Cristina Scaccini

TOTAL ANTIOXIDANT CAPACITY AS A TOOL TO ASSESS REDOX STATUS: CRITICAL VIEW AND EXPERIMENTAL DATA

The measure of antioxidant capacity (AC) considers the cumulative action of all the antioxidants present in plasma and body fluids, thus providing an integrated parameter rather than the simple sum of measurable antioxidants. The capacity of known and unknown antioxidants and their synergistic interaction is therefore assessed, thus giving an insight into the delicate balance in vivo between oxidants and antioxidants. Measuring plasma AC may help in the evaluation of physiological, environmental, and nutritional factors of the redox status in humans. Determining plasma AC may help to identify conditions affecting oxidative status in vivo (e.g., exposure to reactive oxygen species and antioxidant supplementation). Moreover, changes in the plasma AC after supplementation with galenic antioxidants or with antioxidant-rich foods may provide information on the absorption and bioavailability of nutritional compounds. Consequently, this review discusses the rationale, interpretation, confounding factors, measurement limits, and human applications of the measure of plasma AC.

Beer increases plasma antioxidant capacity in humans

The positive association of a moderate intake of alcoholic beverages with a low risk for cardiovascular disease, in addition to ethanol itself, may be linked to their polyphenol content. This article describes the effect of acute ingestion of beer, dealcoholized beer, and ethanol (4.5% v/v) on the total plasma antioxidant status of subjects, and the change in the high performance liquid chromatography profile of some selected phenolic acids (caffeic, sinapic, syringic, and vanillic acids) in 14 healthy humans. Plasma was collected at various times: before (T0), 1 hour after (T1), and 2 hours after (T2) drinking. The study is part of a larger research planned to identify both the impact of brewing on minor components potentially present in beer and their metabolic fate in humans. Beer was able to induce a significant (P < 0.05) increase in plasma antioxidant capacity at T1 (mean +/- SD: T0 1,353 +/- 320 microM; T1 1,578 +/- 282 microM), returning close to basal values at T2. All phenolic acids measured in plasma tended to increase after beer intake (20% at T1, 40% at T2). Syringic and sinapic acid reached statistical significance (P < 0.05 by one-way analysis of variance-Fishers test) at T1 and T2, respectively. Plasma metabolic parameters (glucose, total cholesterol, triglycerides, and uric acid) and plasma antioxidants (alpha-tocopherol and glutathione) remained unchanged. Ethanol removal impaired the absorption of phenolic acids, which did not change over the time of the experiment, accounting for the low (and not statistically significant) increase in plasma antioxidant capacity after dealcoholized beer drinking. Ethanol alone did not affect plasma antioxidant capacity or any of the antioxidant and metabolic parameters measured.

Role of coffee in modulation of diabetes risk

Coffee consumption has been associated with a lower risk of type 2 diabetes. This association does not depend on race, gender, geographic distribution of the study populations, or the type of coffee consumed (i.e., caffeinated or decaffeinated). This review discusses the strength of this relationship, examines the possibility that the pattern of coffee consumption could influence the association, and evaluates the possible relationship between coffee consumption and other risk factors associated with diabetes. Particular attention is paid to the identification, on the basis of the scientific evidence, of the possible mechanisms by which coffee components might affect diabetes development, especially in light of the paradoxical effect of caffeine on glucose metabolism. In addition to the role of coffee in reducing the risk of developing type 2 diabetes, the possible role of coffee in the course of the illness is explored. Finally, the possibility that coffee can also affect the risk of other forms of diabetes (e.g., type 1 diabetes and gestational diabetes) is examined.

Modulation of ceramide-induced NF-κB binding activity and apoptotic response by caffeic acid in U937 cells: comparison with other antioxidants

Ceramide acts as second messenger in the signal transduction triggered by a variety of stress stimuli and extracellular agents. Stress response through ceramide is involved in the development of many human diseases, such as atherosclerosis, inflammation, neurodegenerative disorders, and acquired immunodeficiency syndrome. Dietary polyphenols have been reported to exert a beneficial effect on the onset and development of most of these human chronic-degenerative pathologies. However, the mechanisms underlying this beneficial effect are mostly not understood at the present. To investigate the ability of polyphenols in modulating fundamental cellular functions, we studied the effect of caffeic acid, a widespread phenolic acid largely present in human diet, in the modulation of ceramide-induced signal transduction pathway leading to apoptosis in U937 cells, in comparison with other established antioxidants of nutritional interest (N-acetylcysteine, d-alpha-tocopherol acetate and ascorbic acid). Our results indicate that caffeic acid efficiently inhibits both ceramide-induced NF-kappaB binding activity and apoptosis at micromolar concentration. Other antioxidants tested are totally ineffective in inhibiting apoptosis, although affecting NF-kappaB activation. Caffeic acid was found to inhibit protein tyrosine kinase activity, suggesting that this mechanism can be on the basis of the inhibition of apoptosis. Our results suggest that dietary caffeic acid might modulate ceramide-induced signal transduction pathway and NF-kappaB activation through either antioxidant and nonantioxidant mechanisms.

Role of dietary polyphenols in platelet aggregation. A review of the supplementation studies.

Epidemiological studies suggest that high polyphenols intake from diet is associated with reduced risk for cardiovascular diseases. Platelet aggregation is a crucial mechanism in the pathogenesis and clinical expression of coronary acute syndrome, and there is extensive evidence that antiplatelet therapy reduces cardiovascular disease risk. In this review, the available literature on the effect of polyphenols supplementation on platelet aggregation in humans or animal models has been critically analyzed, taking into consideration the different experimental protocols employed. In some studies, polyphenols supplementation did not show any effect on platelet aggregation. However, in the most of the studies, polyphenols supplementation, either as purified compounds or food extracts, showed some inhibitory effects, both in humans and in animal models. The extent of the inhibition varies in a wide range, depending on the experimental conditions used. The observed inhibitory effect of polyphenols on platelet aggregation might explain, at least in part, the epidemiological data on beneficial effect of dietary polyphenols on cardiovascular disease risk and suggests a role for polyphenols in helping to prevent cardiovascular diseases.

4-methylcoumarins as antioxidants: scavenging of peroxyl radicals and inhibition of human low-density lipoprotein oxidation.

The antioxidant activity of eight synthetic 4-methylcoumarins was systematically studied. The antioxidant capacity was measured using: (i) a competition kinetic test, to measure the relative capacity to quench peroxyl radical; (ii) the in vitro oxidative modification of human low-density lipoprotein, initiated by AAPH or catalyzed by copper. In both models, the ortho-OH substitutes were found to be better antioxidant than the meta one. The most efficient antioxidant was the 7,8-dihydroxy-4-methylcoumarin and the corresponding diacetoxy-substituted was unexpectedly a good antioxidant. Finally, the presence of an ethoxycarbonylethyl substituent at the C-3 position increased the antioxidant capacity of both 7,8-dihydroxy-4-methylcoumarin and 7,8-diacetoxy-4-methylcoumarin.

White wine phenolics are absorbed and extensively metabolized in humans.

Despite the vast literature describing the biological effects of phenolic compounds, rather scarce data are available on their absorption from diet in humans. The present study focused on the absorption in humans of phenolic acids from white wine, particularly hydroxycinnamic acids and their esters with tartaric acid. The results obtained indicate that, following a single wine drink, hydroxycinnamic acids from white wine are absorbed from the gastrointestinal tract and circulate in the blood after being largely metabolized to the form of glucuronide and sulfate conjugates. Unmodified tartaric acid esters of hydroxycinnamic acids from wine are present in human plasma at low levels, if any. Wine hydroxycinnamic acids, although present in wine as conjugated forms, are still bioavailable to humans.

Beer Affects Oxidative Stress due to Ethanol in Rats

The relationship between chronic moderate beerconsumption and oxidative stress was studied in rats.Animals were fed three different isocaloric diets forsix weeks: a beercontaining diet (30% w/w), an ethanol-supplemented diet (1.1 g/100 g, thesame as in the beer diet) and an alcohol-free basaldiet. At the end of the feeding period, rats wereanalyzed for plasma and liver oxidative status. Somelivers were isolated and exposed toischemiareperfusion to assess the additional oxidativestress determined by reperfusion. No significantdifferences in plasma antioxidant status were foundamong the three dietary groups. Lipoproteins from the beer group,however, showed a greater propensity to resist lipidperoxidation. Ischemia caused a decrease in liver energyand antioxidant status in all groups. Nevertheless, ATP was lower in the livers of rats exposed tothe ethanol diet. During reperfusion, lipoperoxidationincreased significantly in all groups. However, liversobtained from ethanoltreated rats showed the higher formation of lipoperoxides. Inconclusion, a moderate consumption of beer in awell-balanced diet did not appear to cause oxidativestress in rats; moreover, probably through its minorcomponents, beer could attenuate the oxidative action ofethanol by itself.

A liquid chromatography-mass spectrometry approach to study "glucosinoloma" in broccoli sprouts.

Glucosinolates are an important class of secondary plant metabolites, possessing health-promoting properties. Young broccoli plants are a very good source of glucosinolates with concentrations several times greater than in mature plants. The aim of our study was to develop a liquid chromatography-mass spectrometry and liquid chromatography/tandem mass spectrometry qualitative and quantitative method for the measure of glucosinolates in broccoli sprouts. The described method provides high sensitivity and specificity, allowing a rapid and simultaneous determination of 14 glucosinolates. The proposed method has been validated for eight glucosinolates: glucobrassicin, glucoraphanin, glucoiberin, glucoerucin, progoitrin, gluconapin, sinigrin and glucocheirolin. The linear range was 1-150 µg ml(-1), the intra-day and inter-day precision values are within 6% and 8% at the lower limit of quantification, while the overall recovery of the eight glucosinolates was 99 ± 9%. This validated method was used successfully for analysis of glucosinolates content of broccoli sprouts grown in different conditions.

Lipid peroxidation in liver microsomes of rats fed soybean, olive, and coconut oil☆

Abstract The effect of varying unsaturation degree of dietary lipid on the oxidative response of rat liver microsomes was studied. Three groups of growing male rats were maintained for 6 weeks on 15% fat diets containing either soybean oil, olive oil, or coconut oil, with the same level of vitamin E. After 6 weeks, microsomal malondialdehyde, vitamin E, and fatty acid composition were measured in liver microsomes. The relative abundance of saturated and unsaturated fatty acids in the microsomes reflected the composition of the dietary lipid. When dietary requirement for vitamin E was satisfied, the increased polyunsaturated fatty acid intake from vegetable oils did not enhance lipid peroxidation in physiological conditions, as demonstrated by similar malondialdehyde concentrations found in the three groups. However, the somewhat lower vitamin E content measured in soybean oil-fed rats confirms an enhanced requirement for dietary antioxidant caused by the increased intake of polyunsaturated fatty acids. The susceptibility of liver microsomes to lipid peroxidation stimulated by the ADP/iron/ascorbate system was also studied. Membranes of soybean oil-fed rats exhibited the highest peroxidation rate, as shown by oxygen consumption and malondialdehyde and 4-hydroxy-2,3-trans-neonenal production, because of the lower concentration of vitamin E and of the higher content of polyunsaturated fatty acids. Microsomes of olive oil- and coconut oil-fed rats showed highest protection against lipid peroxidation.