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Biomedical subjects

H Tanizawa

Publications and source records attributed to H Tanizawa.

At least 37 records · Page 2Linked to original sources
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↗