研究者詳細 - 豊國　伸哉

論文 - 豊國　伸哉

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Helicobacter pylori eradication attenuates oxidative stress in human gastric mucosa

Pignatelli B, Bancel B, Plummer M, Toyokuni S, Patricot LM, Ohshima H

AMERICAN JOURNAL OF GASTROENTEROLOGY 96 巻 ( 6 ) 頁： 1758 - 1766 2001年6月

Difference in thioredoxin expression in viral myocarditis in inbred strains of mice 国際誌 Open Access

Miyamoto M, Kishimoto C, Shioji K, Nakamura H, Toyokuni S, Nakayama Y, Kita M, Yodoi J, Sasayama S

JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION 65 巻 ( 6 ) 頁： 561 - 564 2001年6月

Helicobacter pylori eradication attenuates oxidative stress in human gastric mucosa 国際誌

Pignatelli B, Bancel B, Plummer M, Toyokuni S, Patricot LM, Ohshima H

AMERICAN JOURNAL OF GASTROENTEROLOGY 96 巻 ( 6 ) 頁： 1758 - 1766 2001年6月

Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice Open Access

MIYAMOTO Miki, KISHIMOTO Chiharu, SHIOJI Keisuke, NAKAMURA Hajime, TOYOKUNI Shinya, NAKAYAMA Yukie, KITA Masakazu, YODOI Junji, SASAYAMA Shigetake

Japanese circulation journal 65 巻 ( 6 ) 頁： 561 - 564 2001年5月

掲載種別：研究論文（学術雑誌）出版者・発行元：社団法人日本循環器学会

Redox regulating mechanisms may be involved in the pathogenesis of viral myocarditis and thioredoxin (TRX) is a small multifunctional protein that contains a redox active sequence. The present study investigated the histopathology and characteristics of TRX expression in acute coxsackievirus B3 myocarditis in inbred strains of mice (severe myocarditis in DBA/2 mice, moderate myocarditis in BALB/c mice and mild myocarditis in C57BL/6 mice). Thioredoxin was upregulated and its expression correlated with the severity of the disease. In addition, 8-hydroxy-2'-deoxyguanosine, which is an established marker for oxidative stress, was concominantly positive in damaged myocytes. Thus, TRX may be specifically induced by the acute inflammatory stimuli in murine viral myocarditis, and the severity and development of acute viral myocarditis may be regulated by the cellular redox state. (Jpn Circ J 2001; 65: 561-564)

DOI： 10.1253/jcj.65.561

Open Access

CiNii Research

Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice Open Access

MIYAMOTO Miki, KISHIMOTO Chiharu, SHIOJI Keisuke, NAKAMURA Hajime, TOYOKUNI Shinya, NAKAYAMA Yukie, KITA Masakazu, YODOI Junji, SASAYAMA Shigetake

Japanese circulation journal 65 巻 ( 6 ) 頁： 561 - 564 2001年5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：社団法人日本循環器学会

DOI： 10.1253/jcj.65.561

Open Access

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Spontaneous loss-of-function mutations of the 8-oxoguanine DNA glycosylase gene in mice and exploration of the possible implication of the gene in senescence

Mori M., Toyokuni S., Kondo S., Kasai H., Naiki H., Toichi E., Hosokawa M., Higuchi K.

Free Radical Biology and Medicine 30 巻 ( 10 ) 頁： 1130 - 1136 2001年5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：Free Radical Biology and Medicine

8-Oxoguanine is one of the major premutagenic oxidative base legions in vivo and is suspected to play a crucial role in various pathophysiological processes, such as cancer and aging. Mammalian 8-oxoguanine DNA glycosylase (OGG1) is thought to play a major role in the removal of 8-oxoguanine adducts in vivo. We have identified several inbred mouse strains with a spontaneous mutation, OGG1-R336H or double mutations, OGG1-R304W/R336H. R304W mutation caused a complete loss of OGG1 activity, while the R336H mutation led to disruption of nuclear localization of the enzyme although the activity remained normal. Among the double mutants was SAMP1, which exhibits accelerated senescence and short lifespan. We assessed the possible implication of the mutant OGG1 and 8-oxoguanine in aging utilizing SAMP1 mice. SAMP1 retained 1.5- to 1.9-fold increase in 8-oxoguanine level of hepatic nuclear DNA as compared with normal mice, until at least 12 months of age. A genetic association study, however, indicated that the mutant Ogg1 gene per se is not responsible for the accelerated senescence and short lifespan of SAMP1. Mutant OGG1 may be associated with pathologic conditions in other mouse strains. © 2001 Elsevier Science Inc.

DOI： 10.1016/S0891-5849(01)00511-1

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Spontaneous loss-of-function mutations of the 8-oxoguanine DNA glycosylase gene in mice and exploration of the possible implication of the gene in senescence

Mori M, Toyokuni S, Kondo S, Kasai H, Naiki H, Toichi E, Hosokawa M, Higuchi K

FREE RADICAL BIOLOGY AND MEDICINE 30 巻 ( 10 ) 頁： 1130 - 1136 2001年5月

Angiosarcoma of the scalp: Absence of vascular endothelial cadherin in primary and metastatic lesions

Tanioka M., Ikoma A., Morita K., Fujii H., Toda K.I., Takahashi K., Tanaka T., Nishigori C., Jin G., Higashi S., Toyokuni S., Miyachi Y.

British Journal of Dermatology 144 巻 ( 2 ) 頁： 380 - 383 2001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：British Journal of Dermatology

A 73-year-old man with angiosarcoma of the scalp died about 1 year after disease onset, despite systemic and topical administration of recombinant interleukin-2. Histopathology showed typical changes of endothelial cells with very sparse lymphocytic infiltration into the tumour. An autopsy revealed that the primary site penetrated cranial bone and invaded vertically into the subarachnoid space. Multiple metastases to lung, chest wall, vertebrae and ribs were also found. On immunofluorescence staining, the expression of vascular endothelial cadherin, which is present in normal endothelium, was absent from both primary and metastatic sites. This may have promoted local invasion and metastasis.

DOI： 10.1046/j.1365-2133.2001.04032.x

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Pericardial fluid from patients with ischemic heart disease induces myocardial cell apoptotis via an oxidant stress-sensitive p38 mitogen-activated protein kinase pathway. 査読有り国際誌

Iwakura A, Fujita M, Hasegawa K, Toyokuni S, Sawamura T, Nohara R, Sasayama S, Komeda M

Journal of molecular and cellular cardiology 33 巻 ( 3 ) 頁： 419 - 30 2001年3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：Journal of Molecular and Cellular Cardiology

Factors produced by the heart are accumulated at high concentrations in pericardial fluid. We recently reported that pericardial fluid from patients with ischemic heart disease induces apoptosis in an F2 cell line. To characterize factors in pericardial fluid from patients with ischemic heart disease, we investigated signaling pathways by which this pericardial fluid induces apoptosis in cardiac myocytes. Pericardial fluid from patients with ischemic heart disease markedly increased the percentage of TUNEL-positive myocytes compared with fetal bovine serum. Apoptosis was also confirmed by ladder formation and morphologic features. Apoptosis mediated by this pericardial fluid occurs as readily in cardiac myocytes prepared from neonatal mice nullizygous for p53 as in wild-type littermates. This indicates that p53 is not required for this process. We have found that pericardial fluid from ischemic heart disease elicits a robust increase in phosphorylation of p38 mitogen-activated protein kinase. Specific inhibition of the p38 mitogen-activated protein kinase pathway with SB 203580 almost completely blocked apoptosis mediated by pericardial fluid from ischemic heart disease. Activation of p38 mitogen-activated protein kinase is caused by cellular stress, including oxidants. We have also found that anti-oxidant catalase inhibited pericardial fluid-induced activation of p38 mitogen-activated protein kinase and apoptosis. These findings demonstrate that myocardial cell apoptosis induced by pericardial fluid from patients with ischemic heart disease is mediated by an oxidant stress-sensitive p38 mitogen-activated protein kinase pathway. A possible application of SB 203580 to preserve cardiac function in patients with ischemic heart disease should be discussed.

DOI： 10.1006/jmcc.2000.1314

Web of Science

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PubMed

Angiosarcoma of the scalp: absence of vascular endothelial cadherin in primary and metastatic lesions

Tanioka M, Ikoma A, Morita K, Fujii H, Toda KI, Takahashi K, Tanaka T, Nishigori C, Jin G, Higashi S, Toyokuni S, Miyachi Y

BRITISH JOURNAL OF DERMATOLOGY 144 巻 ( 2 ) 頁： 380 - 383 2001年2月

Angiosarcoma of the scalp: absence of vascular endothelial cadherin in primary and metastatic lesions

Tanioka M, Ikoma A, Morita K, Fujii H, Toda KI, Takahashi K, Tanaka T, Nishigori C, Jin G, Higashi S, Toyokuni S, Miyachi Y

BRITISH JOURNAL OF DERMATOLOGY 144 巻 ( 2 ) 頁： 380 - 383 2001年2月

An electron spin resonance study on alkylperoxyl radical in thin-sliced renal tissues from ferric nitrilotriacetate-treated rats: the effect of alpha-tocopherol feeding

Toyokuni S, Masumizu T, Ozeki M, Kondo S, Hiroyasu M, Kohno M, Hiai H

FREE RADICAL RESEARCH 35 巻 ( 3 ) 頁： 245 - 255 2001年

Difference in Thioredoxin Expression in Viral Myocarditis in Inbred Strains of Mice Open Access

Miyamoto Miki, Kishimoto Chiharu, Shioji Keisuke, Nakamura Hajime, Toyokuni Shinya, Nakayama Yukie, Kita Masakazu, Yodoi Junji, Sasayama Shigetake

JAPANESE CIRCULATION JOURNAL 65 巻 ( 6 ) 頁： 561 - 564 2001年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：社団法人日本循環器学会

DOI： 10.1253/jcj.65.561

Open Access

PubMed

CiNii Research

境界悪性卵巣粘液性腫ようの再発との細胞学的鑑別が困難であった子宮頚部上皮内腺癌の１例国際誌

小椋聖子, 清水恵子, 小林八郎, 豊國伸哉, 桜井幹己

日本臨床細胞学会雑誌 40 巻 ( 6 ) 頁： 636 - 640 2001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

背景:近年, 診断法や治療法の進歩に伴う治癒率の向上とともに, 婦人科領域の重複癌発生率が上昇している. 婦人科領域の細胞診断の際に重複癌を疑う像に遭遇することがあるが, その判定に苦慮することは少なくない. 今回われわれは, 境界悪性卵巣粘液性腫瘍の再発との鑑別が困難であった子宮頸部上皮内腺癌の1例を報告する. 症例:55歳, 女性. 3年前に右卵巣腫瘍破裂のため, 右付属器摘出術が施行され, 右卵巣境界悪性粘液性腫瘍, 腸上皮型, Ic期と診断された. 外来での経過観察中, 子宮頸部擦過細胞診にて異型腺細胞集団が認められ, 子宮頸部腺系病変あるいは卵巣粘液性腫瘍の再発が疑われた. 単純子宮全摘術および左付属器摘出術が施行され, 摘出標本の組織診で子宮頸部上皮内腺癌と診断された. 子宮体部, 左付属器に悪性所見は認められなかった. 結論:婦人科領域における重複癌の診断においては, 細胞所見のみならず臨床所見や画像診断を加味した総合的な判断が必要である.

DOI： 10.5795/jjscc.40.636

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Iron-induced oxidative damage in colon carcinoma (Caco-2) cells

Núñez M., Tapia V., Toyokuni S., Okada S.

Free Radical Research 34 巻 ( 1 ) 頁： 57 - 68 2001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：Free Radical Research

Intestinal epithelial cells have an active apical iron uptake system that is involved in the regulated absorption of iron. By the action of this system, intestinal cells acquire increasing amounts of iron with time. Since intracellular reactive iron is a source of free radicals and a possible cause of colon carcinoma, this study analyzed the oxidative damages generated by iron accumulation in Caco-2 cells. Cells cultured with increasing concentrations of iron increased both total intracellular iron and the reactive iron pool, despite an active IRE/IRP system, which regulates intracellular iron levels. Increasing concentrations of iron resulted in increased protein oxidative damage, as shown by the immunoreactivity for 4-hydroxy-2-nonenal-modified proteins, and markedly induced DNA oxidation determined by 8-hydroxy-2′-deoxyguanidine production. Iron also impaired cell viability, resulting in increased cell death after 6 days of culture. In summary, iron accumulation by intestinal Caco-2 cells correlated with oxidative damage to proteins and DNA. Oxidative damage finally resulted in loss of cell viability. The Fe-induced oxidative damage observed may be relevant in understanding the cascade of events associated with iron-mediated colon carcinogenesis.

DOI： 10.1080/10715760100300061

Scopus

Helicobacter pylori eradication attenuates oxidative stress in human gastric mucosa

Pignatelli B., Bancel B., Plummer M., Toyokuni S., Patricot L.M., Ohshima H.

American Journal of Gastroenterology 96 巻 ( 6 ) 頁： 1758 - 1766 2001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：American Journal of Gastroenterology

OBJECTIVE: Helicobacter pylori infection causes gastric diseases, but the responsible mechanisms are not completely understood. They can involve DNA and tissue damage induced by reactive oxygen and nitrogen species. Our aim is to investigate the effects of bacterial eradication on oxidative stress by measuring changes of relevant markers. METHODS: Antral biopsies were obtained from 34 patients with chronic atrophic gastritis and peptic ulcer disease before and after bacterial eradication. The expression of inducible nitric oxide synthase (iNOS) and levels of nitrotyrosine (NTYR) and 8-hydroxy-2′-deoxyguanosine were assessed immunohistochemically as markers of nitric oxide (NO) production and of damage to proteins and DNA, respectively. RESULTS: Before treatment, the percentages of patients with staining were: 56 for iNOS in inflammatory cells, 79 and 61 for NTYR and 8-hydroxy-2′-deoxyguanosine in foveolar cells, respectively, and 82 for 8-hydroxy-2′-deoxyguanosine in lymphoid follicles. NTYR staining was associated with the intensity of inflammation (p = 0.04) and gastritis activity (p = 0.07). The prevalence of 8-hydroxy-2′-deoxyguanosine tended to be associated with that of NTYR. After successful H. pylori eradication, the prevalence of iNOS and NTYR (in mild gastritis) staining decreased (p < 0.001 and p < 0.06, respectively). 8-Hydroxy-2′-deoxyguanosine staining disappeared in 24% of cases but appeared in 18% of previously negative cases despite eradication. CONCLUSION: Targets of oxidative stress associated with H. pylori infection are inflammatory and deep foveolar cells and lymphoid follicles. This is the first report of 8-hydroxy-2′-deoxyguanosine localization in gastric mucosa. Oxidative stress is reduced by bacterial eradication in the first stages of mild gastritis. Moderate-severe gastritis may be a step that is reversible for iNOS, but partly irreversible for NTYR and 8-hydroxy-2′-deoxyguanosine. © 2001 Am. Coll. of Gastroenterology.

DOI： 10.1016/S0002-9270(01)02432-7

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Helicobacter pylori eradication attenuates oxidative stress in human gastric mucosa 国際誌

Pignatelli B., Bancel B., Plummer M., Toyokuni S., Patricot L., Ohshima H.

American Journal of Gastroenterology 96 巻 ( 6 ) 頁： 1758 - 1766 2001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：American Journal of Gastroenterology

DOI： 10.1111/j.1572-0241.2001.03869.x

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Iron-induced oxidative damage in colon carcinoma (Caco-2) cells 査読有り

MT Nunez, Tapia, V, S Toyokuni, S Okada

FREE RADICAL RESEARCH 34 巻 ( 1 ) 頁： 57 - + 2001年

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：HARWOOD ACAD PUBL GMBH

Intestinal epithelial cells have an active apical iron uptake system that is involved in the regulated absorption of iron. By the action of this system, intestinal cells acquire increasing amounts of iron with time. Since intracellular reactive iron is a source of free radicals and a possible cause of colon carcinoma, this study analyzed the oxidative damages generated by iron accumulation in Caco-2 cells. Cells cultured with increasing concentrations of iron increased both total intracellular iron and the reactive iron pool, despite an active IRE/IRP system, which regulates intracellular iron levels. Increasing concentrations of iron resulted in increased protein oxidative damage, as shown by the immunoreactivity for 4-hydroxy-2-nonenal-modified proteins, and markedly induced DNA oxidation determined by 8-hydroxy-2'-deoxyguanidine production. Iron also impaired cell viability, resulting in increased cell death after 6 days of culture. In summary, iron accumulation by intestinal Caco-2 cells correlated with oxidative damage to proteins and DNA. Oxidative damage finally resulted in loss of cell viability. The Fe-induced oxidative damage observed may be relevant in understanding the cascade of events associated with iron-mediated colon carcinogenesis.

DOI： 10.1080/10715760100300061

Web of Science

researchmap

Iron-induced oxidative damage in colon carcinoma (Caco-2) cells

Nunez MT, Tapia V, Toyokuni S, Okada S

FREE RADICAL RESEARCH 34 巻 ( 1 ) 頁： 57 - + 2001年

Curcumin and especially tetrahydrocurcumin ameliorate oxidative stress-induced renal injury in mice

Okada K., Wangpoengtrakul C., Tanaka T., Toyokuni S., Uchida K., Osawa T.

Journal of Nutrition 131 巻 ( 8 ) 頁： 2090 - 2095 2001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 Nutrition

Protective effects of curcumin (U1), one of the major yellow pigments in turmeric and its derivative, tetrahydrocurcumin (THU1), against ferric nitrilotriacetate (Fe-NTA)-induced oxidative renal damage were studied in male ddY mice. Single Fe-NTA treatment (5 mg Fe/kg body intraperitoneally) transiently causes oxidative stress, as shown by the accumulation of lipid peroxidation products and 8-hydroxy-2′-deoxyguanosine in the kidney. Mice were fed with a diet containing 0.5 g/100 g U1 or THU1 for 4 wk. THU1 significantly inhibited 2-thiobarbituric acid reactive substances and 4-hydroxy-2-nonenal-modified proteins and 8-hydroxy-2′-deoxyguanosine formation in the kidney; U1 inhibited only 4-hydroxy-2-nonenal-modified protein formation. To elucidate the mechanisms of protection by U1 and THU1, the pharmacokinetics and radical-scavenging capacities of U1 and THU1 were investigated by HPLC and electron spin resonance spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide, respectively. Induction of antioxidant enzymes was also investigated. The amounts of THU1 and its conjugates (as sulfates and glucuronides) in the liver and serum were larger in the THU1 group than in the U1 group. The amounts of U1 and its conjugates were small even in the U1 group. These results suggest that THU1 is more easily absorbed from the gastrointestinal tract than U1. Furthermore, THU1 induced antioxidant enzymes, such as glutathione peroxidase, glutathione S-transferase and NADPH: quinone reductase, as well as or better than U1 and scavenged Fe-NTA-induced free radicals in vitro better than U1. These results suggest that U1 is converted to THU1 in vivo and that THU1 is a more promising chemopreventive agent.

DOI： 10.1093/jn/131.8.2090

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