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Abstract: Casein phosphopeptides (CPPs) have been proposed as potential dietary antioxidants on designing new functional products. A fruit beverage, with/without milk, was subjected to in vitro digestion. Caco-2 cultures were preincubated with soluble fractions or isolated CPPs, the latter obtained from skimmed milk. The mitochondrial activities (MTT test), intracellular GSH and GSH-reductase activity (GSH-Rd), cell cycle analysis and RNA distribution in cycle phases were studied after inducing oxidative stress status (5mM H2O2). MTT conversion was better preserved by soluble fractions of fruit beverages, either with or without milk. GSH concentration was equally decreased, and GSH-Rd was increased in all preincubations. However, failed to inhibit a decreased G1 cell population. CPPs produced RNA accumulation in the G2 phase, suggesting a modulating effect on cell response. We can postulate an antioxidant effect derived from dietary CPPs on a biological system which can be synergistic with other antioxidant compounds derived from fruit beverage. [Copyright &y& Elsevier]

Abstract: Foods and drinking water are the main routes for human exposure to inorganic arsenic, the intestinal epithelium being the first barrier against such exogenous toxicants. The present study evaluates the effect of As(III) (0.5–25μM) upon Caco-2 cells as an intestinal epithelia model. Cell viability, intracellular formation of reactive oxygen species (ROS), mitochondrial membrane potential (Δψm) changes, and cell cycle distribution in exposed cultures were evaluated. The intracellular production of ROS was seen to increase in a non-dose dependent manner at all concentrations tested, with impairment of cell mitochondrial enzyme function secondary to a loss of Δψm. Concentrations between 0.5 and 5μM induce cell cycle transition from phase G1 to phase S, with no significant alteration in the proportion of cells in phase G2. These data suggest that As(III) could induce intestinal oxidative stress-cytotoxicity at mitochondrial functional level, and affect cell cycle progression. The data presented in this work may also suggest the impairment of essential survival processes in Caco-2 cells, induced after exposure to As(III) (1–25μM). Oxidative stress and alteration of mitochondrial functionality could be early indicators of arsenic-induced cytotoxicity, with the resulting abnormal progression of the cell cycle. [Copyright &y& Elsevier]