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Plant sterols (PS) have been incorporated to foods due to their cholesterol-lowering effect. Because of their low intestinal absorption (0.5–2%), they can reach the colon and exert local actions. The aim of this study was to evaluate the antiproliferative effect of individual (β-sitosterol, campesterol and stigmasterol) and combined PS in colon cancer cells (Caco-2) at human colonic concentrations after simulated gastrointestinal digestion of a PS enriched milk-based fruit beverage. β-Sitosterol, campesterol and stigmasterol induced significant cell viability reduction (13–59% vs control), but only stigmasterol produced an overproduction of reactive oxygen species (92% vs control). Individual PS induced reversible arrest in phase G 0 /G 1 of the cell cycle, suggesting that they act as cytostatic agents. Combined PS showed a greater effect than individual PS, inducing also cell necrosis and irreversible cell cycle arrest (G 0 /G 1 phase). The consumption of PS-enriched foods therefore could exert a potential preventive effect against colon cancer. [ABSTRACT FROM AUTHOR]

Sterol oxidation products (SOPs) have shown cytotoxic effect in human intestinal cells; however, their effect within a food matrix has not been assayed yet. This study evaluated the possible cytotoxic effect of SOPs within bioaccessible fractions (BFs) of two milk-based fruit beverages with (BFA)/without (BFB) plant sterols in differentiated Caco-2 cells and if the BFs counteracted the cytotoxic effect induced by COPs mixture (30 and 60 μM). BFs did not evoke cytotoxic effect in any of the tests carried out and they protected against the loss of intestinal cohesion, mitochondrial depolarization and necrosis induced by COPs mixture. Moreover, BFB sample protected from cell cycle arrest, lessened lysosomal injury and overproduction of ROS at 30 μM. Therefore, the formation of SOPs within milk-based fruit beverages with/without plant sterols does not contribute to intestinal epithelium damage and these types of food matrices confer additional protection against COPs at dietary concentrations. [ABSTRACT FROM AUTHOR]