ABSTRACT
The mammalian lignans enterolactone (ENL) and enterodiol, commonly found in human plasma and urine, are phytoestrogens that may contribute to the prevention of breast cancer and coronary heart disease. They are formed by the conversion of dietary precursors such as secoisolariciresinol and matairesinol lignans by the colonic microflora. The identification of lignins, cell-wall polymers structurally related to lignans, as precursors of mammalian lignans is reported here for the first time. In study 1, rats were fed rye or wheat bran (15% diet) for 5 d. Untreated brans and brans extracted with solvents to remove lignans were compared. ENL was estimated in urine samples collected for 24 h by time-resolved fluoroimmunoassay. ENL urinary excretion was reduced from 18.6 to 5.3 nmol/d (n=8; P<0.001) when lignans were removed from rye bran and from 30.5 to 6.2 nmol/d (P<0.001) when they were removed from wheat bran. These results suggest that lignins, embedded in the cell wall and retained in the bran during solvent extraction, account for 26-32% of the ENL formed from cereal brans. In study 2, rats were fed a deuterated synthetic lignin (0.2% diet) together with wheat bran (15%) for 3 d. The detection of deuterated ENL by LC-tandem MS in urine (20 nmol/d) clearly confirms the conversion of lignin into mammalian lignans. More research is warranted to determine the bioavailability of lignins in the human diet.
Subject(s)
4-Butyrolactone/analogs & derivatives , Diet , Lignans/biosynthesis , Lignin/administration & dosage , Lignin/metabolism , 4-Butyrolactone/biosynthesis , 4-Butyrolactone/urine , Animals , Biological Availability , Cell Wall/metabolism , Cellulases/metabolism , Chromatography, Liquid , Deuterium , Gas Chromatography-Mass Spectrometry , Glycoside Hydrolases/metabolism , Isoflavones/biosynthesis , Lignans/analysis , Lignans/urine , Male , Phytoestrogens , Plant Preparations , Rats , Rats, Wistar , Secale/chemistry , Spectrometry, Mass, Electrospray Ionization , Triticum/chemistryABSTRACT
Quercetin (3,3',4',5,7-pentahydroxyflavone) is one of the most abundant flavonol-type flavonoids rich in diet and suggested to possess a beneficial role in blood circulation. This study was conducted to know the effect of quercetin aglycone and one of its possible metabolite, quercetin-3-O-beta-D-glucuronide on cigarette tar extract-induced impairment of erythrocyte deformability. Erythrocyte suspension containing quercetin aglycone, quercetin-3-O-beta-D-glucuronide or quercetin-3-O-beta-D-glucoside was forced to flow through microchannels with equivalent diameter of 7 &mgr;m and its transit time was measured as an index of erythrocyte deformability using microchannel array method. Both quercetin aglycone and quercetin-3-O-beta-D-glucuronide, but not quercetin-3-O-beta-D-glucoside, substantially increased erythrocyte deformability indicating that the former two compounds affect the physicochemical state of erythrocyte by interacting with its membranes. Aqueous cigarette tar extract caused marked decrease in erythrocyte deformability with concomitant increase of membranous lipid peroxidation. In that case, quercetin aglycone suppressed the impairment of erythrocyte deformability as well as membranous lipid peroxidation. The same effect was found in quercetin-3-O-beta-D-glucuronide, eventhough its effect was lower than that of quercetin aglycone. Thus, not only quercetin aglycone but also its conjugate metabolite protects erythrocyte membrane from the damage of smoking by scavenging reactive oxygen species generated from cigarette tar. Intake of quercetin-rich food may be helpful to protect membranous damage in erythrocytes from smoking.
ABSTRACT
Alpha-tocotrienol (alpha-T3) has been suggested to protect cellular membranes against free radical damage. This study was done to estimate the effect of alpha-T3 on free radical-induced impairment of erythrocyte deformability by comparing it to alpha-tocopherol (alpha-T). An erythrocyte suspension containing 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH) was forced to flow through microchannels with an equivalent diameter of 7 microm for measuring erythrocyte deformability. A higher concentration of AAPH caused a marked decrease in erythrocyte deformability with concomitant increase of membranous lipid peroxidation. Treatment of erythrocytes with alpha-T or alpha-T3 suppressed the impairment of erythrocyte deformability as well as membranous lipid peroxidation and they also increased erythrocyte deformability even in the absence of AAPH. In these cases, the protecting effect of alpha-T3 was significantly higher than that of alpha-T. We emphasize that higher incorporating activity of alpha-T3 into erythrocyte membranes seems to be the most important reason for higher protection against erythrocyte oxidation and impairment its deformability.
