研究者詳細 - 豊國　伸哉

論文 - 豊國　伸哉

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Oxidative stress in pancreatic β-cells of GK rat, a model of non-obese NIDDM 国際誌

Ihara, Y, Yamada, Y, Uchida, K, Toyokuni, S, Seino, Y

DIABETES 47 巻頁： A263 - A263 1998年5月

Significant deposition of 4-hydroxy-2-nonenal-modified-protein adducts in human alcoholic liver disease; Positive correlation with parenchymal iron. 国際誌

Ohhira, M; Ohtake, T; Matsumoto, A; Saito, H; Kawashima, T; Ikuta, K; Tanaka, K; Fujimoto, Y; Ono, M; Toyokuni, S; Kohgo, Y

GASTROENTEROLOGY 114 巻 ( 4 ) 頁： A1315 - A1315 1998年4月

The role of oxidative DNA damage in human arsenic carcinogenesis: Detection of 8-OHdG in arsenic related Bowen's disease.

Matsui, M; Nishigori, C; Toyokuni, S; Takada, J; Akaboshi, M; Ochi, H; Ishikawa, M; Imamura, S

JOURNAL OF INVESTIGATIVE DERMATOLOGY 110 巻 ( 4 ) 頁： 526 - 526 1998年4月

The role of oxidative DNA damage in human arsenic carcinogenesis: Detection of 8-OHdG in arsenic related Bowen's disease. 国際誌

Matsui, M, Nishigori, C, Toyokuni, S, Takada, J, Akaboshi, M, Ochi, H, Ishikawa, M, Imamura, S

JOURNAL OF INVESTIGATIVE DERMATOLOGY 110 巻 ( 4 ) 頁： 526 - 526 1998年4月

Enhanced hepatic lipid peroxidation in chronic hepatitis C 査読有り国際誌

Kageyama F., Kobayashi Y., Koide S., Murohisa G., Otake M., Shimizu E., Sasada Y., Suzuki F., Kawasaki T., Nakamura H., Toyokuni S., Uchida K.

Japanese Pharmacology and Therapeutics 26 巻 ( SUPPL. 2 ) 頁： 149 - 152 1998年4月

Enhanced hepatic lipid peroxidation in chronic hepatitis C 査読有り国際誌

Kageyama F, Kobayashi Y, Koide S, Murohisa G, Otake M, Shimizu E, Sasada Y, Suzuki F, Kawasaki T, Nakamura H, Toyokuni S, Uchida K

Japanese Pharmacology and Therapeutics 26 巻 ( SUPPL. 2 ) 頁： 149 - 152 1998年4月

Involvement of nitric oxide in survival of random pattern skin flap

Um SC, Suzuki S, Toyokuni S, Kim BM, Tanaka T, Hiai H, Nishimura Y

PLASTIC AND RECONSTRUCTIVE SURGERY 101 巻 ( 3 ) 頁： 785 - 792 1998年3月

Involvement of nitric oxide in survival of random pattern skin flap

Um S.C., Suzuki S., Toyokuni S., Kim B.M., Tanaka T., Hiai H., Nishimura Y.

Plastic and Reconstructive Surgery 101 巻 ( 3 ) 頁： 785 - 792 1998年3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：Plastic and Reconstructive Surgery

A free radical gas, nitric oxide, has many useful functions when produced under physiological conditions by neurons and endothelial cells. However, excess nitric oxide has been reported to exert cytotoxic effects by direct toxicity or by reaction with superoxide. The effect of nitric oxide on the microcirculation in the periphery of a flap remains unclear, and its effect on flap survival is also unknown because nitric oxide has a dual action. Thus, we attempted to clarify the effect of nitric oxide on survival of rat random pattern skin flaps by the use of an endothelial constitutive nitric oxide synthase inhibitor (IP administration of 50 mg/kg N(G)-nitro-L- arginine) and the substrate of nitric oxide synthase (IP administration of 1 g/kg L-arginine). Three kinds of experiments were done using a total number of 120 animals: (1) time course measurement of blood flow in the flap periphery was performed using a laser Doppler flowmeter (30 rats), (2) tile length of the surviving area of flaps was measured 1 week after raising the flap (60 rats), and (3) Western blot analysis was used to determine the time course of changes ill tile amount of endothelial constitutive nitric oxide synthase and the formation of 3-nitro-L-tyrosine, which is it marker of peroxynitrite-mediated (i.e., nitric oxide-dependent) tissue damage (30 rats). Inhibition of endothelial constitutive nitric oxide synthase by N(G)- nitro-L-arginine significantly decreased the length of the surviving area of skin flap (p < 0.01 compared with the control), which was associated with a decrease in tim blood flow of the proximal portion of the flap. On the other hand, exogenous L-arginine increased the survival length of skin flap significantly (p < 0.01 compared with the control), which was associated with all increase in blood flow of the distal portion of the flap even though there was nitric oxide-mediated oxidative tissue damage. These results suggest that nitric oxide produced by endothelial constitutive nitric oxide synthase plays a role in maintaining circulation in the skin flap periphery and that L-arginine administration contributes to reduction of ischemic necrosis in the skin flap.

DOI： 10.1097/00006534-199803000-00030

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Major targets of ROS-induced cancer in rats are p15/p16 oncosuppressor genes

Toyokuni, S; Tanaka, T; Iwasa, Y; Kondo, S; Hiai, H

FREE RADICAL BIOLOGY AND MEDICINE 25 巻頁： S119 - S119 1998年

A processed grain food AOB inhibits hepatic injury in endotoxemic rats

Minamiyama, Y; Takemura, S; Toyokuni, S; Tanimoto, Y; Sato, EF; Inoue, M

BIOLOGICAL OXIDANTS AND ANTIOXIDANTS: MOLECULAR MECHANISMS AND HEALTH EFFECTS 頁： 349 - 357 1998年

A processed grain food inhibits hepatic injury in endotoxemic rats 査読有り

Minamiyama Y., Takemura S., Toyokuni S., Tanimoto Y., Sato E.F., Inoue M.

Journal of Nutritional Science and Vitaminology 44 巻 ( 4 ) 頁： 547 - 559 1998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：Journal of Nutritional Science and Vitaminology

Although various antioxidants have been tested as therapeutics for endotoxemic subjects, the results of their efficacy are conflicting. Antioxidant biofactor (AOB) is a unique processed grain food that exhibits strong antioxidant activity (Minamiyama et al, J Nutr Sci Vitaminol, 40: 467- 477, 1994). The present study was carried out to test the effect of AOB on hepatic injury in rats induced by lipopolysaccharide (LPS). Intravenous administration of LPS induced liver injury with a concomitant increase in hepatic generation of nitric oxide (NO) and 4-hydroxy-2-nonenal (HNE) modified proteins in the control group. The administration of AOB significantly inhibited the LPS-induced hepatic injury and generation of HNE- modified proteins and increased the survival rate of endotoxemic rats without affecting NO generation and plasma levels of tumor necrosis factor-α (TNF- α) and interferon-γ (IFN-γ). AOB scavenged superoxide radicals without affecting NO production by LPS-stimulated macrophage cell line J 774.2 cells. AOB also inhibited lipid peroxidation induced by LPS in the cells. These results suggested that AOB might scavenge superoxide radicals and decrease toxic metabolites including HNE, thereby inhibiting liver injury in endotoxemic rats.

DOI： 10.3177/jnsv.44.547

その他リンク： https://jlc.jst.go.jp/DN/JALC/00085275768?from=CiNii

Oxidative stress and cancer: The role of redox regulation

Toyokuni S

BIOTHERAPY 11 巻 ( 2-3 ) 頁： 147 - 154 1998年

卵巣粘液性腫ようの術中腫よう捺印細胞像の検討境界悪性例を中心に:境界悪性例を中心に国際誌

清水恵子, 小椋聖子, 村田匡好, 高尾由美, 豊國伸哉, 桜井幹己

日本臨床細胞学会雑誌 37 巻 ( 6 ) 頁： 583 - 590 1998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：特定非営利活動法人日本臨床細胞学会

卵巣腫瘍は良悪性の術前診断が困難なことが多く, 当院では術中腫瘍捺印細胞診を積極的に施行している. 1990年から1997年の8年間に術中腫瘍捺印細胞診が施行された卵巣粘液性腫瘍は34例で, 良性が16例, 境界悪性が12例, 悪性が6例であった. 術中腫瘍捺印細胞診の正診率は, 良性と悪性に関しては100%であったが, 境界悪性では75%で誤判定例はすべて良性と判定していた. 今回, われわれは境界悪性例を中心とした細胞像と, 誤判定を防ぐための新しい圧挫標本の併用について検討したので報告する.<BR>境界悪性腫瘍の細胞像の特徴は, 背景が比較的きれいで, 良性例に比べて重積性が増し, 乳頭状の集団やボール状の集団が出現していることであった. 個々の細胞異型に関しては, 良性例に比べてN/C比の増大や, 核クロマチン増量, 核小体の肥大が部分的に観察されるものの著明ではなく, 悪性例とは区別が可能と思われた. 良性と誤判定した例については, 上皮性成分の出現i数の少なさがその最大の原因と思われ, 圧挫標本の作製を加えることにより正診率の向上が期待できるものと思われた.

DOI： 10.5795/jjscc.37.583

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Oxidative stress and cancer: The role of redox regulation 査読有り

S Toyokuni

BIOTHERAPY 11 巻 ( 2-3 ) 頁： 147 - 154 1998年

Immunohistochemical detection of 4-hydroxy-2-nonenal-modified-protein adducts in human alcoholic liver diseases

Ohhira M., Ohtake T., Matsumoto A., Saito H., Ikuta K., Fujimoto Y., Ono M., Toyokuni S., Kohgo Y.

Alcoholism: Clinical and Experimental Research 22 巻 ( 3 SUPPL. 1 ) 1998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：Alcoholism: Clinical and Experimental Research

4-Hydroxy-2-nonenal (HNE) is one of the major components of lipid peroxidation product and has been shown to react with proteins to form HNE-protein adducts. HNE-protein adducts are relatively stable and can be used as a marker of radical-mediated cellular damage. We report herein the immunohistochemical analysis of HNE-protein adducts in human alcoholic liver diseases using a specific monoclonal antibody HNEJ-2. Cytoplasm of hepatocytes and bile duct epithelia was positively stained for HNE-protein adducts, and the nucleus was negligibly stained. The immunohistochemical intensity of hepatocytes was classified into three groups: strong, moderate, and faint staining. Strong staining was found in 43% of alcoholic liver diseases and in 4% of viral liver diseases. Hepatocytes of alcoholic liver diseases contained a higher amount of HNE-protein adducts than those of viral liver diseases, and the difference was statistically significant (p = 0.005; χ2 test). Semiquantitative analysis of the histological intensities of HNE-protein adducts and iron indicated a significant positive correlation (p = 0.084; Spearman's rank correlation). The localization of HNE-protein adducts and iron in hepatocytes appeared to be identical. These data suggested the correlation between HNE-protein adducts and iron. Our results indicate that HNE-protein adducts, a marker of oxidative stress-induced damage, are increased in human alcoholic liver damage, and that hepatic siderosis may act on the production of free radicals. Copyright © 1998 by The Research Society on Alcoholism.

DOI： 10.1111/acer.1998.22.s3_part1.145s

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A processed grain food AOB inhibits hepatic injury in endotoxemic rats 査読有り国際誌

Minamiyama, Y, Takemura, S, Toyokuni, S, Tanimoto, Y, Sato, EF, Inoue, M

BIOLOGICAL OXIDANTS AND ANTIOXIDANTS: MOLECULAR MECHANISMS AND HEALTH EFFECTS 頁： 349 - 357 1998年

New biomarker evidence of oxidative DNA damage in patients with non-insulin-dependent diabetes mellitus

Leinonen J., Lehtimäki T., Toyokuni S., Okada K., Tanaka T., Hiai H., Ochi H., Laippala P., Rantalaiho V., Wirta O., Pasternack A., Alho H.

FEBS Letters 417 巻 ( 1 ) 頁： 150 - 152 1997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：FEBS Letters

Urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) has been reported to serve as a sensitive biomarker of oxidative DNA damage and also of oxidative stress. We have investigated oxidative DNA damage in patients with non-insulin-dependent diabetes mellitus (NIDDM) by urinary 8-OHdG assessments. We determined the total urinary excretion of and OHdG from 24 h urine samples of 81 NIDDM patients 9 years after the initial diagnosis and of 100 non-diabetic control subjects matched for age and gender. The total 24 h urinary excretion of 8-OHdG was markedly higher in NIDDM patients than in control subjects (68.2 ± 39.4 μg vs, 49.6 ± 37.7 μg, P= 0.001). High glycosylated hemoglobin was associated with a high level of urinary 8-OHdG. The increased excretion of urinary and OHdG is seen as indicating an increased systemic level of oxidative DNA damage in NIDDM patients.

DOI： 10.1016/S0014-5793(97)01273-8

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New biomarker evidence of oxidative DNA damage in patients with non-insulin-dependent diabetes mellitus

Leinonen J, Lehtimaki T, Toyokuni S, Okada K, Tanaka T, Hiai H, Ochi H, Laippala P, Rantalaiho V, Wirta O, Pasternack A, Alho H

FEBS LETTERS 417 巻 ( 1 ) 頁： 150 - 152 1997年11月

Protein modification by lipid peroxidation products: Formation of malondialdehyde-derived N epsilon-(2-propenal)lysine in proteins 査読有り国際誌

Uchida K, Sakai K, Itakura K, Osawa T, Toyokuni S

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 346 巻 ( 1 ) 頁： 45 - 52 1997年10月

Protein modification by lipid peroxidation products: Formation of malondialdehyde-derived N(ε)(2-propenal)lysine in proteins

Uchida K., Sakai K., Itakura K., Osawa T., Toyokuni S.

Archives of Biochemistry and Biophysics 346 巻 ( 1 ) 頁： 45 - 52 1997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：Archives of Biochemistry and Biophysics

Malondialdehyde (MDA), a naturally occurring dialdehyde produced in the membrane lipid peroxidation, is known to react with lysine residues of proteins, but the MDA-lysine adducts generated in the proteins have not been characterized adequately. In the present study, we provide evidence that the enaminal-type MDA-lysine adduct, N(ε)-(2-propenal)lysine, is formed in human low-density lipoprotein (LDL) upon reaction with MDA or Cu2+. We found that the incubation of N(α)acetyllysine with MDA generated N(α)-acetyl-N(ε)- (2-propenal)lysine as the predominant product. In addition, a polyclonal antiserum raised against the MDA-modified protein was found to contain antibody populations that could be purified by affinity gel prepared by covalent attachment of N(α)-acetyl-N(ε)-(2-propenal)lysine. It was concluded that the affinity-purified anti-N(ε)-(2-propenal) lysine antibody was highly specific to the enaminal derivative of both lysine residues and phosphatidylethanolamine, based on the observations that (i) MDA was the only aldehyde which generated immunoreactive materials in proteins; (ii) among structurally defined MDA-lysine adducts tested, the antibody recognized the enaminal adduct only; and (iii) immunoreactivity to N(2-propenal)serine was still significant but much weaker than its reactivity to N-(2- propenal)ethanol- amine. Furthermore, analysis of antibody recognition sites with a variety of N-(2-propenal)alkylamines revealed that the mono-specific antibody recognized the N-2-propenal-N-ethyl moiety [-(CH2)2-NH-CH=CH - CHO] of enaminal adducts. Determination by a competitive enzyme-linked immunosorbent assay demonstrated that N(ε)-(2-propenal)lysine accounted for 33.7 and 3.1% of the lysine residues that disappeared during in vitro incubation of LDL with MDA and Cu2+, respectively. These results suggest that N(ε)-(2-propenal)lysine represents a major form of MDA covalently attached to proteins.

DOI： 10.1006/abbi.1997.0266

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