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Biomedical subjects

H Tanizawa

Publications and source records attributed to H Tanizawa.

At least 19 recordsLinked to original sources
PubMed1992

Studies on natural antioxidants in citrus species. I. Determination of antioxidative activities of citrus fruits.

The antioxidative activities of twenty types of citrus fruits were investigated with a screening method which is based on rat liver microsomal lipid peroxidation induced by dihydronicotinamide adenine dinucleotide phosphate (NADPH) and adenosine diphosphate (ADP). The activities of the exocarp were greater than those of the sarcocarp and the activities from immature fruits (collected in July-August) were greater than those from mature fruits. The strongest antioxidative activity was found in ponkan (Citrus reticulata Blanco) collected in July.

Animals↗
PubMed1992

Studies on absorption, distribution, excretion and metabolism of ginseng saponins. VIII. Isotope labeling of ginsenoside Rb2.

To clarify the pharmacokinetics of absorption, distribution and excretion of ginsenoside Rb2 (Rb2), one of the major saponins of the root of Panax ginseng, following oral administration to rats, a tritium (3H) labeling of Rb2 was examined. The C-12 position of Rb2 was labeled with 3H-sodium borohydride (3H-NaBH4) and 12-3H Rb2 and 12-3H-epi Rb2 was synthesized. This method of specific position labeling of Rb2 may be applicable to other ginsenosides. In the near future, the pharmacokinetics of Rb2 in rats may be clarified with 3H labeled Rb2.

Animals↗
PubMed1991

Studies on absorption, distribution, excretion and metabolism of ginseng saponins. VII. Comparison of the decomposition modes of ginsenoside-Rb1 and -Rb2 in the digestive tract of rats.

In order to clarify some similarities and differences of decomposition modes between 20(S)-protopanaxadiol (20(S)-ppd) saponins, represented by ginsenoside Rb1 (Rb1) and ginsenoside Rb2 (Rb2), the decompositions of Rb1 and Rb2 in the rat gastrointestinal tract, 0.1 N HCl and crude hesperidinase were investigated in detail. As in the case of Rb2 reported previously, Rb1 was hydrolyzed to 20(R,S)-ginsenoside Rg3 in 0.1 N HCl. On the other hand, hydroperoxidation of Rb1 occurred in rat stomach; the major hydroperoxide was separated and identified as the 25-hydroperoxy-23-ene derivative of Rb1 (VIII) by 1H- and 13C-nuclear magnetic resonance and fast atom bombardment mass spectrometry. The decomposition modes of 20(S)-ppd saponins (Rb1 and Rb2) differed from that of 20(S)-protopanaxatriol saponin (Rg1) in rat stomach. In rat large intestine, five decomposition products of Rb1 were observed by thin-layer chromatography, and these were identified as gypenoside XVII (G-XVII), ginsenoside Rd (Rd), ginsenoside F2 (F2), compound K (C-K) and VIII. The decomposition modes of Rb1 and Rb2, both 20(S)-ppd saponins, are considered to be different because of the hydrolysis rate in the terminal sugar moiety at the C-20 hydroxyl group in the rat large intestine. Using crude hesperidinase, Rb1 was decomposed to G-XVII, F2 and C-K, and Rb2 was decomposed to 3-O-beta-D-glucopyranosyl-20-O-[alpha-L-arabinopyranosyl(1----6)-b eta-D- glucopyranosyl]-20-(S)-ppd, F2 and C-K. Consequently, it appears that hydrolysis by beta-glucosidase, which is present in the rat large intestine, is distinct from that by crude hesperidinase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Studies on absorption, distribution, excretion and metabolism of ginseng saponins. VI. The decomposition products of ginsenoside Rb2 in the stomach of rats.

The decomposition of ginsenoside Rb2 (Rb2) in rat stomach (in vivo) and in 0.1 N HCl solution (in vitro) was investigated in detail. By treating with 0.1 N HCl, the acidity of which is similar to that of gastric juice, a part of Rb2 was hydrolyzed to 20(R,S)-ginsenoside Rg3. On the other hand, Rb2 was little decomposed in rat stomach and a small quantity of an unidentified metabolite, which was different from the hydrolyzed products in 0.1 N HCl, was observed. The metabolite was separated into four compounds, which were identified by 1H- and 13C-nuclear magnetic resonance and fast atom bombardment mass spectrometry. These compounds were determined to be 25-hydroxy-23-ene (IV), 24-hydroxy-25-ene (V), 25-hydroperoxy-23-ene (VI) and 24-hydroperoxy-25-ene (VII) derivative of Rb2, respectively. In this study, it is suggested that 20(S)-protopanaxatriol saponins undergo hydrolysis of the C-20 glycosyl moiety and hydration of the side chain, on the other hand, 20(S)-protopanaxadiol saponins undergo oxygenation of the side chain.

Absorption↗
PubMed1990

Calcium ionophore potentiates chemotactic peptide and platelet activating factor in stimulating thromboxane B2 and leukotriene B4 biosynthesis in human neutrophils.

Formyl-Met-Leu-Phe (FMLP) and platelet activating factor (PAF) stimulated the synthesis of thromboxane B2 (TXB2) and leukotriene B4 (LTB4) to a small degree in human neutrophils. Calcium ionophore A-23187 enhanced synergistically both FMLP and PAF induced eicosanoid synthesis, whereas phorbol ester PMA attenuated PAF but not FMLP stimulated arachidonate metabolism. These results suggest that calcium mobilization may be a rate limiting step in FMLP and PAF induced synthesis of TXB2 and LTB4 and that protein kinase C activation may play a negative regulatory role in PAF stimulated eicosanoid synthesis.

Calcimycin↗
PubMed1990

Studies of aloe. III. Mechanism of cathartic effect. (2).

The mechanism of action of aloe-emodin-9-anthrone, a decomposition product of barbaloin, in causing a significant increase in the water content of the rat large intestine, was investigated. Aloe-emodin-9-anthrone inhibited rat colonic Na+, K(+)-adenosine triphosphatase (ATPase) in vitro, and increased the paracellular permeability across the rat colonic mucosa in vivo. Therefore, it seemed that the increase in water content of the rat large intestine produced by aloe-emodin-9-anthrone was due to both inhibition of absorption and stimulation of secretion without stimulation of peristalsis. Furthermore, pretreatment with loperamide, an antidiarrheal agent, completely prevented the increase of paracellular permeability induced by aloe-emodin-9-anthrone but did not completely reduce the concomitant increase in residual fluid volume. These findings suggest that aloe-emodin-9-anthrone has multiple mechanisms of action involved in the increase of water content in the rat large intestine.

Aloe↗
PubMed1990

Studies on absorption, distribution, excretion and metabolism of ginseng saponins. V. The decomposition products of ginsenoside Rb2 in the large intestine of rats.

The decomposition of ginsenoside Rb2 (Rb2) in the rat large intestine after oral administration was investigated in detail. A part of Rb2 was decomposed and six decomposition products (I-VI) were observed on thin-layer chromatogram. Among them, five products (I-V) were isolated, and identification of these compounds was done by carbon-13 nuclear magnetic resonance (13C-NMR). On the basis of 13C-NMR analysis, these compounds were identified as ginsenoside Rd (I), 3-O-beta-D-glucopyranosyl-20-O- [alpha-L-arabinopyranosyl(1----6)-beta-D-glucopyranosyl]-20(S)- proto-panaxadiol (II), ginsenoside F2 (III), 20-O-[alpha-L-arabinopyranosyl(1----6)-beta-D-glucopyranosyl]-20(S )- protopanaxadiol (IV), and compound K (V), respectively.

Animals↗
PubMed1989

Synergism between chemotactic peptide and platelet-activating factor in stimulating thromboxane B2 and leukotriene B4 biosynthesis in human neutrophils.

Formyl-Met-Leu-Phe (FMLP) and platelet-activating factor (PAF) were capable of stimulating thromboxane B2 (TXB2) and leukotriene B4 (LTB4) syntheses in human neutrophils, albeit in a relatively poor degree. A combination of FMLP and PAF, however, was synergistic in stimulating TXB2 and LTB4 syntheses. Phorbol myristate acetate (PMA) appeared to attenuate PAF- but not FMLP-induced arachidonate metabolism. These results suggest that cooperative action of FMLP and PAF on arachidonate release and metabolism does exist and that PMA-mediated protein kinase C activation may regulate FMLP and PAF actions in a different manner.

Arachidonic Acid↗
PubMed1989

Effect of adriamycin on DNA, RNA and protein biosyntheses in mouse tissues, in connection with its cardiotoxicity.

We examined whether the cause of the remarkable decreases in the activities of lipid peroxidation-preventive enzymes in the heart of adriamycin (ADR)-treated mice might be related to inhibition of DNA, RNA or protein biosynthesis. It was found that biosyntheses of DNA, RNA and protein in the heart, liver and kidney of mice were markedly inhibited by ADR (15 mg/kg, ip). The inhibitory effects of ADR on each type of biosynthesis were particularly marked in the heart among the tissues examined. Strong correlations between the percentage inhibition of DNA and protein biosynthesis by ADR, and the percentage decrease in the activities of lipid peroxidation-preventive enzymes were observed in the heart, liver, kidney and lung, especially for the decrease of glutathione peroxidase activity and the inhibition of DNA and protein biosyntheses. We also found that marked decreases of DNA, RNA and protein biosynthesis in ADR-treated mice occurred not only in the heart but also in tumor tissues. From these results, we conclude that the increment of cardiac lipid peroxide in ADR-treated mice, which is closely related to the cardiotoxicity of ADR, results from inhibition of DNA, RNA and protein biosyntheses after the distribution of ADR.

Aclarubicin↗
PubMed1989

Effect of adriamycin on the activities of superoxide dismutase, glutathione peroxidase and catalase in tissues of mice.

The increment of lipid peroxide in the hearts of mice treated with adriamycin (ADR) was examined in relation to the decrease in the activities of superoxide dismutase (SOD), glutathione peroxidase (GSHpx) and catalase. The natural activities of these enzymes in mouse heart are lower than those in the liver. The biggest decrease in enzyme activity observed in the heart after ADR administration was that of GSHpx. Therefore, the increment of lipid peroxide was attributable to the decrease in the activities of these enzymes, especially GSHpx. Subsequently, the effects of antioxidants on the decreases in activities of SOD, GSHpx and catalase in the hearts of mice treated with ADR were examined. However, the decrease in the activities of the enzymes were not accompanied with any increment of lipid peroxide. This result suggests that active oxygen radicals produced by ADR through the agent's redox cycling have no effect on the activities of these enzymes. Therefore, it appears that the decrease in the activities of these enzymes induced by ADR in the mouse results from inhibition of enzyme protein biosynthesis.

Animals↗
PubMed1989

Effect of aclacinomycin on lipid peroxide levels in tissues of mice.

We have examined the lipid peroxide levels in aclacinomycin (ACM)-treated mice by using adriamycin (ADR) as a comparative drug. There was no increase in the lipid peroxide level of the heart at either 3h or 4d after ACM administration (15 mg/kg, i.p.), although the level in the heart of ADR-treated mice was elevated to 257% of that in normal mice. The effect of ACM and its glycoside-type metabolites on the increase of reduced nicotinamide adenine dinucleotide phosphate (NADPH)-dependent microsomal lipid peroxidation (in vitro) was weaker than that of ADR. Then, we examined the tissue concentrations of ACM. The AUC0-24h of ACM was the lowest in the heart among the tissues examined, being only 29.3% of that obtained with ADR. However, the concentrations of the glycoside-type metabolites of ACM in all tissues determined were higher than the concentration of ACM. In the heart, the T1/2 and AUC0-24h of ACM glycosides were somewhat higher than those of ADR. In conclusion, ACM and its metabolites do not lead to an increase in lipid peroxide level in the heart of mouse, and the difference in lipid peroxide increment in the mouse heart induced by ADR and ACM is independent of the tissue concentration of the drugs.

Aclarubicin↗
PubMed1988

[Spontaneous heart failure in BALB/c mice].

The hearts of BALB/c mice are known to acquire pronounced greyish white spots (cardiac white spots). BALB/c male mice were examined for the relationship between the incidence of cardiac white spots and weekly age, and compared with DDY male mice. During the observation period of 0.4-30 weeks, cardiac white spots on the right ventricle of BALB/c mice were first detected at three weeks (6 of 20 mice; 30%), and the maximal incidence of cardiac white spots was obtained at nine weeks (39 of 44 mice; 88%). In contrast, DDY mice were completely devoid of cardiac spots. Histopathologically, the cardiac spots were dystrophic calcinosis. There were significant increases in the relative organ weights of the heart and kidney of BALB/c mice compared with those of DDY mice. However, there was no significant difference between BALB/c and DDY mice in serum calcium concentration or histological characteristics of the parathyroid gland or bone marrow. The cardiac white spots of BALB/c mice were considered to be controlled by genetic susceptibility that occurred spontaneously with aging. The results described here suggest that BALB/c mice are adequate experimental animals for the study of myocardial disease that occurs spontaneously.

Aging↗
PubMed1987

Selective inhibition of 5-lipoxygenase pathway in rat pulmonary alveolar macrophages by cigarette smoking.

Pulmonary alveolar macrophages from sham or cigarette-smoke-exposed rats were examined for their ability to transform exogenously added arachidonate to metabolites of lipoxygenase and cyclooxygenase pathways. Synthesis of 5-HETE and leukotriene B4 was selectively inhibited by cigarette smoke exposure, whereas the formation of prostaglandin E2 and thromboxane B2 remained unchanged. Selective inhibition of the lipoxygenase pathway was further reflected by the reduced content of leukotriene B4 in bronchoalveolar fluid of smoke-exposed rats. These results suggest that lipoxygenase-derived products may play a unique role in smoking-induced pulmonary diseases.

Animals↗
PubMed1987

Increase in thromboxane B2 and decrease in prostaglandin E2 and 6-keto-prostaglandin F1 alpha release into rat bronchoalveolar fluid as a consequence of cigarette smoking.

Rats were exposed to cigarette smoke once daily for 4 to 8 weeks. Bronchoalveolar lavage fluid was obtained from each animal and assayed for immunoreactive PGE2, TXB2 and 6-Keto-PGF1 alpha. Significant increase in TXB2 and decrease in PGE2 and 6-Keto-PGF1 a release into bronchoalveolar fluid as a consequence of cigarette smoking were observed. These changes of arachidonate metabolites in lung alveoli may account in part for bronchoconstriction induced by cigarette smoking.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Effect of doxorubicin on lipid peroxide levels in tissues of mice.

The tissue concentrations of doxorubicin (DOX, 15 mg/kg, ip) and daunorubicin (DAU, 15 mg/kg, ip) in mice were investigated to clarify their relationship to the cardiotoxicity, which is considered to be closely related to the lipid peroxide level in the heart. The largest Cmax of DOX after intraperitoneal injection was obtained in the liver and was equivalent to 1.8 times that in the heart. Elimination of DOX from the heart was not delayed. Nevertheless, the increases of lipid peroxide in the heart found in in vivo and in vitro experiments were considerably higher than those in the liver. Therefore, the cardiotoxicity of DOX can not be explained simply in terms of the relative concentrations of DOX in various tissues. On the other hand, experiments on the tissue concentration of DAU, which shows weaker cardiotoxicity than DOX, and on lipid peroxidation in vitro, suggested that the relative cardiotoxicities of DOX and DAU are directly related to their relative concentrations in the mouse heart. We observed a metabolite of DOX, doxorubicinone, and an unknown metabolite of DAU in various tissues of mouse after drug injection, but these metabolites did not seem to be involved in the cardiotoxicities of DOX and DAU.

Animals↗