Sesamol induces mitochondrial apoptosis pathway in HCT116 human colon cancer cells via pro-oxidant effect

AimsSesamol lignan is a phenolic compound found in sesame seeds. We investigated the effect of different concentrations of sesamol on oxidative stress in colorectal carcinoma cells (HCT116).Main methodsAntioxidation in vitro was determined from elimination of the DPPH radical, ferric reducing-antioxidant power (FRAP), O2−, and peroxyl radical scavenging activity. Intracellular O2−, H2O2 and GSH levels were determined by DHE, DCFH-DA, and CMF-DA assay, respectively. Cell viability was detected by neutral red assay. Cell cycle proportion and mode of apoptotic HCT116 cells death was analyzed by flow cytometry. Apoptosis in sesamol-treated HCT116 cells was confirmed by morphological changes in the nuclei using DAPI staining and changes in mitochondrial membrane potential using the DiOC6(3) assay.Key findingsSesamol at both low (0.05 and 0.25 mM) and high (0.5, 2, 5, and 10 mM) concentrations concurrently reduced FRAP reagent and scavenged DPPH, and O2−. Sesamol at low concentrations scavenged ROO, but ROO-scavenging was decreased at higher concentrations. Sesamol suppressed cell viability via disruption of cell cycle progression at high concentrations (0.5, 1, 2, and 5 mM), thereby causing S-phase arrest and inducing apoptosis—through the production of intracellular O2−, mitochondrial dysfunction, and DNA fragmentation.SignificanceHigh concentrations of sesamol induced the mitochondrial apoptosis pathway in human colon cancer HCT116 cells via a pro-oxidant effect.