Faculty Profiles - TOYOKUNI Shinya

Papers - TOYOKUNI Shinya

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Improvement in hepatic lipid peroxidation in patients with complete response to interferon-α treatment for chronic hepatitis C. International journal

Kageyama, F; Kobayashi, Y; Kawasaki, T; Toyokuni, S; Uchida, K; Nakamura, H

HEPATOLOGY Vol. 28 ( 4 ) page： 250A - 250A 1998.10

Role of cytochrome P450 isoforms and free radicals in endotoxemic liver injury.

Minamiyama, Y; Takemura, S; Imaoka, S; Toyokuni, S; Funae, Y; Kinoshita, H; Inoue, M

HEPATOLOGY Vol. 28 ( 4 ) page： 251A - 251A 1998.10

Role of cytochrome P450 isoforms and free radicals in endotoxemic liver injury. Reviewed

Minamiyama Y, Takemura S, Imaoka S, Toyokuni S, Funae Y, Kinoshita H, Inoue M

HEPATOLOGY Vol. 28 ( 4 ) page： 251A - 251A 1998.10

Improvement in hepatic lipid peroxidation in patients with complete response to interferon-alpha treatment for chronic hepatitis C. Reviewed International journal

Kageyama F, Kobayashi Y, Kawasaki T, Toyokuni S, Uchida K, Nakamura H

HEPATOLOGY Vol. 28 ( 4 ) page： 250A - 250A 1998.10

Improvement in hepatic lipid peroxidation in patients with complete response to interferon-α treatment for chronic hepatitis C. International journal

Kageyama, F, Kobayashi, Y, Kawasaki, T, Toyokuni, S, Uchida, K, Nakamura, H

HEPATOLOGY Vol. 28 ( 4 ) page： 250A - 250A 1998.10

Heat shock preconditioning ameliorates liver injury following normothermic ischemia-reperfusion in steatotic rat livers

Yamagami K, Yamamoto Y, Kume M, Kimoto S, Yamamoto H, Ozaki N, Yamamoto M, Shimahara Y, Toyokuni S, Yamaoka Y

JOURNAL OF SURGICAL RESEARCH Vol. 79 ( 1 ) page： 47 - 53 1998.9

Heat shock preconditioning ameliorates liver injury following normothermic ischemia-reperfusion in steatotic rat livers

YAMAGAMI K

J Surg Res Vol. 79 ( 1 ) page： 47 - 53 1998.9

Development of High-grade Renal Cell Carcinomas in Rats Independently of Somatic Mutations in the Tsc2 and VHL Tumor Suppressor Genes

TOYOKUNI Shinya, OKADA Kunihiko, KONDO Shohei, NISHIOKA Hiroaki, TANAKA Tomoyuki, NISHIYAMA Yasuyuki, HINO Okio, HIAI Hiroshi

Vol. 89 ( 8 ) page： 814 - 820 1998.8

Development of High-grade Renal Cell Carcinomas in Rats Independently of Somatic Mutations in the Tsc2 and VHL Tumor Suppressor Genes International journal

TOYOKUNI Shinya, OKADA Kunihiko, KONDO Shohei, NISHIOKA Hiroaki, TANAKA Tomoyuki, NISHIYAMA Yasuyuki, HINO Okio, HIAI Hiroshi

Vol. 89 ( 8 ) page： 814 - 820 1998.8

Development of high-grade renal cell carcinomas in rats independently of somatic mutations in the Tsc2 and VHL tumor suppressor genes

Toyokuni S, Okada K, Kondo S, Nishioka H, Tanaka T, Nishiyama Y, Hino O, Hiai H

JAPANESE JOURNAL OF CANCER RESEARCH Vol. 89 ( 8 ) page： 814 - 820 1998.8

A processed grain food inhibits hepatic injury in endotoxemic rats

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

JOURNAL OF NUTRITIONAL SCIENCE AND VITAMINOLOGY Vol. 44 ( 4 ) page： 547 - 559 1998.8

Development of high-grade renal cell carcinomas in rats independently of somatic mutations in the Tsc2 and VHL tumor suppressor genes

Toyokuni S., Okada K., Kondo S., Nishioka H., Tanaka T., Nishiyama Y., Hino O., Hiai H.

Japanese Journal of Cancer Research Vol. 89 ( 8 ) page： 814 - 820 1998.8

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

Ferric nitrilotriacetate (Fe-NTA) induces renal proximal tubular damage that ultimately leads to a high incidence of renal cell carcinoma (RCC) in rats. The RCCs are characterized by 1) high incidence of pulmonary metastasis and peritoneal invasion, 2) high incidence of tumor-associated mortality and 3) possible involvement of reactive oxygen species in carcinogenesis. The present study investigated the possible role of Tsc2 and VHL tumor suppressor genes in this model. Thirty-four Fe-NTA-induced primary RCCs and 20 other primary or metastatic tumors of rats were searched for genetic alteration in all the coding exons of both genes by polymerase chain reaction-single-strand-conformation polymorphism analysis and sequencing in conjunction with morphological evaluation. In the Fe-NTA-induced RCCs, frequency of metastasis or invasion was proportionally associated with the nuclear grade of the tumor (grades 1-3). Only one Fe-NTA-induced RCC of grade 1 revealed missense mutations with loss of heterozygosity in exon 10 of the Tsc2 gene (codons 334, GTG (Val) to GCG (Ala), and 336, TAT (Tyr) to CAT (His)). No mutation was found in the VHL gene. The results suggest that 1) high-grade RCCs can develop in the absence of mutations in the Tsc2 and VHL genes in rats, and that 2) Tsc2 gene somatic mutation can nonetheless be one of the causes of non-Eker rat RCCs.

DOI： 10.1111/j.1349-7006.1998.tb00633.x

Scopus

Development of high-grade renal cell carcinomas in rats independently of somatic mutations in the Tsc2 and VHL tumor suppressor genes

Toyokuni S, Okada K, Kondo S, Nishioka H, Tanaka T, Nishiyama Y, Hino O, Hiai H

JAPANESE JOURNAL OF CANCER RESEARCH Vol. 89 ( 8 ) page： 814 - 820 1998.8

Oxidative stress and cancer: The role of redox regulation

Toyokuni S.

Biotherapy Vol. 11 ( 2-3 ) page： 147 - 154 1998.7

Over-expression of glutathione S-transferase Yp isozyme and concomitant down-regulation of Ya isozyme in renal cell carcinoma of rats induced by ferric nitrilotriacetate Reviewed International journal

Tanaka T, Nishiyama Y, Okada K, Satoh K, Fukuda A, Uchida K, Osawa T, Hiai H, Toyokuni S

CARCINOGENESIS Vol. 19 ( 5 ) page： 897 - 903 1998.5

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

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

DIABETES Vol. 47 page： A263 - A263 1998.5

Oxidative stress in pancreatic beta-cells of GK rat, a model of non-obese NIDDM International journal

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

DIABETES Vol. 47 page： A263 - A263 1998.5

Over-expression of glutathione S-transferase Yp isozyme and concomitant down-regulation of Ya isozyme in renal cell carcinoma of rats induced by ferric nitrilotriacetate

Tanaka T., Nishiyama Y., Okada K., Satoh K., Fukuda A., Uchida K., Osawa T., Hiai H., Toyokuni S.

Carcinogenesis Vol. 19 ( 5 ) page： 897 - 903 1998.5

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：Carcinogenesis

An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces renal proximal tubular damage, a consequence of iron-catalysed Fenton-like reactions, that finally leads to a high incidence of renal cell carcinoma (RCC) in rodents. Glutathione S-transferase (GST) is a family of enzymes that play an important role in detoxification of hydrophobic and electrophilic molecules, and has been associated with putative preneoplastic foci of rat hepatocarcinogenesis and chemotherapy-resistance of human cancers. Our previous study revealed an induction of π-class glutathione S-transferase (Yp) mRNA in the kidney 3 h after administration of Fe-NTA. In the present study, expression of GST isozymes were further investigated in the Fe-NTA-induced RCCs of rats which are characterized by (1) high incidence of metastasis and invasion, (2) high incidence of tumour-associated mortality, and (3) possible involvement of reactive oxygen species in carcinogenesis. In the Fe-NTA-induced RCCs, the levels of α-class GST (Ya) mRNA and proteins were markedly decreased with no apparent change in the copy number of the gene. In contrast, GST-Yp mRNA and proteins were significantly increased in the RCCs while the total GST enzymatic activity was decreased. Immunohistochemical analysis revealed intense staining of GST-Yp not only in the primary RCCs and its metastatic sites, but also in their non-tumorous part of proximal tubules. The contrastive expression of GST isozymes in this renal carcinogenesis model suggests an alteration of its transcription mechanisms and warrants further investigation of this particular detoxifying enzyme from the viewpoint of reactive oxygen species-induced carcinogenesis.

DOI： 10.1093/carcin/19.5.897

Scopus

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 Vol. 22 ( 3 ) page： 145S - 149S 1998.5

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

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

ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH Vol. 22 ( 3 ) page： 145S - 149S 1998.5

Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT WILLIAMS & WILKINS

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; chi(2) 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.

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