1,721,185 research outputs found
Factors influencing the bioavailability of antioxidants in foods : a critical appraisal
An important aspect when studying the role of antioxidants in human health is the evaluation of their bioavailability from foods. This aspect is gaining increasing interest as food industries are continually involved in developing new products, defined as ‘‘functional’’ by virtue of the presence
of specific antioxidants or phytochemicals. The bioavailability of these substances is, however, not always well known.
Although, from a theoretical point of view, several
definitions of bioavailability have been suggested, the most appropriate seems to be as that fraction of an ingested nutrient or compound that reaches the systemic circulation and the specific sites where it can exert its biological
action. In this definition, three main steps are implicit: release from the carrier matrix, intestinal absorption and tissue uptake.
These aspects are discussed in the paper
Lymphocyte lycopene concentration and DNA protection from oxidative damage is increased in women after a short period of tomato consumption
Several epidemiologic studies have suggested a role of tomato products in protecting against cancer and chronic diseases. In nine adult women, we evaluated whether the consumption of 25 g tomato puree (containing 7 mg lycopene and 0.3 mg β-carotene) for 14 consecutive days increased plasma and lymphocyte carotenoid concentration and whether this was related to an improvement in lymphocyte resistance to an oxidative stress (500 μmol/L hydrogen peroxide for 5 min). Before and after the period of tomato intake, carotenoid concentrations were analyzed by HPLC and lymphocyte resistance to oxidative stress by the Comet assay, which detects DNA strand breaks. Intake of tomato puree increased plasma (P < 0.001) and lymphocyte (P < 0.005) lycopene concentration and reduced lymphocyte DNA damage by ~50% (P < 0.0001). β-Carotene concentration increased in plasma (P < 0.05) but not in lymphocytes after tomato puree consumption. An inverse relationship was found between plasma lycopene concentration (r = -0.82, P < 0.0001) and lymphocyte lycopene concentration (r = -0.62, P < 0.01) and the oxidative DNA damage. In conclusion, small amounts of tomato puree added to the diet over a short period can increase carotenoid concentrations and the resistance of lymphocytes to oxidative stress
Determination of carotenoids in vegetable foods and plasma
In this paper a HPLC method for the determination of lutein, zeaxanthin, β-cryptoxanthin, α-carotene, β-carotene and lycopene in mixed vegetables and fruit and in human plasma is described. The carotenoids were well separated and the separation was achieved within fifteen minutes using a HPLC system consisting of a 5 μm Vydac 20ITP54 C18 column, an UV detector, methanol-tetrahydrofuran (95:5 v/v) as mobile phase and a flow rate of 1.0 ml/min. The validity of the separation method was determined by evaluating the linearity of the calibration graphs of each carotenoid (between 0.1 and 1.0 μg/ml for all compounds except lycopene between 0.1 and 0.8 μg/ml, r = 0.999) and the accuracy of the chromatographic response (CV < 10%). The re-producibility of the retention times was also good. In the foods samples the extraction procedure was very effective whereas, the saponification step significantly damaged some of the carotenoids. In the plasma the extraction and separation of these compounds were also effective and the qualitative data obtained comparable with those reported in literature. The use of echinenone as internal standard helped to improve quality control
The comet assay for the evaluation of cell resistance to oxidative stress
Oxidative stress caused by reactive species of oxygen, damages cellular DNA, proteins and lipids and is widely recognised as one of the causes of the development of chronic disease. If we could understand to what extent a cell can contrast such oxidants, it would help towards preliminary screening of the antioxidant action in the organism. We used a technique that quantifies cellular DNA damage, the Comet assay or Single Cell Gel Electrophoresis to evaluate the resistance of human primary lymphocytes to an ex vivo treatment with H2O2, before and after the intake of a diet with high or low amounts of antioxidants. Two concentrations of H2O2 (300 μM and 500 μM) were used and a dose dependent damage of cellular DNA was registered [F(1,18)=13.003; p=0.002]. A lower DNA damage was produced by H2O2 at both the concentrations after the intake of the diet rich in antioxidants. The results obtained in our conditions seem to demonstrate that the evaluation of DNA damage by means of the Comet assay is a useful method to analyse the oxidative stress and the antioxidant capacity of the cells when challenged with H2O2
Malondialdehyde production in Jurkat T cells subjected to oxidative stress
OBJECTIVE: We investigated the relation between membrane lipid peroxidation, as evaluated by malondialdehyde (MDA), and oxidative stimuli in the Jurkat T-cell line and designed a cellular model to assess the antioxidant potential of compounds. METHODS: Jurkat T cells were subjected to different concentrations of Fe(2+) ions (from 25 to 150 micromol/L) or H(2)O(2) (from 0.1 to 5 mmol/L), and MDA was determined after separation in high-performance liquid chromatography of the adduct with thiobarbituric acid. MDA production also was investigated in cells supplemented with epigallocatechin gallate and genistein and subjected to Fe(2+) oxidative treatment. RESULTS: MDA production increased with the concentration of Fe(2+), whereas H(2)O(2) had no effect at any concentration. Oxidative stress for 15 min or 2 h produced similar MDA levels. The supplementation of epigallocatechin gallate partly prevented MDA production (about 40%, P < 0.05), whereas genistein exerted no preventive effect on lipid peroxidation. CONCLUSION: We propose this cellular model, consisting of Jurkat T cells subjected to 100 micromol/L of Fe(2+) for 15 min, to study the protective effect of antioxidant supplementation against membrane lipid peroxidation
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