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(−)-Epicatechin is a phenolic compound with antioxidant activity that is present in natural food and drinks, such as cocoa and red wine. Evidence suggests that (−)-epicatechin exhibits anticancer activity; however, its mechanism of action is poorly understood. Here, we investigated the anticancer effects of (−)-epicatechin and its mechanism of action in breast cancer cells. We assessed the anticancer activity by cell proliferation assays, apoptosis by DNA fragmentation and flow cytometry. The expression of proteins associated with apoptosis was analyzed by the human apoptosis array. MitoSOXTM Red and biomarkers of oxidative damage were used to measure the effect of (−)-epicatechin on mitochondrial reactive oxygen species (ROS) and cellular damage, respectively. (−)-Epicatechin treatment caused a decreasing in the viability of MDA-MB-231 and MCF-7 cells. This cell death was associated with DNA fragmentation and an apoptotic proteomic profile. Further, (−)-epicatechin in MDA-MB-231 cells upregulated death receptor (DR4/DR5), increased the ROS production, and modulated pro-apoptotic proteins. In MCF-7 cells, (−)-epicatechin did not involve death receptor; however, an increase in ROS and the upregulation of pro-apoptotic proteins (Bad and Bax) were observed. These changes were associated with the apoptosis activation through the intrinsic pathway. In conclusion, this study shows that (−)-epicatechin has anticancer activity in breast cancer cells and provides novel insight into the molecular mechanism of (−)-epicatechin to induce apoptosis.

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Background: Studies show that diet and exercise are important in the treatment of obesity. The aim of this study was to determine whether additional regular moderate aerobic exercise during a treatment with hypocaloric diet has a beneficial effect on oxidative stress and molecular damage in the obese patient. Methods: Oxidative stress of 16 normal-weight (NW) and 32 obese 1 (O1) subjects (BMI 30–34.9 kg/m²) were established by biomarkers of oxidative stress in plasma. Recombinant human insulin was incubated with blood from NW or O1 subjects, and the molecular damage to the hormone was analyzed. Two groups of treatment, hypocaloric diet (HD) and hypocaloric diet plus regular moderate aerobic exercise (HDMAE), were formed, and their effects in obese subjects were analyzed. Results: The data showed the presence of oxidative stress in O1 subjects. Molecular damage and polymerization of insulin was observed more frequently in the blood from O1 subjects. The treatment of O1 subjects with HD decreased the anthropometric parameters as well as oxidative stress and molecular damage, which was more effectively prevented by the treatment with HDMAE. Conclusion: HD and HDMAE treatments decreased anthropometric parameters, oxidative stress, and molecular damage in O1 subjects.

Natural compounds such as (−)-epicatechin show a variety of biological properties including anticancer activity.

Obesity and its associated disorders constitute a growing epidemic across the world. Numerous studies have demonstrated the presence of systemic oxidative stress in patients with obesity. In this study, we show the effects of oxidative stress present in the blood from obese patients on recombinant human insulin. Insulin was incubated with whole blood (WB) from overweight subjects (OW), obese 1 patients (O1), or normal weight volunteers (NW) (n=16 for each group). Whole blood from OW and O1, unlike WB from NW, increased the carbonyl content of insulin; however, only whole blood from O1 patients increased the amount of formazan present in the hormone. Interestingly, the incubation of insulin with WB from O1 provoked a decrease in the hypoglycemic activity of the hormone (18%), an effect due to insulin polymerization. In addition, we showed that the formation of the insulin polymer generated the formation of new epitopes and the development of a new immunogenicity. These observations show that oxidative stress present in the WB of O1 patients can result in abolition of the biological activity of insulin and contribute to the development of an immune response to the hormone.