Faculty Profiles - TOYOKUNI Shinya

Papers - TOYOKUNI Shinya

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A case of cervical adenocarcinoma in situ with difficulty in cytological differentiation from recurrent ovarian tumor of borderline malignancy

OGURA Seiko, SHIMIZU Keiko, KOBAYASHI Hachiro, TOYOKUNI Shinya, SAKURAI Masami

The Journal of the Japanese Society of Clinical Cytology Vol. 40 ( 6 ) page： 636 - 640 2001.11

A case of cervical adenocarcinoma in situ with difficulty in cytological differentiation from recurrent ovarian tumor of borderline malignancy

OGURA Seiko, SHIMIZU Keiko, KOBAYASHI Hachiro, TOYOKUNI Shinya, SAKURAI Masami

The Journal of the Japanese Society of Clinical Cytology Vol. 40 ( 6 ) page： 636 - 640 2001.11

A novel selectin blocker alleviates oxidative stress of lung reperfusion injury

Yoshimura, T; Kawashima, M; Nakamura, T; Isowa, N; Bando, T; Hasegawa, S; Kondo, H; Toyokuni, S; Wada, H

JOURNAL OF SURGICAL RESEARCH Vol. 101 ( 1 ) page： 91 - 98 2001.11

Language：English Publishing type：Research paper (scientific journal) Publisher：Journal of Surgical Research

Background. The importance of reactive oxygen species released through interaction of leukocyte/endothelial cell in ischemia-reperfusion injury of the lung is not yet fully understood. A novel selectin blocker, OJ-R9188, which inhibits the interaction, may alleviate oxidative stress and pulmonary dysfunction after warm ischemia-reperfusion. Materials and methods. Rat lungs were reperfused at 37°C for 60 min with an ex vivo model and were divided into three groups (n = 10). In the fresh group, lungs were reperfused immediately after harvest. In the OJ-R (-) and OJ-R (+) groups, lungs were reperfused after warm ischemia at 37°C for 90 min. In the OJ-R (+) group, rats received 100 μg per body of OJ-R9188 intravenously 10 min before the harvest. The electron spin resonance method was used to assess the direct scavenging activity of OJ-R9188. Results. Both shunt fractions and wet/dry weight ratios of the lung tissue after reperfusion in the OJ-R (+) group were significantly lower than those in the OJ-R (-) group. Oxidative DNA damage in the alveolar wall of the OJ-R (+) group, assessed by immunohistochemical quantitation of 8-hydroxy-2′-deoxyguanosine, was significantly lower than that of the OJ-R (-) group. Immunostaining of 3-nitro-L-tyrosine, which represents nitric oxide-mediated oxidative damage, was also more intense in the OJ-R (-) group than in the OJ-R (+) group. Direct scavenging activity of OJ-R9188 was not observed, and the number of leukocytes infiltrated to the lung tissue as seen by myeloperoxidase activity was not different between the OJ-R (-) and OJ-R (+) groups. Conclusions. A novel selectin blocker, OJ-R9188, improves pulmonary function after warm ischemia-reperfusion and alleviates reperfusion-induced oxidative alveolar damage. © 2001 Academic Press.

DOI： 10.1006/jsre.2001.6258

Characterization of a vitamin D receptor knockout mouse as a model of colorectal hyperproliferation and DNA damage

Kallay E, Pietschmann P, Toyokuni S, Bajna E, Hahn P, Mazzucco K, Bieglmayer C, Kato S, Cross HS

CARCINOGENESIS Vol. 22 ( 9 ) page： 1429 - 1435 2001.9

Characterization of a vitamin D receptor knockout mouse as a model of colorectal hyperproliferation and DNA damage

Kallay E, Pietschmann P, Toyokuni S, Bajna E, Hahn P, Mazzucco K, Bieglmayer C, Kato S, Cross HS

CARCINOGENESIS Vol. 22 ( 9 ) page： 1429 - 1435 2001.9

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

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

JOURNAL OF NUTRITION Vol. 131 ( 8 ) page： 2090 - 2095 2001.8

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

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

JOURNAL OF NUTRITION Vol. 131 ( 8 ) page： 2090 - 2095 2001.8

Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds

Kawanishi S, Inoue S, Oikawa S, Yamashita N, Toyokuni S, Kawanishi M, Nishino K

FREE RADICAL BIOLOGY AND MEDICINE Vol. 31 ( 1 ) page： 108 - 116 2001.7

Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds

Kawanishi S., Inoue S., Oikawa S., Yamashita N., Toyokuni S., Kawanishi M., Nishino K.

Free Radical Biology and Medicine Vol. 31 ( 1 ) page： 108 - 116 2001.7

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：Free Radical Biology and Medicine

DNA damage in cultured cells and in lungs of rats induced by nickel compounds was investigated to clarify the mechanism of nickel carcinogenesis. DNA strand breaks in cultured cells exposed to nickel compounds were measured by using a pulsed field gel electrophoresis technique. Among nickel compounds (Ni3S2, NiO (black), NiO (green), and NiSO4), only Ni3S2, which is highly carcinogenic, induced lesions of both double- and single-stranded DNA in cultured human cells (Raji and HeLa cells). Treatment of cultured HeLa cells with Ni3S2 (10 μg/ml) induced a 1.5-fold increase in 8-hydroxy-2′-deoxyguanosine (8-OH-dG) compared with control, whereas NiO (black), NiO (green), and NiSO4 did not enhance the generation of 8-OH-dG. Intratracheal instillation of Ni3S2, NiO(black), and NiO(green) to Wistar rats increased 8-OH-dG in the lungs significantly. NiSO4 induced a smaller but significant increase in 8-OH-dG. Histological studies showed that all the nickel compounds used induced inflammation in lungs of the rats. Nitric oxide (NO) generation in phagocytic cells induced by Ni3S2, NiO(black), and NiO(green) was examined using macrophage cell line RAW 264.7 cells. NO generation in RAW 264.7 cells stimulated with lipopolysaccharide was enhanced by all nickel particles. Two mechanisms for nickel-induced oxidative DNA damage have been proposed as follows: all the nickel compounds used induced indirect damage through inflammation, and Ni3S2 also showed direct oxidative DNA damage through H2O2 formation. This double action may explain relatively high carcinogenic risk of Ni3S2. © 2001 Elsevier Science Inc.

DOI： 10.1016/S0891-5849(01)00558-5

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Oxidative DNA damage in cultured cells and rat lungs by carcinogenic nickel compounds Reviewed

S Kawanishi, S Inoue, S Oikawa, N Yamashita, S Toyokuni, M Kawanishi, K Nishino

FREE RADICAL BIOLOGY AND MEDICINE Vol. 31 ( 1 ) page： 108 - 116 2001.7

Language：English Publishing type：Research paper (scientific journal) Publisher：PERGAMON-ELSEVIER SCIENCE LTD

DNA damage in cultured cells and in lungs of rats induced by nickel compounds was investigated to clarify the mechanism of nickel carcinogenesis. DNA strand breaks in cultured cells exposed to nickel compounds were measured by using a pulsed held gel electrophoresis technique. Among nickel compounds (Ni3S2, NiO (black), NiO (green), and NiSO4), only Ni3S2, which is highly carcinogenic, induced lesions of both double- and single-stranded DNA in cultured human cells (Raji and HeLa cells). Treatment of cultured HeLa cells with Ni3S2 (10 mug/ml) induced a 1.5-fold increase in 8-hydroxy-2'-deoxyguanosine (8-OH-dG) compared with control, whereas NiO (black), NiO (green), and NiSO4 did not enhance the generation of 8-OH-dG. Intratracheal instillation of Ni3S2, NiO(black), and NiO(green) to Wistar rats increased 8-OH-dG in the lungs significantly. NiSO4 induced a smaller but significant increase in 8-OH-dG. Histological studies showed that all the nickel compounds used induced inflammation in lungs of the rats. Nitric oxide (NO) generation in phagocytic cells induced by Ni3S2, NiO(black). and NiO(green) was examined using macrophage cell line RAW 264.7 cells. NO generation in RAW 264.7 cells stimulated with lipopolysaccharide was enhanced by all nickel particles. Two mechanisms for nickel-induced oxidative DNA damage have been proposed as follows: all the nickel compounds used induced indirect damage through inflammation, and Ni3S2 also showed direct oxidative DNA damage through H2O2 formation. This double action may explain relatively high carcinogenic risk of Ni3S2. (C) 2001 Elsevier Science Inc.

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Endogenous formation of protein adducts with carcinogenic aldehydes - Implications for oxidative stress Reviewed International journal

Ichihashi K, Osawa T, Toyokuni S, Uchida K

JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 276 ( 26 ) page： 23903 - 23913 2001.6

Endogenous formation of protein adducts with carcinogenic aldehydes: Implications for oxidative stress

Ichihashi K., Osawa T., Toyokuni S., Uchida K.

Journal of Biological Chemistry Vol. 276 ( 26 ) page： 23903 - 23913 2001.6

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：Journal of Biological Chemistry

In the present study, we characterize the covalent modification of a protein by crotonaldehyde, a representative carcinogenic aldehyde, and describe the endogenous production of this aldehyde in vivo. The crotonaldehyde preferentially reacted with the lysine and histidine residues of bovine serum albumin and generated a protein-linked carbonyl derivative. Upon incubation with the histidine and lysine derivatives, crotonaldehyde predominantly generated β-substituted butanal adducts of histidine and lysine and N ε-(2,5-dimethyl-3-formyl-3,4-dehydropiperidino)lysine (dimethyl-FDP-lysine) as the putative carbonyl derivatives generated in the crotonaldehyde-modified protein. To verify the endogenous formation of crotonaldehyde in vivo, we raised the monoclonal antibody (mAb82D3) against the crotonaldehyde-modified protein and found that it cross-reacted with the protein-bound 2-alkenals, such as crotonaldehyde, 2-pentenal, and 2-hexenal. The anti-2-alkenal antibody recognized multiple crotonaldehyde-lysine adducts, including dimethyl-FDP-lysine and an unknown product, which showed the greatest immunoreactivity with the antibody. On the basis of the chemical and spectroscopic evidence, the major antigenic product was determined to be a novel Schiff base-derived crotonaldehyde-lysine adduct, Nε -(5-ethyl-2-methylpyridinium)lysine (EMP-lysine). It was found that the lysine residues that had disappeared in the protein treated with crotonaldehyde were partially recovered by EMP-lysine. The presence of immunoreactive materials with mAb82D3 in vivo was demonstrated in the kidney of rats exposed to the renal carcinogen, ferric nitrilotriacetate. In addition, the observations that the metal-catalyzed oxidation of polyunsaturated fatty acids in the presence of proteins resulted in an increase in the antigenicity of the protein indicated that lipid peroxidation represents a potential pathway for the formation of crotonaldehyde/2-alkenals in vivo. These data suggest that the formation of carcinogenic aldehydes during lipid peroxidation may be causally involved in the pathophysiological effects associated with oxidative stress.

DOI： 10.1074/jbc.M101947200

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Difference in thioredoxin expression in viral myocarditis in inbred strains of mice

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

JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION Vol. 65 ( 6 ) page： 561 - 564 2001.6

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 Vol. 96 ( 6 ) page： 1758 - 1766 2001.6

Difference in thioredoxin expression in viral myocarditis in inbred strains of mice

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

JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION Vol. 65 ( 6 ) page： 561 - 564 2001.6

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

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

Japanese circulation journal Vol. 65 ( 6 ) page： 561 - 564 2001.5

Publishing type：Research paper (scientific journal) Publisher：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)

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

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

Japanese circulation journal Vol. 65 ( 6 ) page： 561 - 564 2001.5

Language：English Publishing type：Research paper (scientific journal) Publisher：社団法人日本循環器学会

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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 Vol. 30 ( 10 ) page： 1130 - 1136 2001.5

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：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 Vol. 30 ( 10 ) page： 1130 - 1136 2001.5

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 Vol. 144 ( 2 ) page： 380 - 383 2001.3

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：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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Papers - TOYOKUNI Shinya