Soft-hydrothermal processing of red cedar bedding reduces its induction of cytochrome P450 in mouse liver.

Red cedar-derived bedding materials cause changes in cytochrome P450-dependent microsomal enzyme systems in laboratory animals. We examined the effect of essential oil of red cedar (EORC), as well as the effect of bedding from which it had been removed, on the hepatic expression cytochrome P450s in mice. EORC was obtained from liquid extracts of red cedar bedding by a soft-hydrothermal process and was administered orally to mice. Between days 1 and 2 after administration, hepatic P450s were significantly induced as follows: CYP3As, 7.1x; CYP1As, 1.6x; CYP2E1, 1.5x; CYP2Cs, 1.6x. A housing study of mice indicated that red cedar bedding increased the levels of these P450s in mouse liver, whereas mice housed in cedar bedding from which EORC had been removed (ST-cedar bedding) showed significantly lower levels of P450s, especially CYP3As, CYP1As and CYP2E1. Soft-hydrothermal processing partially removed many components of EORC. In particular, several volatile sesquiterpenes, naphthalene-derived aromatics and 4,4-dimethyl-13alpha-androst-5-ene were decreased in the ST-cedar bedding, suggesting that these may be responsible for P450 induction. This study demonstrated that the removal of these volatile compounds by soft-hydrothermal processing can decrease the hepatic P450-inducing effect of red cedar bedding.

Various cooking methods and the flavonoid content in onion.

Onion is a major source of flavonoids and is cooked in various ways in the world. The major flavonoids in onion are two quercetin glycosides, quercetin 4'-O-beta-glucoside (Q4'G) and quercetin 3,4'-O-beta-diglucosides (Q3,4'G), which are recognized as bioactive substances that are good for our health. We have investigated the effect of cooking procedures on the content of antioxidants. We selected quercetin conjugates, total phenol compounds, and ascorbic acid to estimate the amount of flavonoid ingestion from onion. We examined the following cooking methods: boiling, frying with oil and butter, and microwave cooking. Various cooking methods do not consider the degradation of quercetin conjugates when cooking onion. Microwave cooking without water better retains flavonoids and ascorbic acid. Frying does not affect flavonoid intake. The boiling of onion leads to about 30% loss of quercetin glycosides, which transfers to the boiling water. At that time, the effect of additives on the quercetin conjugates is different according to the compounds. The hydrolysis of quercetin glycosides for daily cooking might occur with the addition of seasonings such as glutamic acid. Additional ferrous ions accelerated the loss of flavonoids.

beta-Glucosidase activity in the rat small intestine toward quercetin monoglucosides.

In order to evaluate the positional specificity for a glucoside group in the hydrolysis of flavonoid glucosides in the rat small intestine, beta-glucosidase activity was measured with the quercetin monoglucosides, quercetin-3-O-beta-D-glucopyranoside (Q3G), quercetin-4'-O-beta-D-glucopyranoside (Q4'G) and quercetin-7-O-beta-D-glucopyranoside (Q7G), as well as with quercetin-3-O-rutinoside (rutin) and p-nitrophenyl-beta-D-glucopyranoside (NPG) by using the HPLC technique. Enzymes were prepared from rat small intestinal mucosa of the duodenum, jejunum and ileum, among which the enzyme activity of the jejunum was highest for all the glycosides tested. Q4'G was the richest substrate for a beta-glucosidase solution among these glycosides, while rutin and NPG were both poor substrates. This suggests that dietary flavonoid glucosides are primarily hydrolyzed and liberated aglycones in the jejunum.

Influence of surface microstructure on the reaction of the active ceramics in vivo.

When porosity and macro-pore size differ in the same ceramic, the mode of bone regeneration and the degradation of ceramics in vivo is said to be different. However, the reactions in vivo of ceramics that have a different microstructure with the same porosity and the same macro-pore size, are not so far known. In this study, two kinds of beta-tricalcium phosphate (TCP) that had different microstructures but the same porosity and macro-pore size, were manufactured. These TCP were implanted in the distal femurs of 20 mature male rabbits, and their respective areas of ceramics and of regenerated bone were measured after 4, 12 and 24 wk. In both TCPs, the regenerated bone similarly decreased from 4-24 wk in a different way. The area of ceramics in one of these TCPs significantly decreased gradually throughout the observation period. On the other hand, the other TCP showed no marked decrease during the same period. This suggested a possibility that the difference in micro-structure has a large effect on the reaction of the ceramics in the bone.

Antioxidative activity of quercetin and quercetin monoglucosides in solution and phospholipid bilayers.

The antioxidative effect of quercetin, quercetin 3-O-beta-D-glucopyranoside (Q3G), quercetin 4'-O-beta-D-glucopyranoside (Q4'G) and quercetin 7-O-beta-D-glucopyranoside (Q7G) was examined in solution and liposomal phospholipid suspension. First, their peroxyl radical-scavenging activities were investigated by measuring the inhibition of hydroperoxidation of methyl linoleate initiated by a radical initiator, 2,2'-azobis(2,4-dimethylvaleronitrile) (AMVN). Quercetin exhibited the highest peroxyl radical-scavenging activity judging from the rate of hydroperoxidation during the induction period (Rinh) and the length of induction period (tinh). Although Q7G showed an induction period, its Rinh was higher and its tinh was lower than that of quercetin. Neither Q3G nor Q4'G gave a clear induction period in the curve of hydroperoxide formation. The rate of hydroperoxidation in the presence of Q3G was higher than Rinh of quercetin and the oxidative loss of Q3G was much slower than quercetin or Q7G when exposed to AMVN in solution. Q4'G exerted little inhibition compared to Q3G or Q7G. Next, the antioxidative activity of quercetin and its monoglucosides in phospholipid bilayers was examined by measuring the inhibition of lipid peroxidation in large unilamellar vesicles composed of egg yolk phosphatidylcholine (PC) and a water-soluble radical initiator. They retarded the accumulation of PC-hydroperoxides and the induction period increased in the order of Q4'G < Q3G approximately Q7G < quercetin. It is therefore concluded that quercetin acts as an antioxidant more efficiently than its monoglucosides when phospholipid bilayers are exposed to aqueous oxygen radicals.

Effects of rat bile-pancreatic juice on Fe2+ induced peroxidation of phospholipids.

The effects of rat bile-pancreatic juice (BPJ) on Fe2+ induced oxidation of soybean phosphatidylcholine (PC) was monitored to investigate the influence of this digestive juice on oxidative damage in the gastrointestinal tract. A large volume of BPJ (50% in the suspension of PC, v/v) suppressed the lipid peroxidation, but a smaller volume had the reverse effect. BPJ could decompose free fatty acid hydroperoxides (FFA-OOH) at a lower concentration (approximately 0.2 mM) completely, although its phospholipase activity liberated FFA-OOH from PC hydroperoxides. Sodium deoxycholate enhanced the Fe2+ induced oxidation of PC in a concentration-dependent manner when PC was suspended in the buffer. Boiled BPJ suppressed Fe2+ induced and peroxyl radical initiated oxidation of sodium deoxycholate micelles of soybean PC up to approximately 50% (v/v). It was strongly suggested that rat BPJ had a biphasic effect on Fe2+ induced oxidation of phospholipids depending on the enhancement by bile salts and the inhibition by antioxidant components with radical-scavenging activity and hydroperoxide-decomposing activity.

Preparation and characterization of porous apatite ceramics coated with beta-tricalcium phosphate.

Hydroxyapatite (Ca10(PO4)6(OH)2; HA) is one of the most biocompatible materials with bones, and porous HA is promising bone substitute materials for clinical applications. While there are reports that beta-tricalcium phosphate (Ca3(PO4)2; TCP) has higher resorbability than HA when the material is implanted in a bone defect. In the present study, porous HA coated with beta-TCP was prepared by our unique method. The porous HA of about 60% porosity with interconnecting pore structure was soaked in diammonium hydrogen phosphate solution, and then the HA was sintered at 900 degrees C for 3 h. beta-TCP was revealed by X-ray diffractometry on the surface of porous HA. It was possible to control the content of surface-formed beta-TCP arbitrary by varying the concentration of the solution. The obtained HA coated with 33 wt% beta-TCP (33TCP) had about 60% open porosity with the pore size from 150 to 400 microns. The average compressive strength of this porous ceramics was 17.5 MPa. Surface coated HA with beta-TCP deprived of the brittleness in handling. The weight of HA implanted into muscles was increased obviously at 4 weeks because of formation of carbonate hydroxyapatite on the surface of HA. The weight of 33TCP was scarcely changed up to 12 weeks, but the weight tended to increase at 24 weeks. The carbonate hydroxyapatite was not formed on 33TCP at 4 weeks, but formed on it at 24 weeks. Therefore beta-TCP coated porous HA behaved like beta-TCP initially after implantation, and then behaved like HA.

Microstructure and mechanical properties of hydroxyapatite ceramics with zirconia dispersion prepared by post-sintering.

Hydroxyapatite ceramics with zirconia dispersion from fine powders synthesized hydrothermally were post-sintered at 1000-1300 degrees C under 200 MPa of argon for 1 h without capsules, after normal sintering in air at 1200 degrees C for 3 h. Densification was most significant with post-sintering at 1200 degrees C. Fracture toughness, Vickers hardness and elastic properties of these materials were investigated. Post-sintering gave twice the K1c value of transparent pure hydroxyapatite ceramics. Vickers hardness and Young's modulus of the ceramics were increased by post-sintering.