研究者詳細 - 豊國　伸哉

論文 - 豊國　伸哉

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CONGENITAL MYOTONIC-DYSTROPHY WITH PROGRESSIVE EDEMA AND HYPOPROTEINEMIA

FUJII T, YORIFUJI T, OKUNO T, TOYOKUNI S, OKADA S, MIKAWA H

BRAIN & DEVELOPMENT 13 巻 ( 1 ) 頁： 58 - 60 1991年

CONGENITAL MYOTONIC-DYSTROPHY WITH PROGRESSIVE EDEMA AND HYPOPROTEINEMIA

FUJII T, YORIFUJI T, OKUNO T, TOYOKUNI S, OKADA S, MIKAWA H

BRAIN & DEVELOPMENT 13 巻 ( 1 ) 頁： 58 - 60 1991年

Congenital myotonic dystrophy with progressive edema and hypoproteinemia

Fujii T., Yorifuji T., Okuno T., Toyokuni S., Okada S., Mikawa H.

Brain and Development 13 巻 ( 1 ) 頁： 58 - 60 1991年

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Brain and Development

We report a patient with congenital myotonic dystrophy who had progressive edema and hypoproteinemia. An atrioseptal defect and patent ductus arteriosus were noted and were considered to be the cause of the right heart failure and edema. Although urinary protein levels were minimal, infusion of albumin did not improve the hypoproteinemia. Administration of dexamethasone increased the serum protein level, but the edema was not ameliorated. Autopsy revealed a slight lymphatic dilatation in the small intestine, suggesting protein-losing enteropathy. © 1991, All rights reserved.

DOI： 10.1016/S0387-7604(12)80300-7

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A CASE OF BIOPSY-PROVEN MYOCARDITIS PROGRESSING TO AUTOPSY-PROVEN DILATED CARDIOMYOPATHY

MATOBA Y, MATSUMORI A, OHTANI H, TOMINAGA M, FUJIWARA H, TOYOKUNI S, TAKAHASHI K, MIDORIKAWA O, KAWAI C

CLINICAL CARDIOLOGY 13 巻 ( 10 ) 頁： 732 - 737 1990年10月

A case of biopsy‐proven myocarditis progressing to autopsy‐proven dilated cardiomyopathy Open Access

Matoba Y., Matsumori A., Ohtani H., Tominaga M., Fujiwara H., Kawai C., Toyokuni S., Midorikawa O., Takahashi K.

Clinical Cardiology 13 巻 ( 10 ) 頁： 732 - 737 1990年10月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Clinical Cardiology

A 22‐year‐old man presented with congestive heart failure following flulike symptoms. The diagnosis of acute myocarditis was confirmed by endomyocardial biopsy, which revealed mild infiltration of inflammatory cells. A favorable response to beta‐adrenergic receptor blockade was seen, and the patient was discharged without symptoms. Five months later, however, congestive heart failure recurred, and intracardiac thrombi were demonstrated. The patient died after two months. Postmortem examination revealed left ventricular dilatation with slight interstitial fibrosis; the diagnosis was dilated cardiomyopathy. Thus, progression of biopsy‐proven myocarditis to dilated cardiomyopathy 10 months after the onset of disease was documented. Copyright © 1990 Wiley Periodicals, Inc.

DOI： 10.1002/clc.4960131013

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A CASE OF BIOPSY-PROVEN MYOCARDITIS PROGRESSING TO AUTOPSY-PROVEN DILATED CARDIOMYOPATHY

MATOBA Y, MATSUMORI A, OHTANI H, TOMINAGA M, FUJIWARA H, TOYOKUNI S, TAKAHASHI K, MIDORIKAWA O, KAWAI C

CLINICAL CARDIOLOGY 13 巻 ( 10 ) 頁： 732 - 737 1990年10月

COMBINED HISTOCHEMICAL AND BIOCHEMICAL-ANALYSIS OF SEX-HORMONE DEPENDENCE OF FERRIC NITRILOTRIACETATE-INDUCED RENAL LIPID-PEROXIDATION IN DDY-MICE

TOYOKUNI S, OKADA S, HAMAZAKI S, MINAMIYAMA Y, YAMADA Y, LIANG P, FUKUNAGA Y, MIDORIKAWA O

CANCER RESEARCH 50 巻 ( 17 ) 頁： 5574 - 5580 1990年9月

COMBINED HISTOCHEMICAL AND BIOCHEMICAL-ANALYSIS OF SEX-HORMONE DEPENDENCE OF FERRIC NITRILOTRIACETATE-INDUCED RENAL LIPID-PEROXIDATION IN DDY-MICE

TOYOKUNI S, OKADA S, HAMAZAKI S, MINAMIYAMA Y, YAMADA Y, LIANG P, FUKUNAGA Y, MIDORIKAWA O

CANCER RESEARCH 50 巻 ( 17 ) 頁： 5574 - 5580 1990年9月

Combined Histochemical and Biochemical Analysis of Sex Hormone Dependence of Ferric Nitrilotriacetate-induced Renal Lipid Peroxidation in ddY Mice 査読有り国際誌

Toyokuni S., Okada S., Hamazaki S., Minamiyama Y., Yamada Y., Liang P., Fukunaga Y., Midorikawa O.

Cancer Research 50 巻 ( 17 ) 頁： 5574 - 5580 1990年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Cancer Research

Ferric nitrilotriacetate (Fe-NTA) induces renal proximal tubular necrosis, a consequence of lipid peroxidation, that finally leads to a high incidence of renal adenocarcinoma in rats and mice. Male animals are much more susceptible than female animals to both effects. Moreover, the distribution of the susceptible proximal tubules is different between male and female animals. The present study investigated the effects of castration and sex hormones on Fe-NTA-induced renal lipid peroxidation. Male and female ddY mice were either left untreated, castrated, and/or treated with testosterone or estriol. Histochemical (reactivity to cold SchifTs reagent) and biochemical (thiobarbSturic acid-reactive substance) evaluations were performed 1 h after the i.p. injection of Fe-NTA (5 mg iron/kg). Testosterone treatment and/or oophorectomy increased the Schiff pos-itivity of the renal cortical proximal tubules and the amount of thiobar-bituric acid-reactive substance (testosterone-treated female > intact female, P < 0.005; castrated female > intact female, P < 0.1; castrated and testosterone-treated female >intact female, P < 0.005). In contrast, estriol treatment and/or orchiectomy decreased the Schiff positivity of the renal cortical proximal tubules and the amount of thiobarbituric acid-reactive substance (estriol-treated male < intact male, P < 0.01; castrated male < intact male, P < 0.01; castrated and estriol-treated male < intact male, P < 0.005). Estradiol treatment produced similar results to estriol treatment (estradiol-treated male <intact male, P < 0.005). Castration and/or administration of the opposite sex hormone reversed the sex difference in the distribution of proximal tubules susceptible to lipid peroxidation. However, the i.v. injection to male mice, 5 min prior to the Fe-NTA treatment, of conjugated estrogen that is promptly excreted via the urine produced no significant effect. Thus, altered metabolic pathways rather than the direct scavenging activity of estrogens seem to be involved in the sex hormone-dependent difference of lipid peroxidation. Genetically determined sex hormone status appears to have influenced the incidence of Fe-NTA-induced renal adenocarcinoma in intact animals. © 1990, American Association for Cancer Research. All rights reserved.

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Combined histochemical and biochemical analysis of sex hormone dependence of ferric nitrilotriacetate-induced renal lipid peroxidation in ddY mice.

Toyokuni S, Okada S, Hamazaki S, Minamiyama Y, Yamada Y, Liang P, Fukunaga Y, Midorikawa O

Cancer research 50 巻 ( 17 ) 頁： 5574 - 80 1990年9月

THIOBARBITURIC ACID-REACTIVE SUBSTANCE FORMATION OF RAT-KIDNEY BRUSH-BORDER MEMBRANE-VESICLES INDUCED BY FERRIC NITRILOTRIACETATE

HAMAZAKI S, OKADA S, TOYOKUNI S, MIDORIKAWA O

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 274 巻 ( 2 ) 頁： 348 - 354 1989年11月

Thiobarbituric acid-reactive substance formation of rat kidney brush border membrane vesicles induced by ferric nitrilotriacetate

Hamazaki S., Okada S., Toyokuni S., Midorikawa O.

Archives of Biochemistry and Biophysics 274 巻 ( 2 ) 頁： 348 - 354 1989年11月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Archives of Biochemistry and Biophysics

An iron chelate, ferric nitrilotriacetate (Fe3+-NTA), is nephrotoxic and also carcinogenic to the kidney in experimental animals. Iron-promoted lipid peroxidation in the proximal tubules is thought to be responsible for the pathologic process. In the present study, iron-promoted lipid peroxidation, with thiobarbituric acid (TBA) formation as an indication, in the tubular surface was simulated in vitro using rat kidney brush border membrane vesicles and the results were compared with those using linoleate micelles and rat liver microsomal lipid liposomes. Addition of ascorbate, cysteine, or dithiothreitol to the Fe3+-NTA solution resulted in consumption of dissolved oxygen and promoted the lipid peroxidation in the micelles and in the liposomes. In contrast, addition of glutathione to the Fe3+-NTA solution caused only sluggish oxygen consumption and far less peroxidation in these lipid systems. When the brush border membrane vesicles were used for the peroxidation substrate, Fe3+-NTA and glutathione could promote TBA formation at a rate comparable to that elicited by Fe3+-NTA with cysteine or dithiothreitol. Acivicin, a γ-glutamyl transpeptidase inhibitor, suppressed the peroxidation of the brush border membrane vesicles promoted by Fe3+-NTA and glutathione. These results suggest the following mechanism of proximal tubular cell lipid peroxidation promoted by Fe-NTA: Fe3+-NTA filtered through glomeruli is rapidly reduced by cysteine and Fe2+-NTA starts lipid peroxidation at the site, leading to proximal tubular necrosis. Cysteine is amply supplied by the decomposition of glutathione within the lumen by the action of γ-glutamyl transpeptidase and dipeptidase situated at the proximal tubular brush border membrane. © 1989.

DOI： 10.1016/0003-9861(89)90448-7

Scopus

INDUCTION OF MESOTHELIOMA BY INTRAPERITONEAL INJECTIONS OF FERRIC SACCHARATE IN MALE WISTAR RATS

OKADA S, HAMAZAKI S, TOYOKUNI S, MIDORIKAWA O

BRITISH JOURNAL OF CANCER 60 巻 ( 5 ) 頁： 708 - 711 1989年11月

THIOBARBITURIC ACID-REACTIVE SUBSTANCE FORMATION OF RAT-KIDNEY BRUSH-BORDER MEMBRANE-VESICLES INDUCED BY FERRIC NITRILOTRIACETATE 査読有り

S HAMAZAKI, S OKADA, S TOYOKUNI, O MIDORIKAWA

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 274 巻 ( 2 ) 頁： 348 - 354 1989年11月

Induction of mesothelioma by intraperitoneal injections of ferric saccharate in male wistar rats

Okada S., Hamazaki S., Toyokuni S., Midorikawa O.

British Journal of Cancer 60 巻 ( 5 ) 頁： 708 - 711 1989年11月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：British Journal of Cancer

Iron appears to play a major role in catalysing free radical production, leading to lipid peroxidation and DNA damage. We, therefore, investigated the effect of colloidal iron deposited in the peritoneum. Wistar male rats were given either ferric saccharate, ferric saccharate and nitrilotriacetic acid (NTA), NTA or saline. NTA was shown previously to ‘free’ iron to promote lipid peroxidation and an iron chelate of NTA is known to be carcinogenic to the kidney. Iron at a dose of 5 mg kg-1 day-1, and saline at a dose of 0.5 ml day-1 were injected i.p. for 3 months. NTA at a dose of 83.5 mg kg-1 day1 was give i.p for 5 months. All the rats were killed about a year later for histological examination. In nine of the 19 rats treated with ferric saccharate, mesothelial tumors were induced in the serosa of the tunica vaginalis or the length of the spermatic cord. Among rats treated with ferric saccharate and NTA, seven had localised mesotheliomas in the above locations and six had wide-spread peritoneal mesotheliomas. No mesothelial tumors developed in either NTA treated or saline treated rats. No pleural mesotheliomas were found in any group. These findings add to the evidence that iron is involved in some carcinogenic processes. © The Macmillan Press Ltd., 1989.

DOI： 10.1038/bjc.1989.344

Scopus

INDUCTION OF MESOTHELIOMA BY INTRAPERITONEAL INJECTIONS OF FERRIC SACCHARATE IN MALE WISTAR RATS

OKADA S, HAMAZAKI S, TOYOKUNI S, MIDORIKAWA O

BRITISH JOURNAL OF CANCER 60 巻 ( 5 ) 頁： 708 - 711 1989年11月

OXYGEN REDUCTION AND LIPID-PEROXIDATION BY IRON CHELATES WITH SPECIAL REFERENCE TO FERRIC NITRILOTRIACETATE

HAMAZAKI S, OKADA S, LI JL, TOYOKUNI S, MIDORIKAWA O

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 272 巻 ( 1 ) 頁： 10 - 17 1989年7月

OXYGEN REDUCTION AND LIPID-PEROXIDATION BY IRON CHELATES WITH SPECIAL REFERENCE TO FERRIC NITRILOTRIACETATE 査読有り

S HAMAZAKI, S OKADA, JL LI, S TOYOKUNI, O MIDORIKAWA

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 272 巻 ( 1 ) 頁： 10 - 17 1989年7月

Oxygen reduction and lipid peroxidation by iron chelates with special reference to ferric nitrilotriacetate

Hamazaki S., Okada S., Li J., Toyokuni S., Midorikawa O.

Archives of Biochemistry and Biophysics 272 巻 ( 1 ) 頁： 10 - 17 1989年7月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：Archives of Biochemistry and Biophysics

A certain iron chelate, ferric nitrilotriacetate (Fe3+-NTA) is nephrotoxic and also carcinogenic to the kidney in mice and rats, a distinguishing feature not shared by other iron chelates tested so far. Iron-promoted lipid peroxidation is thought to be responsible for the initial events. We examined its ability to initiate lipid peroxidation in vitro in comparison with that of other ferric chelates. Chelation of Fe2+ by nitrilotriacetate (NTA) enhanced the autoxidation of Fe2+. In the presence of Fe2+-NTA, lipid peroxidation occurred as measured by the formation of conjugated diene in detergent-dispersed linoleate micelles, and by the formation of thiobarbituric acid-reactive substances in the liposomes of rat liver microsomal lipids. Addition of ascorbic acid to Fe3+-NTA solution promoted dose-dependent consumption of dissolved oxygen, which indicates temporary reduction of iron. On reduction, Fe3+-NTA initiated lipid peroxidation both in the linoleate micelles and in the liposomes. Fe3+-NTA also initiated NADPH-dependent lipid peroxidation in rat liver microsomes. Although other chelators used (deferoxamine, EDTA, diethylenetriaminepentaacetic acid, ADP) enhanced autoxidation, reduction by ascorbic acid, or in vitro lipid peroxidation of linoleate micelles or liposomal lipids, NTA was the sole chelator that enhanced all the reactions. © 1989.

DOI： 10.1016/0003-9861(89)90188-4

Scopus

CIRRHOSIS OF THE LIVER INDUCED BY CUPRIC NITRILOTRIACETATE IN WISTAR RATS - AN EXPERIMENTAL-MODEL OF COPPER TOXICOSIS

TOYOKUNI S, OKADA S, HAMAZAKI S, FUJIOKA M, LI JL, MIDORIKAWA O

AMERICAN JOURNAL OF PATHOLOGY 134 巻 ( 6 ) 頁： 1263 - 1274 1989年6月

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