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Flavanones are found specifically and abundantly in citrus fruits. Their beneficial effect on vascular function is well documented. However, little is known about their cellular and molecular mechanisms of action in vascular cells. The goal of the present study was to identify the impact of flavanone metabolites on endothelial cells and decipher the underlying molecular mechanisms of action. We investigated the impact of naringenin and hesperetin metabolites at 0·5, 2 and 10 μm on monocyte adhesion to TNF-α-activated human umbilical vein endothelial cells (HUVEC) and on gene expression. Except hesperetin-7-glucuronide and naringenin-7-glucuronide (N7G), when present at 2 μm, flavanone metabolites (hesperetin-3′-sulphate, hesperetin-3′-glucuronide and naringenin-4′-glucuronide (N4′G)) significantly attenuated monocyte adhesion to TNF-α-activated HUVEC. Exposure of both monocytes and HUVEC to N4′G and N7G at 2 μm resulted in a higher inhibitory effect on monocyte adhesion. Gene expression analysis, using TaqMan Low-Density Array, revealed that flavanone metabolites modulated the expression of genes involved in atherogenesis, such as those involved in inflammation, cell adhesion and cytoskeletal organisation. In conclusion, physiologically relevant concentrations of flavanone metabolites reduce monocyte adhesion to TNF-α-stimulated endothelial cells by affecting the expression of related genes. This provides a potential explanation for the vasculoprotective effects of flavanones.
Effects of different inulin-type fructan fractions were studied on atherosclerotic plaque formation in male apo E-deficient mice. Thirty-two mice were randomly divided into four groups and received either a semi-purified sucrose-based diet (control group), or diets in which sucrose was replaced in part by various inulin-type fructans (10 g/100 g): long-chain inulin, oligofructose, or an oligofructose-enriched inulin for 16 weeks. The presence of atherosclerotic plaques was assessed by histomorphometry in the aortic sinus. The apo E-deficient mice fed long-chain inulin or an oligofructose-enriched inulin had about 35 % and 25 % less atherosclerotic lesion area compared with the control group, respectively. Feeding long-chain inulin significantly reduced plasma cholesterol concentrations (P<0·001), and the three inulin-type fructans reduced triacylglycerol (TAG) concentrations compared with the control group (P<0·001). Both the long-chain inulin and an oligofructose-enriched inulin significantly lowered hepatic cholesterol concentrations compared with the control diet (P<0·05). Hepatic TAG concentrations were significantly lower in all three groups fed the fructan-supplemented diets v. the control group (P<0·0001). The results of the present study suggest that inhibition of atherosclerotic plaque formation is more potent in the presence of long-chain inulin, either alone or in combination with oligofructose (an oligofructose-enriched inulin), and that this probably is related to changes in lipid metabolism.
Zn has been shown to possess antioxidant properties in vitro and in vitro. As inadequate dietary Zn intake has been reported in these populations, Zn supplementation may protect against oxidative stress and thereby limit the progression of degenerative diseases in such populations. We conducted the present study to evaluate the long-term supplementation effects of two moderate doses of Zn on in vitro Cu-induced LDL oxidation in French men and women.Three groups of sixteen healthy subjects aged 55–70 years from each sex participated in this randomized double-blind, placebo-controlled study. Each group received for six months either 0, 15 or 30mg supplemental Zn per d. At the beginning and at the end of the supplementation periods, dietary intakes of Zn, Cu, Fe and vitamin E were estimated using 4d food-intake records (including the weekend) and the GENI program. Zn, Cu, Fe and vitamin E statuswere also determined. In vitro LDL oxidizability (basal conjugated diene level, maximal conjugated diene formation and lag time) and lipid parameters were also determined. Dietary intakes of Zn, Cu, Fe and vitamin E were adequate in this population. Zn supplementation significantly increased serum Zn levels but did not significantly modify Cu, Fe or vitamin E status. However, Zn supplementation had no effect on in vitro LDL oxidation parameters, nor were there any sex-related differences in in vitro LDL oxidizability. The present study showed that long-term Zn supplementation of healthy subjects aged 55–70 years had no effect on in vitro Cu-induced LDL oxidation under the study conditions.
Excessive dietary NaCl in association with a paucity of plant foods, major sources of K alkaline salts, is a common feature in Western eating habits which may lead to acid–base disorders and to Ca and Mg wasting. In this context, to evaluate the effects of potato, rich in potassium citrate, on acid–base homeostasis and mineral retention, Wistar rats were fed wheat starch (WS) or cooked potato (CP) diets with a low (0·5 %) or a high (2 %) NaCl content during 3 weeks. The replacement of WS by CP in the diets resulted in a significant urinary alkalinisation (pH from 5·5 to 7·3) parallel to a rise in citrate and K excretion. Urinary Ca and Mg elimination represented respectively 17 and 62% of the daily absorbed mineral in rats fed the high-salt WS diet compared with 5 and 28% in rats fed the high-salt CP diet. The total SCFA concentration in the caecum was 3-fold higher in rats fed the CP diets compared with rats fed the WS diets, and it led to a significant rise in Ca and Mg intestinal absorption (Ca from 39 to 56 %; Mg from 37 to 60 %). The present model of low-grade metabolic acidosis indicates that CP may be effective in alkalinising urine, enhancing citrate excretion and ameliorating Ca and Mg balance.
The underlying mechanisms for the detrimental consequences of a high-fructose diet in animal models are not clear. However, the possibility exists that fructose feeding facilitates oxidative damage. Thus, the aim of the present study was to assess, in weaning rats, the effect of a high-sucrose diet v. starch diet for 2 weeks on oxidative stress variables. Plasma lipid levels were measured and lipid peroxidation was evaluated by urine and plasma thiobarbituric acid-reactive substances (TBARS). The susceptibilities of several tissues to peroxidation were determined in tissue homogenates after in vitro lipid peroxidation. Antioxidant defence variables were evaluated by measuring plasma and heart vitamin E levels, and heart superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities. Higher plasma triacylglycerol (P<0·01) and TBARS (P<0·01) levels were found in rats fed the sucrose diet as compared with the starch-fed group, whereas plasma α-tocopherol levels were significantly decreased in the sucrose-fed group compared with the starch-fed group (P<0·01). Higher urine TBARS (P<0·01) were found in the sucrose-fed group compared with the starch-fed group, suggesting increased production of these substances from lipid peroxidation in vivo. Higher susceptibility to peroxidation in heart, thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group. No statistical differences were observed for liver TBARS level between the two groups. Heart SOD activity was significantly decreased (P<0·001) in the sucrose-fed group compared with the starch-fed group, whereas heart vitamin E level and GPX activity were not different between the groups. However, the in vitro generation of superoxide radical in heart homogenate, measured by electron spin resonance detection and spin trapping, was not increased in the sucrose-fed group compared with starch-fed rats. Altogether, the results indicate that a short-term consumption of a high-sucrose diet negatively affects the balance of free radical production and antioxidant defence in rats, leading to increased lipid susceptibility to peroxidation.
Recent studies underline the importance of the immunoinflammatory processes in the pathology of Mg deficiency. Neutrophils possess a superoxide anion-generating NADPH oxidase and its inappropriate activation may result in tissue damage. The aim of the present study was to assess the effect of experimental Mg deficiency in the rat on polymorphonuclear leucocytes (PMN) activity and the role of increasing extracellular Mg. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 d. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of PMN. Higher plasma interleukin 6 and NO concentrations and increased lipid peroxidation in the heart were found in Mg-deficient rats as compared with control rats. As shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared with neutrophils from control rats. Moreover, the chemiluminescence of PMN from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. PMN from Mg-deficient rats also showed an increased activity of phagocytosis in comparison with neutrophils from control animals. Increasing extracellular Mg concentration in the incubating medium of PMN (0·8 v. 8·0 mM) decreased the chemiluminescence activity of PMN from control rats following opsonized zymosan activation. Chemiluminescence activities of PMN from Mg-deficient rats following phorbol myristate acetate or opsonized zymosan challenge were also decreased by high extracellular Mg concentration. From this work, it appears that PMN activation is an early consequence of Mg deficiency and that high extracellular Mg concentration inhibits free radicals generation.
Experimental Mg deficiency leads to alterations in the immune response. Reduction of thymus weight and histological changes were previously observed in Mg-deficient rats after several weeks on a deficient diet, suggesting that functions of this immune organ may be affected by Mg deficiency. More recently, changes in the immune system during early Mg deficiency were shown. Thus, in the present study we examined modifications in the thymus during the early stages of Mg deficiency in weanling rats. From our results, it appears that Mg deficiency accelerates thymus involution. The assessment of apoptosis (enumeration of apoptotic cells on the basis of morphological criteria and intranucleosomal degradation of genomic DNA) showed greater values in thymuses from Mg-deficient rats as compared with controls. This was observed very early, since a significant difference was shown on the second day of deficiency, before reduced weight of thymus, which was recorded in the later period. These results indicate the relationship of accelerated thymus involution with an active process of cell death. Mg deficiency led to histological changes in the thymus. In the early stage of deficiency (second day) the presence of inflammatory cells was shown, suggesting that the inflammatory process was already occurring in the tissue studied. Later (eighth day) an increased proportion of epithelial reticular cells in the cortex was shown, indicating a remodelling process occurring in this period. Enhanced susceptibility to peroxidation also occurred very early during Mg deficiency. It may be hypothesized that disturbances in Mg status of short duration could have cellular effects with various deleterious consequences.
Triacylglycerol-rich lipoproteins (TGRLP) were isolated from Cu-deficient and control rats. TGRLP from Cu-deficient rats appeared more fluid than those from controls as sensed by the fluorescence anisotropy of 1,6-diphenyl-l-3,5-hexatriene (DPH). This high fluidity was related to alow cholesterol: phospholipid ratio and high triacylglycerol content in these lipoproteins. TGRLP from Cu-deficient rats were more susceptible to in vitro peroxidation than lipoproteins from control rats as shown by the rate of diene conjugation. The damage induced by the peroxidation resulted in a more ordered state of the lipid fraction especially in lipoproteins from Cu-deficient rats. Thus, after in vitro peroxidation, TGRLP from Cu-deficient rats were more rigid than those from controls. These results suggest that Cu deficiency induces modifications in physicochemical properties of TGRLP which could affect their metabolism.
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