Effect of a barley-vegetable soup on plasma carotenoids and biomarkers of cardiovascular disease.

Functional foods that provide benefits beyond their traditional nutritional value have attracted much interest. Aim of the study was to evaluate the nutritional and the functional properties of a frozen ready-to-eat soup containing barley and pigmented vegetables. Both glycaemic index and the glyceamic load of ready-to-eat soup were evaluated in vivo. Moreover the bioavailability of carotenoids (lutein and beta-carotene) and the effect on lipid profile and lipid peroxidation were studied in 38 volunteers whose diet was supplemented for two weeks with a daily portion (250 g) of the ready-to-eat soup. Plasma levels of carotenoids (lutein and beta-carotene) and plasma total antioxidant capacity significantly increased after 2 weeks of treatment. Furthermore, we observed a decrease in the levels of lipids (total cholesterol and low density lipoprotein-cholesterol) and of markers of lipid peroxidation (oxidized low density lipoprotein and lipid hydroperoxides) in plasma of all subjects. The glyceamic index of the product was 36, therefore it could be considered a low glyceamic index food. An accurate selection of vegetable foods results in a palatable and healthy product that provides benefits on plasma lipids and lipid peroxidation (Protocol number 211525).

Lipid peroxidation in hemodialysis patients: effect of vitamin C supplementation.

OBJECTIVES: Renal failure is associated with several metabolic disturbances and increasing evidences support a role of oxidative stress and impaired antioxidant defence in the pathologic mechanisms that may contribute to accelerated atherogenesis in these patients. Aim of the study was to further investigate the relationship between oxidative stress and chronic renal failure. DESIGN AND METHODS: We compared the paraoxonase (PON1) activity, the levels of lipid hydroperoxides and AGE adducts in plasma of hemodialysis patients before and after intravenous administration of vitamin C. RESULTS: An increase in lipid hydroperoxides, AGE adducts and a decrease in the activity of PON1 were observed in patients with respect to controls. The comparison before and after supplementation with vitamin C showed an increase of PON1 activity and a decrease of AGE and lipid hydroperoxides levels. CONCLUSIONS: The results provide further evidence that lipid peroxidation and impairment of antioxidant system in plasma of patients may play a role in renal disease and suggest that evaluation of PON1 activity could represents an useful approach to monitor antioxidant treatment and new dialysis therapies.

Effect of acylethanolamides on lipid peroxidation and paraoxonase activity.

N-acylethanolamides (NAEs) are hydrophobic molecules synthesized in many tissues. An increase in the plasma levels of NAEs has been observed in human diseases. Previous studies have suggested that NAEs could exert a protective effect against oxidative stress. Aim of the study was to investigate whether NAEs (oleoylethanolamide, palmitoylethanolamide and anandamide), differing for acyl chain length and unsaturation, exert a protective role against plasma lipid peroxidation triggered by incubation with Cu2+2 or AAPH (2,2'-azobis(2-amidinopropane) dihydrochloride). Moreover, we investigated the effect of NAEs on the activity of HDL-associated paraoxonase (PON1), an enzyme involved in the antioxidant end anti-inflammatory role of human high density lipoproteins (HDL). The results demonstrated that the NAEs protect plasma lipids and PON1 activity against AAPH and/or copper-induced oxidation.

Glycation of human high density lipoprotein by methylglyoxal: effect on HDL-paraoxonase activity.

OBJECTIVE: Methylglyoxal (MG), a reactive carbonyl compound formed primarily from triose phosphates, appears to be involved in the molecular mechanisms of diabetes, end-stage renal disease and neurodegenerative diseases. Methylglyoxal exerts several biological activities. Among these it promotes advanced glycation end products (AGEs), which are crucial in pathogenesis of human disease. Previous studies have demonstrated that MG reacts with proteins and compositional modifications reflect loss of biological activity. The aim of the study was to investigate the effect of in vitro MG-induced glycation on human high density lipoprotein (HDL) and on the activity of the enzyme paraoxonase-1 (PON1). METHODS: HDL was incubated in the absence or in the presence of MG (0.2mmol/L and 1.0mmol/L) (MG-HDL) for different times (3, 6, 24h) at 37° C. We evaluated apoprotein compositional changes, in both control and MG treated HDL, using intrinsic fluorescence of tryptophan and monitoring the decrease of free amino groups. Furthermore we evaluated fluorescent advanced glycation end products (Ex=370nm, Em=440nm) and the activity of HDL-paraoxonase. RESULTS: We demonstrated that human HDL is susceptible to glycation by MG (0.2mmol/L and 1mmol/L). The decrease of free amino groups and of intrinsic fluorescence of tryptophan demonstrates HDL apoprotein modifications in HDL incubated with MG. The compositional changes are associated with a significant increase in fluorescent advanced glycation end products and with a significant decrease of paraoxonase-1 enzyme activity associated with the HDL surface. CONCLUSIONS: HDL-associated paraoxonase is responsible for the anti-inflammatory and anti-oxidative properties of HDL and detoxification against homocysteine-thiolactone. Therefore, modifications of apoprotein composition and the decrease of paraoxonase-1 activity in MG-treated HDL could affect the protective effect exerted by HDL against oxidative damage and could contribute to complications in patients affected by diseases associated with aging and oxidative stress.

Altered inflammation, paraoxonase-1 activity and HDL physicochemical properties in obese humans with and without Prader-Willi syndrome.

Prader-Willi syndrome (PWS) represents the most common form of genetic obesity. Several studies confirm that obesity is associated with inflammation, oxidative stress and impairment of antioxidant systems; however, no data are available concerning PWS subjects. We compared levels of plasma lipids and C-reactive protein (CRP) in 30 subjects of 'normal' weight (18.5-25 kg/m(2)), 15 PWS obese (>30 kg/m(2)) subjects and 13 body mass index (BMI)-matched obese subjects not affected by PWS. In all subjects, we evaluated the levels of lipid hydroperoxides and the activity of paraoxonase-1 (PON1), an enzyme involved in the antioxidant and anti-inflammatory properties exerted by high-density lipoproteins (HDLs). Furthermore, using the fluorescent molecule of Laurdan, we investigated the physicochemical properties of HDLs isolated from normal weight and obese individuals. Altogether, our results demonstrated, for the first time, higher levels of lipid hydroperoxides and a lower PON1 activity in plasma of obese individuals with PWS with respect to normal-weight controls. These alterations are related to CRP levels, with a lower PON1:CRP ratio in PWS compared with non-PWS obese subjects. The study of Laurdan fluorescence parameters showed significant modifications of physicochemical properties in HDLs from PWS individuals. Whatever the cause of obesity, the increase of adiposity is associated with inflammation, oxidative stress and alterations in HDL compositional and functional properties.

Celiac disease, inflammation and oxidative damage: a nutrigenetic approach.

Celiac disease (CD), a common heritable chronic inflammatory condition of the small intestine caused by permanent intolerance to gluten/gliadin (prolamin), is characterized by a complex interplay between genetic and environmental factors. Developments in proteomics have provided an important contribution to the understanding of the biochemical and immunological aspects of the disease and the mechanisms involved in toxicity of prolamins. It has been demonstrated that some gliadin peptides resistant to complete proteolytic digestion may directly affect intestinal cell structure and functions by modulating gene expression and oxidative stress. In recent years, the creation of the two research fields Nutrigenomics and Nutrigenetics, has enabled the elucidation of some interactions between diet, nutrients and genes. Various dietary components including long chain ω-3 fatty acids, plant flavonoids, and carotenoids have been demonstrated to modulate oxidative stress, gene expression and production of inflammatory mediators. Therefore their adoption could preserve intestinal barrier integrity, play a protective role against toxicity of gliadin peptides and have a role in nutritional therapy of celiac disease.

Effect of homocysteinylation on high density lipoprotein physico-chemical properties.

High density lipoproteins (HDL) exert a protective effect against homocysteinylation due to the activity of the enzyme paraoxonase/thiolactonase associated to the lipoprotein surface. However, a small amount of N-homocysteinylated HDL (N-Hcy-HDL) is present in human plasma, suggesting that homocysteinylation of plasma lipoproteins occurs in vivo. Aim of the present study was to investigate the effect of homocysteinylation on apoprotein structure and physico-chemical properties of HDL using the analysis of the fluorescent emission spectra of tryptophan and Laurdan (6-dodecanoyl-2-dimethyl-aminonaphthalene). Our results demonstrated that the increase in -SH groups in HDL homocysteinylated in vitro (Hcy-HDL) was associated with apoprotein conformational changes and modifications of physico-chemical properties. A significant decrease of paraoxonase and lactonase activity of HDL bound PON1 has also been observed in Hcy-HDL. A significant decrease of the enzyme activity has been observed also in purified PON1 homocysteinylated following the same experimental conditions used for HDL. Moreover, we demonstrated that oxidized HDL were more susceptible to homocysteinylation with respect to control HDL. The modifications of apoprotein conformation and physico-chemical properties in Hcy-HDL and the decrease of paraoxonase-1 activity could affect the protective effect of HDL against oxidative damage and/or homocysteinylation and could contribute to accelerated atherosclerosis in patients affected by diseases associated with oxidative damage, in renal disorders and in patients affected by genetic or nutritional disorders of homocysteine or folate metabolism.

HDL-paraoxonase and membrane lipid peroxidation: a comparison between healthy and obese subjects.

High-density lipoproteins (HDLs) play a key role in the protection against oxidative damage. The enzyme paraoxonase-1 (PON1) associated at the surface of HDL modulates the antioxidant and anti-inflammatory role of HDL. Previous studies have demonstrated a decrease of serum PON in obese patients. The aim of this study was to investigate whether modifications of PON1 activity reflect in a different ability to protect and/or repair biological membranes against oxidative damage. Thirty obese patients at different grades of obesity (BMI ranging from 30.4 to 64.0 kg/m(2)) and 62 age-matched control subjects (BMI <25 kg/m(2)) were included in the study. The ability of HDL to protect membranes against oxidative damage was studied using erythrocyte membranes oxidized with 2,2-azobis(2 amidinopropane)dihydrochloride (AAPH) (ox-membrane). The membrane lipid hydroperoxide levels were evaluated after the incubation of ox-membranes in the absence or in the presence of HDL of controls or obese patients. The results confirm that HDL exerts a protective effect against lipid peroxidation. The ability of HDL to repair erythrocyte membranes was positively correlated with HDL-PON activity and negatively correlated with lipid hydroperoxide levels in HDL. These results suggest that PON modulates the HDL repairing ability. HDL from obese patients repaired less efficiently erythrocyte membranes against oxidative damage with respect to HDL from healthy subjects. A negative relationship has been established between BMI of obese patients and the protective effect of HDL. In conclusion, the decrease of HDL-PON activity and the lower HDL protective action against membrane peroxidation in obese patients could contribute to accelerate the cellular oxidative damage and arteriosclerosis in obesity.

Effect of phytosterols on copper lipid peroxidation of human low-density lipoproteins.

OBJECTIVE: Phytosterols and stanols have received much attention in the past several years because of their cholesterol-lowering properties, and several studies have shown a protective effect against cardiovascular disease and colon and breast cancer development. A significant decrease of plasma low-density lipoprotein (LDL) cholesterol and apolipoprotein B has been demonstrated in subjects whose diet was supplemented with 2g/d of plant sterols. Changes in plasma lipoprotein levels were associated with a decrease of oxidized LDL, suggesting that plant sterols could exert an antioxidant effect. The aim of the present study was to further investigate the interaction between the major dietary phytosterols and plasma lipoproteins. Moreover, their antioxidant effect against in vitro-induced lipid peroxidation of human LDL was investigated. METHODS: Susceptibility to copper-induced lipid peroxidation was investigated in LDLs isolated from plasma of normolipemic subjects. Concentrations of beta-sitosterol, campesterol, and stigmasterol ranging from 5 to 50 microM were studied. Analyses of the emission fluorescence spectra of tryptophan and of the probe 6-dodecanoyl-2-dimethyl-aminoaphthalene were used to investigate the effect of phytosterols on apoprotein structure and physicochemical properties of LDL. RESULTS: Our results demonstrated that phytosterols exert an inhibitory effect against copper-induced lipid peroxidation of LDLs, as shown by the lowered levels of conjugated dienes in oxidized lipoproteins incubated with different concentrations of plant sterols (5-50 microM). Moreover, analysis of fluorescence emission spectra of tryptophan and 6-dodecanoyl-2-dimethyl-aminoaphthalene demonstrated that phytosterols prevent the alterations of apoprotein structure and physicochemical properties associated with copper-triggered lipid peroxidation of lipoproteins. CONCLUSION: We suggest that the effect exerted by beta-sitosterol, stigmasterol, and campesterol against lipid peroxidation of LDL possibly related to phytosterol-lipoprotein interactions could be of physiologic relevance.

Lipid peroxidation in stroke patients.

BACKGROUND: Paraoxonase is high-density lipoprotein (HDL)-associated esterase/lactonase implicated to play a role in the antioxidant and anti-inflammatory properties exerted by HDL. Increasing evidence support a role of free radicals and oxidative stress in neuronal damage induced by ischemia-reperfusion. The aim of this study was to further investigate the relationship between lipoprotein oxidative damage and stroke. METHODS: We compared the paraoxonase activity and levels of lipid hydroperoxides in plasma isolated from healthy subjects (n=50) and from stroke patients (n=49). Moreover, the correlations between biochemical markers and the National Institute of Health Stroke Scale (NIHSS), which is widely used to study neurological severity, were evaluated. RESULTS: Our results demonstrated, for the first time, that the activity of paraoxonase in plasma of stroke subjects was significantly lower than controls (p<0.001) and the levels of lipid hydroperoxides were significantly higher in plasma from patients (p<0.001). Moreover, using linear regression analysis, significant correlations between the activity of paraoxonase, lipid peroxidation and the severity of neurological deficit at admission were observed. CONCLUSIONS: These results provide further evidence that oxidative stress and impairment of the antioxidant system may play a role in stroke. Antioxidant activity of plasma may be an important factor providing protection from neurological damage caused by stroke-associated oxidative stress.