was observed in the group treated with amygdalin. The differences in TOS, TAS and OSI levels and in 8-OHdG and caspase-3 levels between groups were not statistically significant. Conclusion: Amygdalin shows potential as an anticancer agent and may contribute to the development of different therapeutic approaches for lung cancers.