Abstract
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•First comparative anti-cancer study on persicogenin and homoeriodictyol.•Flavanones induced apoptosis by novel p53-dependent and p53-independent mechanisms.•Persicogenin and homoeriodictyol are active inducers of intracellular ROS.•Flavanones selectively affect mitochondrial functionality (ΔΨm) of cancer cells.•Both flavanones exhibit prospects of potential drugs for cancer treatment.
Herein we examined two flavanones (persicogenin and homoeriodictyol) isolated from Rhus retinorrhoea to elucidate the mechanism of their anticancer effects in MCF-7, HeLa, and HT-29 cells. Based on the [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)] (MTT) cytotoxicity data of persicogenin (500 μg/ml) caused a 58.1 % reduction in HT-29 survival while homoeriodictyol (500 μg/ml) caused a 51.9 %, 66.7 % and 76.2 % reductions in MCF-7, HeLa and HT-29 cell survival, respectively. The neutral red uptake (NRU) assay revealed 53.6 %, 53.9 %, 58.8 % and 83.0 %, 87.7 %, 66.7 % reductions in MCF-7, HeLa, and HT-29 cell survival following persicogenin and homoeriodictyol (500 μg/ml) treatment, respectively. Moreover, the intracellular reactive oxygen species (ROS) was significantly enhanced and dysfunction of mitochondrial membrane potential (ΔΨm) confirmed the mitochondrial injury in all cell types by the flavanones. MCF-7, HeLa, and HT-29 cells exposed to persicogenin and homoeriodictyol (500 μg/ml) had showed 42.5 %, 63.1 %, 62.3 % and 30.7 %, 30.2 %, 23.8 % cells in the sub G1 apoptotic phase. The persicogenin- and homoeriodictyol-treated cell lines had upregulated expressions of p53, caspase-3, caspase-9, bax, and superoxide dismutase 1 (SOD1) genes. Such findings provide novel insight into the comparative anti-cancer efficacy of persicogenin and homoeriodictyol, signifying their promising clinical applications as cancer treatments and their application as bioactive therapeutic agents.