Faculty Profiles - TOYOKUNI Shinya

Papers - TOYOKUNI Shinya

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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

Role of Helicobacter pylori infection in gastroduodenal injury and gastric prostaglandin synthesis during long term/low dose aspirin therapy: A prospective placebo-controlled, double-blind randomized trial Reviewed International journal

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

American Journal of Gastroenterology Vol. 96 ( 6 ) page： 1751 - 1757 2001.7

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

OBJECTIVES: Whether gastric infection with Helicobacter pylori increases the risk of gastric mucosal injury during long term/low dose aspirin therapy is unknown. We examined whether H. pylori infection enhances upper GI mucosal damage, assessed endoscopically, in volunteers given low dose aspirin. We studied 61 healthy men and women, 29 with and 32 without active H. pylori infection. METHODS: We treated volunteers for 45 days with a placebo or aspirin (either 81 mg every day or 325 mg every 3 days). Gastroduodenal mucosal damage was then assessed by endoscopy, as was gastric histology and ex vivo gastric mucosal prostaglandin E2 and F2α synthesis rates. RESULTS: Erosive disease from low dose aspirin (erosions and/or ulcers) occurred in 50% of H. pylori-infected volunteers and in 16% of their noninfected counterparts (p = 0.02). Aspirin caused a significantly higher average mucosal injury score in the gastric antrum in H. pylori-infected participants than in noninfected subjects (p = 0.03), and two H. pylori-infected subjects developed antral gastric ulcers. Subjects with H. pylori gastritis treated with the placebo had nearly 50% higher gastric mucosal prostaglandin (E2 plus F2α) synthesis rates than their noninfected counterparts (108 ± 6 ng/g/min versus 75 ± 6 ng/g/min, p < 0.001). Aspirin reduced mucosal prostaglandin synthesis to similar levels in infected and noninfected participants. CONCLUSIONS: Long term/low dose aspirin therapy led to more gastric mucosal damage when H. pylori gastritis was present than when it was absent, despite similar degrees of gastric mucosal prostaglandin depletion. © 2001 by Am. Coll. of Gastroenterology.

DOI： 10.1016/S0002-9270(01)02491-1

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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

Scopus

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

Scopus

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 International journal

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 International journal

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 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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Pericardial fluid from patients with ischemic heart disease induces myocardial cell apoptotis via an oxidant stress-sensitive p38 mitogen-activated protein kinase pathway. Reviewed International journal

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

Journal of molecular and cellular cardiology Vol. 33 ( 3 ) page： 419 - 30 2001.3

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

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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 Vol. 144 ( 2 ) page： 380 - 383 2001.2

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 Vol. 144 ( 2 ) page： 380 - 383 2001.2

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Papers - TOYOKUNI Shinya