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Chemical screening of digested human milk protein using the oxygen radical absorbance capacity (ORACFL) antioxidant assay confirmed the presence of a peptide fraction (PF23) with high antioxidant activity [5.53 mmol Trolox equivalents (TE)/g] that contained tryptophan as a main component. We evaluated the effects of both PF23 and tryptophan alone on the modulation of oxidative stress in cultured intestinal cells using a dichlorofluorescein diacetate probe. Despite the high ORACFL value, PF23 enhanced (P< 0.05)2, 2′-azobis (2-amidinopropane) dihydrochloride (peroxyl radical generator)-induced intracellular oxidation in the Caco-2 human adenocarcinoma cell line, suggesting prooxidant activity. Compared to selected peptide fractions with relatively lower ORACFL values, PF23 induced oxidative stress more than all other peptide fractions tested (P < 0.05) and contained more tryptophan than the others (P < 0.05). Similar prooxidant activity was observed for tryptophan when it was added to culture medium for both the Caco-2 cells and FHs 74 Int primary fetal enterocytes, while also exhibiting a high ORACFL value (9.69 mmol TE/g). The effect of tryptophan that involves activation of the Nrf-2 pathway and transcription of antioxidant enzymes was therefore investigated in FHs 74 Int cells. Exposure of infant intestinal cells to tryptophan resulted in Nrf-2 activation and an increase in the gene transcript level of glutathione peroxidase 2. We conclude that tryptophan-induced oxidative stress associated with tryptophan-containing milk peptides induces an adaptive response that involves the activation of the antioxidant responsive signaling pathway in intestinal cells. [ABSTRACT FROM AUTHOR]

Prophylactic doses of 120mg of iron (Fe) are commonly used to prevent Fe-deficiency anemia in vulnerable populations, especially in developing countries. Evidence shows that residual Fe in the large bowel may alter the normal antioxidant capacity of the fecal stream. Our objective was to evaluate the effect of dietary antioxidants from the Carotino Tocotrienol-Carotene Mixed Concentrate (CTCMC) on the depletion of fecal antioxidant capacity by oral Fe supplementation. In total, 17 healthy male adults participated in the 2 phases of the study, 5 in the pilot study and 12 in the definitive intervention trial. Participants received different treatments, separated by washout periods. These included: 120 mg Fe; 120 mg Fe and refined palm oil (FeOiI); and 120 mg Fe in refined palm oil combined with 1 of 2 dosages (0.4 g and 0.8 g) of CTCMC/5 mL of refined palm oil (CTCB and CTCA treatments, respectively). Fecal samples were collected and analyzed to quantify the products of hydroxyl radical attack on salicylic acid (2,5 dihydroxybenzoic acid, 2,3-dihydrobenzoic acid, and catechol) at baseline and after active supplementation. Fe supplementation in either form (Fe or FeOil treatments) increased the concentrations of hydroxylated compounds in fecal samples. The production of hydroxylated compounds was significantly lower in treatments CTCB and CTCA than in the FeOil reference. Baseline antioxidant capacity state was virtually restored with dietary carotenoids and tocotrienols from the CTCMC. In conclusion, dietary antioxidants can reverse the depletion of fecal antioxidant capacity induced by oral Fe supplements. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor regarding a study that determined whether folic acid reduces homocysteine levels and masks vitamin B-12 deficiency in elderly people.

Prophylactic doses of 120mg of iron (Fe) are commonly used to prevent Fe-deficiency anemia in vulnerable populations, especially in developing countries. Evidence shows that residual Fe in the large bowel may alter the normal antioxidant capacity of the fecal stream. Our objective was to evaluate the effect of dietary antioxidants from the Carotino Tocotrienol-Carotene Mixed Concentrate (CTCMC) on the depletion of fecal antioxidant capacity by oral Fe supplementation. In total, 17 healthy male adults participated in the 2 phases of the study, 5 in the pilot study and 12 in the definitive intervention trial. Participants received different treatments, separated by washout periods. These included: 120 mg Fe; 120 mg Fe and refined palm oil (FeOiI); and 120 mg Fe in refined palm oil combined with 1 of 2 dosages (0.4 g and 0.8 g) of CTCMC/5 mL of refined palm oil (CTCB and CTCA treatments, respectively). Fecal samples were collected and analyzed to quantify the products of hydroxyl radical attack on salicylic acid (2,5 dihydroxybenzoic acid, 2,3-dihydrobenzoic acid, and catechol) at baseline and after active supplementation. Fe supplementation in either form (Fe or FeOil treatments) increased the concentrations of hydroxylated compounds in fecal samples. The production of hydroxylated compounds was significantly lower in treatments CTCB and CTCA than in the FeOil reference. Baseline antioxidant capacity state was virtually restored with dietary carotenoids and tocotrienols from the CTCMC. In conclusion, dietary antioxidants can reverse the depletion of fecal antioxidant capacity induced by oral Fe supplements. [ABSTRACT FROM AUTHOR]

Prophylactic doses of 120 mg of iron (Fe) are commonly used to prevent Fe-deficiency anemia in vulnerable populations, especially in developing countries. Evidence shows that residual Fe in the large bowel may alter the normal antioxidant capacity of the fecal stream. Our objective was to evaluate the effect of dietary antioxidants from the Carotino Tocotrienol-Carotene Mixed Concentrate (CTCMC) on the depletion of fecal antioxidant capacity by oral Fe supplementation. In total, 17 healthy male adults participated in the 2 phases of the study, 5 in the pilot study and 12 in the definitive intervention trial. Participants received different treatments, separated by washout periods. These included: 120 mg Fe; 120 mg Fe and refined palm oil (FeOil); and 120 mg Fe in refined palm oil combined with 1 of 2 dosages (0.4 g and 0.8 g) of CTCMC/5 mL of refined palm oil (CTCB and CTCA treatments, respectively). Fecal samples were collected and analyzed to quantify the products of hydroxyl radical attack on salicylic acid (2,5 dihydroxybenzoic acid, 2,3-dihydrobenzoic acid, and catechol) at baseline and after active supplementation. Fe supplementation in either form (Fe or FeOil treatments) increased the concentrations of hydroxylated compounds in fecal samples. The production of hydroxylated compounds was significantly lower in treatments CTCB and CTCA than in the FeOil reference. Baseline antioxidant capacity state was virtually restored with dietary carotenoids and tocotrienols from the CTCMC. In conclusion, dietary antioxidants can reverse the depletion of fecal antioxidant capacity induced by oral Fe supplements.