α-Tocopherol (α-Toc) is abundant in LDL and thought to prevent the oxidation of LDL together with various water-soluble antioxidants. Recently, it was reported that α-Toc and γ-Toc metabolites, α-carboxyethyl-6-hydroxychromans (CEHC) and γ-CEHC, are water-soluble antioxidants. In this study, we investigated the interaction between α-Toc and CEHC against 1,1-diphenyl-2-picryl-hydrazyl (DPPH) radicals and LDL oxidation. We administered 600 mg of α-Toc to healthy male volunteers to obtain LDL including high levels of α-Toc before antioxidant administration. The α-Toc content of their LDL was increased after consumption at 24 h (18.3 μg/mL) above the level before consumption (6.6 μg/mL). The lag time of LDL at 24 h after α-Toc consumption (α-Toc rich LDL) with α-CEHC (98.5±8.2 min) or γ-CEHC (101.3±9.0 min) was longer than that of only α-Toc-rich LDL (78.1±9.0 min). Furthermore, we examined the interaction of LDL with CEHC and α-Toc in vitro (5-20 μg/mL). The lag times of 5 and 10 μg/mL α-Toc were 65.5±18.9 min and 69.5±15.5 min, and that of 20 μg/mL α-Toc (83.5±20.2 min) was longer than the control value (55.7±14.1 min). The lag time of 20 μg/mL α-Toc with α-CEHC (98.7±25.7 min) or γ-CEHC (100.6±25.3 min) was longer than that of only α-Toc (83.5±20.2 min). These results suggest that CEHC has the potential to delay the oxidation of LDL, while enhancing the antioxidative activity of α-Toc both in vitro and ex vivo.
As part of a series of non-clinical studies to evaluate the safety of PureSorb-QTM40 (Water-soluble type CoQ10 powder, CoQ10 content is 40 w/w%; hereinafter referred to as P40), male and female rats were treated orally by gavage with P40 once a day for 91 d, and its repeated dose toxicity was assessed. Control animals were treated with a 0.5 w/v% solution of methylcellulose, the vehicle for P40. Each test group consisted of 6 animals of each sex. No adverse effects of P40 were noted in general signs, body weight, food consumption, ophthalmological examination, urinalysis, hematological examination, blood chemical analysis, necropsy, organ weights, or histopathological examination in animals of either sex. From these results, the no observed adverse effect level of P40 was estimated at 2,000 mg/kg in both sexes of rats under the conditions of the present study, and P40 was confirmed to be a food material whose safety is high.
In the present study we investigated the effects of 11 kinds of edible seaweeds (6 brown and 5 red algae) which contain characteristic seaweed dietary fibers on the induction of D-GalN (D-galactosamine)-hepatopathy in rats (Exps. 1 and 2). Then, the efficacy of various components prepared from Gelidium sp., which was found to alleviate the hepatopathy in Exps. 1 and 2, was examined (Exp. 3). The rats were fed the diets containing various kinds of seaweeds (Exps. 1 and 2), or several components of Gelidium sp. such as total dietary fiber (TDF), soluble dietary fiber (SDF), insoluble dietary fiber (IDF) and dietary fiber-free components (DFFC) (Exp. 3), for 8 d. The rats in all experiments were injected with D-GalN (800 mg/kg body weight) intraperitoneally at the 7th day to induce liver injury and were sacrificed 24 h after the injection of D-GalN. The serum transaminase activities (ALT and AST) and lactate dehydrogenase (LDH) were determined to evaluate the levels of hepatopathy. In Exp. 3, the total GSH concentration in the liver, plasma and cecal contents and organic acid concentration in cecal contents were also evaluated. In Exps. 1 and 2, repressive effects against D-GalN-hepatopathy were shown by four seaweeds Laminaria sp., Gelidium sp., Sargassum fulvellum and Eisenia bicyclis. In Exp. 3, it was found that protective activity in Gelidium sp. against D-GalN-hepatopathy existed not only in the SDF but also in the DFFC fraction. The results in Exp. 3 also indicated that the total GSH but not organic acid concentration in the cecal contents were significantly correlated with serum AST activity, suggesting that the protective effect of Gelidium sp. on D-GalN-hepatopathy in rats is related to GSH metabolism in the intestine.
Diabetic cataract is an ocular disease represented as blindness by lens opacification. Oxidative as well as osmotic stress caused by accumulation of polyols within the lens has been shown to be associated with glucose-induced cataractogenesis. Taurine has an antioxidant capacity and its level in diabetic cataractous lens is markedly decreased. Therefore, we investigated whether taurine is a part of antioxidative defense mechanism involved in protecting the lens against high glucose-induced oxidative stress and tissue damage. Lenses were isolated from male Sprague-Dawley rats weighing about 180-200 g and cultured in high glucose medium (55.6 mM) for 6 d as a model of high glucose-induced cataractogenesis. To investigate the antioxidative effect of taurine, 30 mM taurine was added in normal medium for 2 d before the addition of high glucose. The culture of lenses in high glucose medium increased the weight and opacity of lenses of and the carbonylated protein level, and decreased glutathione (GSH) content. Although there were no significant effects of taurine on the weight or opacity of lenses, pretreatment of lenses with 30 mM taurine significantly reversed the level of protein carbonylation and GSH to those of controls. Therefore, taurine might spare GSH and protect the lens from oxidative stress induced by a high concentration of glucose.
Nicotianamine (NA) is a nonprotein amino acid that inhibits the angiotensin I-converting enzyme (ACE) in the renin-angiotensin system (RAS). The purpose of this study is to prove that NA contributes to the suppression of hypertension by preferential inhibition of ACE. On comparison with EDTA—a chelator—we found that the inhibition pattern of NA for ACE is that of mixed inhibition and that NA exhibits weak chelation effects for zinc, copper, and cobalt ions. Therefore, we investigated whether NA inhibited zinc-containing enzymes other than ACE in vitro. The results revealed that NA does not inhibit leucine aminopeptidase or alkaline phosphatase in rat serum. On the other hand, NA demonstrated specific inhibitory effects for rat serum ACE and aortic ACE. These results suggest that the preferential inhibition of circulatory and tissue ACE by NA can contribute to the suppression of hypertension.
The health of individuals is not markedly affected by the nutrients ingested in a single day; rather it is influenced by dietary habits over a long period of time. However, it is impossible to survey usual intake directly because recording diet over a long period of time is burdensome for the subjects, so usual dietary intake is rarely measured directly. Instead, we estimated the distribution of selected nutrients in subjects' usual dietary intake using a statistical method (Best-Power method) described previously. And we assessed the proportion of nutritionally at-risk subjects in individual groups based on the new Japanese Dietary Reference Intakes (DRIs), the Estimated Average Requirement (EAR), or the tentative dietary goal for preventing life-style related diseases (DG) as cut-points. We collected the survey data from 208 men and 251 women, aged 50 to 69 y in 2004 and 2005. The survey was carried out on three non-consecutive days four times each year: in spring, summer, autumn, and winter. The distribution of nutrients in the usual intake was estimated from a dietary survey of 3 d using one-way analyses of variance. We found that the proportion of the population at risk for nutrient deficiency was overestimated in the 1-d intake distribution. On the other hand, the fraction that was nutritionally at-risk in terms of salt intake, according to DG as the cut-point, was underestimated in the 1-d intake distribution: 74.0% of men and 82.5% of women in the 1-d intake, and 90.5% and 93.2%, respectively, for the estimated usual intake adjusted for seasonal variation.
Royal jelly (RJ) has several physiological effects and is widely used in commercial medical products and health foods. We examined the effects of RJ supplementation on serum lipoprotein metabolism in humans. Fifteen volunteers were divided into an RJ intake group (n=7) and a control group (n=8). The RJ group took 6 g per day for 4 wk. Their serum total cholesterol (TC) and serum low-density lipoprotein (LDL) decreased significantly compared with those of the control group (p<0.05). There were no significant differences in serum high-density lipoprotein (HDL) or triglyceride concentrations. Moreover, the relationship between the serum cholesterol and lipoprotein levels was investigated. Among the lipoprotein fractions, small very-low-density lipoprotein was decreased (p<0.05) after RJ intake. Our results suggest that dietary RJ decreases TC and LDL by lowering small VLDL levels.
Corn dextrin preparations with average degradation degrees of 16.7 and 167, or average molecular masses of 2,700 and 27,000, were covalently introduced with 4.5 and 11.2 to 35.4 mol of phosphoric acid, respectively, per mole by dry-heating at 110 to 140°C for 24 h with sodium phosphate, and their effects on cell proliferation and production of immunoglobulin A (IgA) were investigated in C3H/HeN mouse spleen cell cultures. All the phosphorylated dextrin had mitogenic effects and stimulated proliferative responses induced by lipopolysaccharide (LPS) and concanavalin A (ConA). The phosphorylated dextrin with an average degradation degree of 16.7 was divided into 3 fractions, which had 3.6, 4.0 and 6.5 mol of phosphoric acid per mole when the molecular mass of each dextrin was postulated to be 2,700. LPS-induced proliferation was greatest with the preparation having 3.6 mol of phosphoric acid per mole of dextrin, whereas ConA-induced proliferation was strongest with 6.5 mol of phosphoric acid. On the other hand, the divided dextrin enhanced production of IgA by approximately 1.2-, 2.0- and 2.2-fold in accordance with the increasing amount of phosphoric acid. These results indicate that phosphorylated dextrin stimulates humoral immune responses in mouse spleen cell cultures.
Corn dextrin with an average degradation degree of 16.7, or molecular mass of 2,700, was covalently introduced with 4.5 mol of phosphoric acid per mole by dry-heating with sodium phosphate. The effect on immunoglobulin production of the phosphorylated dextrin in mice that orally ingested lipopolysaccharide (LPS) from Salmonella typhimurium was investigated. No significant difference in body weight gain was observed between mice fed a phosphorylated dextrin-containing diet and those fed a control (dextrin-containing) diet. Fecal and intestinal anti-LPS immunoglobulin (Ig) A, intestinal and serum anti-LPS IgG, and fecal and intestinal total IgA levels were significantly higher in the mice given the phosphorylated dextrin. In contrast, serum and intestinal levels of IgM specific to the LPS were similar between the two groups. Moreover, spleen cells from mice fed the phosphorylated dextrin-added diet had significantly higher levels of anti-LPS IgG and IgA than those from mice on the control diet. These results suggest that dietary phosphorylated dextrin protects against local and systemic invasions of pathogenic microorganisms in mice.
Bioavailability of glabridin was elucidated to show that this compound is one of the active components in the traditional medicine licorice. Using a model of intestinal absorption, Caco-2 cell monolayer, incorporation of glabridin was examined. Glabridin was easily incorporated into the cells and released to the basolateral side at a permeability coefficient of 1.70±0.16 cm/s×105. The released glabridin was the aglycone form and not a conjugated form. Then, 10 mg (30 μmol)/kg body weight of standard chemical glabridin and licorice flavonoid oil (LFO) containing 10 mg/kg body weight of glabridin were administered orally to rats, and the blood concentrations of glabridin was determined. Glabridin showed a maximum concentration 1 h after the dose, of 87 nmol/L for standard glabridin and 145 nmol/L for LFO glabridin, and decreased gradually over 24 h after the dose. The level of incorporation into the liver was about 0.43% of the dosed amount 2 h after the dose. These detected glabridins were in the aglycone form and not conjugated forms. The bioavailability was calculated to be AUCinf of 0.825 and 1.30 μM·h and elimination T1/2 of 8.2 and 8.5 h for standard glabridin and LFO, respectively. Adipocytokine levels were determined in the rats. The secreted amount of monocyte chemoattractant protein-1 was significantly lower in the glabridin group compared to control vehicle group. Thus, dietary glabridin was at least partly incorporated into the body in an unchanged form, though most dietary flavonoids are converted to non-active conjugate forms during intestinal absorption.
The liver plays the main role in the secretion of food-derived α-tocopherol into the circulation through the functioning of α-tocopherol transfer protein (α-TTP). However, the effect of liver disease on α-TTP level and α-tocopherol metabolism has not been clarified. We examined the amount of liver α-TTP and its effect on serum α-tocopherol concentration in liver injury. Male Wistar rats were injected intraperitoneally with D-galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, α-tocopherol concentrations, and hepatic α-TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection. On the basis of body weight changes and serum transaminase activities, the livers were found to be in an injured state 24 and 48 h after galactosamine injection but had recovered by 72 h. The hepatic α-TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the α-TTP protein level had begun to decrease. Lipid and α-tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h. Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver α-tocopherol concentration was unchanged. These results show that galactosamine-induced liver injury decreases hepatic α-TTP synthesis in rats. Serum α-tocopherol concentration was not directly affected by the acute change in hepatic α-TTP level, suggesting that the chronic changes in α-TTP activity would be necessary to regulate serum α-tocopherol concentration.
We previously showed that dietary sesame seed and its lignan inhibited γ-tocopherol metabolism to 2,7,8-trimethyl-2(2'-carboxyethyl)-6-hydroxychroman (γ-CEHC), a γ-tocopherol metabolite, and markedly elevated tissue γ-tocopherol concentration in rats. The aim of this study was to clarify the effect of dietary sesame seed on α-tocopherol metabolism. Vitamin E-deficient rats fed a vitamin E-free diet for 4 wk were fed a diet containing α-tocopherol, α- and γ-tocopherol, or α-tocopherol with sesame seed for 7 d. Urinary excretion of 2,5,7,8-tetramethyl-2(2'-carboxyethyl)-6-hydroxychroman (α-CEHC), a α-tocopherol metabolite, in rats fed α-tocopherol with sesame seed was inhibited (p<0.05) as compared with that in rats fed α-tocopherol alone, or α- and γ-tocopherol. The γ-CEHC excretion was also less (p<0.05) in rats fed α-tocopherol with sesame seed than that in rats fed α- and γ-tocopherol. The inhibition of α- and γ-CEHC excretion by sesame seed was accompanied by elevation (p<0.05) of the α- and γ-tocopherol concentration in the liver. These results suggest that dietary sesame seed inhibits not only γ-tocopherol metabolism to γ-CEHC but also α-tocopherol metabolism to α-CEHC in rats.
Microbial breakdown of carbohydrates in the large intestine mainly produces short-chain fatty acids (SCFA). SCFA stimulate epithelial cell proliferation of the digestive tract in vivo. Succinic acid sometimes accumulates in the colonic lumen. However, the effect of succinic acid on colonic epithelial cell proliferation is unknown. Thus, we planned to clarify the influence of succinic acid on colonic epithelial cell proliferation in vivo. We continuously administered infusate with or without succinic acid (100 mM) into the distal colon of rats for 6 d and measured accumulated mitosis per crypt of distal colon of these rats. Succinic acid infused into rat colons significantly inhibited colonic cell proliferation and reduced crypt size. These results clearly indicated the inhibitory effects of succinic acid on colonic epithelial cell proliferation in vivo.
Viscosity of whole pig cecal contents with (2 g/200 mL) or without insoluble dietary fibers prepared from wheat bran of two particle sizes (WB fine 0.22±0.22 mm2, n=1,723; WB coarse 0.51±1.12 mm2, n=1,457, mean±SD) was measured using a rotary viscometer equipped with a vane spindle at the shear rates of 0.05, 0.16, 0.47, 0.78 and 1.56 (s−1) and at 0 and 2 h. Such measurements were repeated twice each for five different donor pig groups. We were able to measure the coefficient of viscosity of such samples over a wide range of shear rate. Coefficient of viscosity depended on shear rate. Addition of insoluble dietary fiber increased the coefficient of viscosity. Insoluble dietary fiber from WB coarse had a significantly stronger effect than that from WB fine. The above results demonstrated that insoluble dietary fibers of wheat bran increase the viscosity of gut contents, and thereby potentially retard digestion and absorption.
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