The total antioxidant capacity of the diet is an independent predictor of plasma beta-carotene.

OBJECTIVE: To investigate the contribution of the total antioxidant capacity (TAC) of the diet to plasma concentrations of beta-carotene. DESIGN: Cross-sectional study. SETTING: Department of Public Health and Department of Internal Medicine and Biomedical Sciences, University of Parma. SUBJECTS: A total of 247 apparently healthy adult men (n=140) and women (n=107). METHODS: A medical history, a physical exam including height, weight, waist circumference and blood pressure measurements, a fasting blood draw, an oral glucose tolerance test and a 3-day food record. RESULTS: We observe a negative trend across quartiles of plasma beta-carotene for most biological variables clustering in the insulin resistance syndrome, as well as for traditional and new risk factors for type II diabetes and cardiovascular disease (CVD), including C-reactive protein and gamma-glutamyltranspeptidase (P<0.05). Regarding dietary characteristics, energy-adjusted intake of fat, fiber, fruits, vegetables, beta-carotene, vitamin C, vitamin E and dietary TAC significantly increased with increasing plasma beta-carotene (P<0.05), whereas alcohol intake decreased (P=0.013). Adjusted geometric means (95% confidence interval) of plasma beta-carotene significantly increased across quartiles of dietary TAC, even when single dietary antioxidants were considered in the model (QI=0.087 mg/dl (0.073-0.102); QII=0.087 mg/dl (0.075-0.103); QIII=0.114 mg/dl (0.098-0.132) and QIV=0.110 mg/dl (0.093-0.130); P for linear trend=0.026). When the population was divided on the basis of alcohol consumption, this trend was also observed in subjects drinking <20 g alcohol/day (P=0.034), but not in those with higher alcohol intake (P=0.448). CONCLUSIONS: Dietary TAC is an independent predictor of plasma beta-carotene, especially in moderate alcohol drinkers. This may explain, at least in part, the inverse relationship observed between plasma beta-carotene and risk of chronic diseases associated to high levels of oxidative stress (i.e., diabetes and CVD), as well as the failure of beta-carotene supplements alone in reducing such risk.

Comparison between daidzein and genistein antioxidant activity in primary and cancer lymphocytes.

The main objective of this study was to compare the protective effect of daidzein and genistein against induced oxidative damage in Jurkat T-cell line and in peripheral blood lymphocytes of healthy subjects. After supplementation of cells with isoflavones (from 2.5 to 20micromol/L in Jurkat T-cell and from 0.01 to 2.5micromol/L in primary lymphocytes, 24h), we determined DNA damage induced by hydrogen peroxide using the comet assay and lipid peroxidation evaluating malondialdehyde (MDA) production after ferrous ion treatment. Supplementation of Jurkat cells and primary lymphocytes with both isoflavones significantly increased DNA protection from oxidative damage at concentrations between 0.1 and 5micromol/L (P<0.05), and with just daidzein, at concentrations higher than 2.5micromol/L, there was a decrease in the production of MDA (P<0.05). Our results seem to support that daidzein is just as effective as genistein in protecting cells against oxidative damage especially with respect to DNA. Moreover, since the protective effect was found at concentrations reachable in plasma after soy consumption (less than 2micromol/L), it can be assumed that the antioxidant activity of isoflavones could really contribute to the healthy properties of soy.

Bioavailability of carotenoids from spinach and tomatoes.

BACKGROUND AND AIM: Few published studies have described the bioavailability of the different carotenoids in spinach. This was designed to evaluate the effects on plasma carotenoid concentrations of a daily consumption of spinach (rich in lutein and beta-carotene), alone or together with lycopene-rich tomato puree. METHODS AND RESULTS: Nine healthy young women consumed a standard low-carotenoid diet during the pre-study phase, the spinach diet (standard diet plus 150 g spinach: 9 mg lutein, 4 mg beta-carotene) from day 0 to day 21, and then, after a wash-out period, the spinach-tomato diet (standard diet plus 150 g spinach and 25 g tomato puree: 9 mg lutein, 4.3 mg beta-carotene and 7 mg lycopene) from day 35 to day 56. The spinach and spinach-tomato supplements were consumed together with 10 g olive oil. Fasting blood samples were collected on day -7, and every week thereafter. Plasma carotenoid concentrations significantly decreased during the standard low-carotenoid diet. Lutein levels gradually increased after spinach consumption from 0.36+/-0.05 to 1.59+/-0.19 micromol/L (p<0.0001), decreased during the wash-out period from 1.59+/-0.19 to 0.62+/-0.07 micromol/L (p<0.001), and rose again after the intake of spinach-tomato puree from 0.62+/-0.07 to 1.55+/-0.17 micromol/L (p<0.0001). beta-carotene levels also increased during both dietary supplementation periods. Lycopene decreased during the spinach diet from 0.20+/-0.03 to 0.07+/-0.01 micromol/L (p<0.001) and increased during the spinach-tomato diet from 0.05+/-0.01 to 0.52+/-0.06 micromol/L (p<0.0001). CONCLUSIONS: The results of this study confirm that a regular intake of selected vegetables leads to a progressive increase in plasma carotenoid concentrations. The addition of tomato puree to spinach does not decrease lutein plasma concentrations. Furthermore, baseline plasma levels of lutein and lycopene are important variables affecting the relative increase in their levels after supplementation: ie more depleted subjects are expected to have a greater percent rise in plasma carotenoid concentrations.

Black tea extract supplementation decreases oxidative damage in Jurkat T cells.

The purpose of this study was to investigate the protective effect of black tea (BT) extract against induced oxidative damage in Jurkat T-cell line. Cells supplemented with 10 or 25 mg/L BT were subjected to oxidation with ferrous ions. Malondialdehyde (MDA) production as marker of lipid peroxidation, DNA single strand breaks as marker of DNA damage, and modification of the antioxidant enzyme activity, glutathione peroxidase (GPX) were measured. Results show the efficacy of BT polyphenols to decrease DNA oxidative damage and to affect GPX activity (P<0.05), while no effect was shown on MDA production. The succeeding investigation of the activity of caffeine and epigallocatechin gallate demonstrated their antioxidant potential with respect to the cellular markers evaluated. In conclusion, this study supports the protective effect of BT against ferrous ions induced oxidative damage to DNA and the ability of BT to affect the enzyme antioxidant system of Jurkat cells.

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.

Tomato consumption does not affect the total antioxidant capacity of plasma.

This study was performed to evaluate the effect of tomato intake on total antioxidant activity of plasma measured by the radical trapping antioxidant parameter assay in 11 healthy female subjects. After 7 d of a diet low in carotenoids and free from lycopene, subjects ate 25 g tomato puree daily (containing 7.0 mg lycopene and 0.25 mg beta-carotene) for 14 consecutive days. At the beginning and end of tomato supplementation, the carotenoid plasma concentration and the total antioxidant activity of plasma were assessed. Before tomato puree consumption, mean +/- SE total lycopene and beta-carotene plasma concentrations were 0.13 +/- 0.02 micromol/L and 0.24 +/- 0.04 micromol/L, respectively. After tomato puree supplementation, both concentrations increased significantly (0.57 +/- 0.06 micromol/L, P < 0.0001 for total lycopene, and 0.31 +/- 0. 04 micromol/L, P = 0.0036 for beta-carotene); however, total plasma antioxidant capacity values did not change significantly. From our results, intake of a food rich in carotenoids does not seem to modify the antioxidant capacity of plasma as evaluated by the radical trapping antioxidant parameter assay.

Supplementation of Jurkat T cells with green tea extract decreases oxidative damage due to iron treatment.

Regular tea consumption has been associated with a reduced risk of cancer. As demonstrated in vitro, green tea contains catechins with antioxidant properties. We evaluated the effect of the supplementation of the Jurkat T-cell line with green tea extract on oxidative damage. Cells grown in medium with or without green tea extract (10 mg/L) were treated with Fe(2+) (100 micromol/L) as an oxidative stimulus for 2 h. Cell membrane lipid peroxidation was evaluated by fatty acids pattern analysis and malondialdehyde production in alpha-linolenic acid-loaded cells. Furthermore, oxidative DNA damage (single strand breaks) was detected in cells by the Comet assay and quantified as relative tail moment (RTM). Supplementation with green tea extract significantly decreased malondialdehyde production (1.6 +/- 0.3 vs. 0.6 +/- 0.1 nmol/mg protein, P < 0.05) and DNA damage (0.32 +/- 0.07 vs. 0.12 +/- 0.04 RTM, P < 0.05) after Fe(2+) oxidative treatment. In control cells, there was no effect on membrane distribution of (n-3) fatty acids due to Fe(2+) treatment. Cell enrichment with alpha-linolenic acid increased total membrane (n-3) fatty acids. However, the oxidative treatment did not modify the distribution of polyunsaturated fatty acids. It is likely that the observed protective effects can be attributed to epigallocatechin gallate, which is present mainly (670 g/kg) in green tea extract; however, we cannot exclude contributions by other catechins. These data support a protective effect of green tea against oxidative damage.