研究者詳細 - 豊國　伸哉

論文 - 豊國　伸哉

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DEGRADATION OF DNA IN DRIED TISSUES BY ATMOSPHERIC OXYGEN

MATSUO S, TOYOKUNI S, OSAKA M, HAMAZAKI S, SUGIYAMA T

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 208 巻 ( 3 ) 頁： 1021 - 1027 1995年3月

Degradation of DNA in dried tissues by atmospheric oxygen

Matsuo S., Toyokuni S., Osaka M., Hamazaki S., Sugiyama T.

Biochemical and Biophysical Research Communications 208 巻 ( 3 ) 頁： 1021 - 1027 1995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：Biochemical and Biophysical Research Communications

Recently, DNA of extinct creatures have been brought into analyses. The difficulty in this field of research is DNA degradation. Oxidative damage is considered to be one of the causes of the DNA degradation. We studied how DNA in dried tissue was affected by atmospheric oxygen using freeze-dried rat liver as a model. In tissues exposed to oxygen, DNA degradation occurred within several months and the amount of 8-hydroxy-2′-deoxyguanosine in DNA rapidly increased. The DNA degradation was inhibited by lipid extraction prior to the exposure to atmospheric oxygen. Purified lambda phage DNA was not affected by oxygen. Cellular DNA and RNA were degraded slowly in nitrogen air. These results suggest that both atmospheric and endogenous oxygens play a role in DNA degradation in dried tissues. © 1995 Academic Press, Inc.

DOI： 10.1006/bbrc.1995.1436

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DEGRADATION OF DNA IN DRIED TISSUES BY ATMOSPHERIC OXYGEN

MATSUO S, TOYOKUNI S, OSAKA M, HAMAZAKI S, SUGIYAMA T

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 208 巻 ( 3 ) 頁： 1021 - 1027 1995年3月

A RENAL CARCINOGEN FERRIC NITRILOTRIACETATE MEDIATES A TEMPORARY ACCUMULATION OF ALDEHYDE-MODIFIED PROTEINS WITHIN CYTOSOLIC COMPARTMENT OF RAT-KIDNEY 査読有り国際誌

UCHIDA K, FUKUDA A, KAWAKISHI S, HIAI H, TOYOKUNI S

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 317 巻 ( 2 ) 頁： 405 - 411 1995年3月

A Renal carcinogen ferric nitrilotriacetate mediates a temporary accumulation of aldehyde-modified proteins within cytosolic compartment of rat-Kidney

Uchida K., Fukuda A., Kawakishi S., Hiai H., Toyokuni S.

Archives of Biochemistry and Biophysics 317 巻 ( 2 ) 頁： 405 - 411 1995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：Archives of Biochemistry and Biophysics

Iron overload with ferric nitrilotriacetate (Fe-NTA) induces acute renal proximal tubular necrosis, a consequence of oxidative tissue damage, that eventually leads to a high incidence of renal adenocarcinoma in rodents. A recent immunohistochemical study has revealed that the materials immunoreactive to the antibody against the aldehyde (4-hydroxy-2-nonenal)-modified proteins are generated in the renal proximal tubules of rats treated with Fe-NTA (S. Toyokuni et al. (1994) Proc. Natl. Acad. Sci. USA 91, 2616-2620). Here we present further evidences that cytosolic proteins modified with lipid peroxidation-derived aldehydes (4-hydroxy-2-nonenal and malondialdehyde) are indeed accumulated in the kidney of rats treated with Fe-NTA. A single intraperitoneaI Fe-NTA treatment (15 or 30 mg Fe/kg body wt) induced a rapid accumulation of thiobarbituric acid-reactive substances, a direct consequence of membrane lipid peroxidation, mostly within the cytosolic compartment of rat kidney. The accumulation of lipid peroxidation-derived aldehydes was associated with an apparent accumulation (from 67.9 nmol in untreated controls to 83.3 nmol/mg protein in Fe-NTA-treated rats at 3 h after treatment) and subsequent elimination of aberrant proteins as assessed by a 2, 4-dinitrophenylhydrazine postlabeling assay. Immunoblot analysis with two different polyclonal antibodies against 4-hydroxy-2-nonenal-modified and malondialdehyde-modified proteins detected a temporary accumulation of aldehyde-modified proteins in the cytosol. An immunohistochemical technique with serial sectioning revealed that immunoreactivities of these antibodies were observed in the identical portion of the renal proximal tubules. The implications of these data in relation to the nephrotoxicity of Fe-NTA-are discussed. © 1995 Academic Press. All rights reserved.

DOI： 10.1006/abbi.1995.1181

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A RENAL CARCINOGEN FERRIC NITRILOTRIACETATE MEDIATES A TEMPORARY ACCUMULATION OF ALDEHYDE-MODIFIED PROTEINS WITHIN CYTOSOLIC COMPARTMENT OF RAT-KIDNEY 査読有り

K UCHIDA, A FUKUDA, S KAWAKISHI, H HIAI, S TOYOKUNI

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS 317 巻 ( 2 ) 頁： 405 - 411 1995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：ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS

Iron overload with ferric nitrilotriacetate (Fe-NTA) induces acute renal proximal tubular necrosis, a consequence of oxidative tissue damage, that eventually leads to a high incidence of renal adenocarcinoma in rodents. A recent immunohistochemical study has revealed that the materials immunoreactive to the antibody against the aldehyde (4-hydroxy-2-nonenal)-modified proteins are generated in the renal proximal tubules of rats treated with Fe-NTA (S. Toyokuni et al. (1994) Proc. Natl. Acad. Sci. USA 91, 2616-2620). Here we present further evidences that cytosolic proteins modified with lipid peroxidation-derived aldehydes (4-hydroxy-2-nonenal and malondialdehyde) are indeed accumulated in the kidney of rats treated with Fe-NTA. A single intraperitoneaI Fe-NTA treatment (15 or 30 mg Fe/kg body wt) induced a rapid accumulation of thiobarbituric acid-reactive substances, a direct consequence of membrane lipid peroxidation, mostly within the cytosolic compartment of rat kidney. The accumulation of lipid peroxidation-derived aldehydes was associated with an apparent accumulation (from 67.9 nmol in untreated controls to 83.3 nmol/mg protein in Fe-NTA-treated rats at 3 h after treatment) and subsequent elimination of aberrant proteins as assessed by a 2,4-dinitrophenylhydrazine postlabeling assay. Immunoblot analysis with two different polyclonal antibodies against 4-hydroxy-2-nonenal-modified and malondialdehyde-modified proteins detected a temporary accumulation of aldehyde-modified proteins in the cytosol. An immunohistochemical technique with serial sectioning revealed that immunoreactivities of these antibodies were observed in the identical portion of the renal proximal tubules. The implications of these data in relation to the nephrotoxicity of Fe-NTA-are discussed. (C) 1995 Academic Press, Inc.

DOI： 10.1111/j.1349-7006.2009.01437.x

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THE MONOCLONAL-ANTIBODY SPECIFIC FOR THE 4-HYDROXY-2-NONENAL HISTIDINE ADDUCT 査読有り国際誌

TOYOKUNI S, MIYAKE N, HIAI H, HAGIWARA M, KAWAKISHI S, OSAWA T, UCHIDA K

FEBS LETTERS 359 巻 ( 2-3 ) 頁： 189 - 191 1995年2月

The monoclonal antibody specific for the 4-hydroxy-2-nonenal histidine adduct Open Access

Toyokuni S., Miyake N., Hiai H., Hagiwara M., Kawakishi S., Osawa T., Uchida K.

FEBS Letters 359 巻 ( 2-3 ) 頁： 189 - 191 1995年2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

Monoclonal antibodies directed against proteins modified with the major membrane lipid peroxidation product, 4-hydroxy-2-nonenal, have been established and characterized. The monoclonal antibodies specific for HNE-modified proteins were raised by immunizing mice with a HNE-keyhole limpet hemocyanin conjugate. The resulting five monoclonal antibodies (mAbs HNEJ-1-5) recognized HNE-modified bovine serum albumin (BSA), but not native BSA in Western blot studies. Of the five mAbs, HNEJ-2 exhibited the highest affinity for HNE-modified proteins and a much higher affinity for the HNE-histidine adduct than the HNE-lysine or HNE-cysteine adducts. mAb HNEJ-2 did not cross-react with proteins that had been treated with other aldehydes, such as 1-hexenal, 2-hexenal, 4-hydroxy-2-hexenal, 2-nonenal, formaldehyde, or glutaraldehyde. These results suggest that the major epitope recognized by mAb HNEJ-2 is the Michael addition-type HNE-histidine adduct. © 1995.

DOI： 10.1016/0014-5793(95)00033-6

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CYTOTOXIC AND MUTAGENIC EFFECTS OF FERRIC NITRILOTRIACETATE ON L5178Y MOUSE LYMPHOMA-CELLS

TOYOKUNI S, SAGRIPANTI JL, HITCHINS VM

CANCER LETTERS 88 巻 ( 2 ) 頁： 157 - 162 1995年1月

CYTOTOXIC AND MUTAGENIC EFFECTS OF FERRIC NITRILOTRIACETATE ON L5178Y MOUSE LYMPHOMA-CELLS

TOYOKUNI S, SAGRIPANTI JL, HITCHINS VM

CANCER LETTERS 88 巻 ( 2 ) 頁： 157 - 162 1995年1月

Cytotoxic and mutagenic effects of ferric nitrilotriacetate on L5178Y mouse lymphoma cells

Toyokuni S., Sagripanti J., Hitchins V.

Cancer Letters 88 巻 ( 2 ) 頁： 157 - 162 1995年1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：Cancer Letters

An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces renal proximal tubular necrosis that leads to a high incidence of renal adenocarcinoma in rodents. Others have shown that Fe-NTA induces modified DNA base products both in vitro and in vivo. However, Fe-NTA is negative in the Ames Salmonella test with or without S9 activation. The goal of this project was to determine if Fe-NTA is cytotoxic and mutagenic using the L5178Y (TK+/-) mouse lymphoma assay. Our experiments showed a relationship between the concentration of Fe-NTA (0 to 1 mM) and the decrease in relative survival. An exposure-dependent increase in the number of mutations was observed with increasing concentrations of Fe-NTA. At 14% relative survival, there was about a 4-fold increase in mutations (trifluorothymidine resistance) over unexposed, control cells. Ferric nitrate or nitrilotriacetic acid alone induced a relatively tow 1.5- or 1.1-fold increase in mutation, respectively. Our results establish that Fe-NTA is mutagenic in the L5178Y mouse lymphoma assay system. © 1995.

DOI： 10.1016/0304-3835(94)03641-U

Scopus

PERSISTENT OXIDATIVE STRESS IN CANCER

TOYOKUNI S, OKAMOTO K, YODOI J, HIAI H

FEBS LETTERS 358 巻 ( 1 ) 頁： 1 - 3 1995年1月

Persistent oxidative stress in cancer

Toyokuni S., Okamoto K., Yodoi J., Hiai H.

FEBS Letters 358 巻 ( 1 ) 頁： 1 - 3 1995年1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

DNA of cancers such as renal cell carcinoma and mammary invasive ductal carcinoma, is persistently exposed to more oxidative stress than that of adjacent nornal tissue. We suggest that the concept of 'persistent oxidative stress in cancer' may open up a new research area, explaining part of the characteristic tumor biology of cancer such as activated transcription factors and proto-oncogenes, genomic instability, chemotherapy-resistance, invasion and metastasis. © 1995.

DOI： 10.1016/0014-5793(94)01368-B

Scopus

PERSISTENT OXIDATIVE STRESS IN CANCER

TOYOKUNI S, OKAMOTO K, YODOI J, HIAI H

FEBS LETTERS 358 巻 ( 1 ) 頁： 1 - 3 1995年1月

ACUTE NEPHROTOXICITY OF A CARCINOGENIC IRON CHELATE - SELECTIVE-INHIBITION OF A PROTEOLYTIC CONVERSION OF ALPHA(2U)-GLOBULIN TO THE KIDNEY FATTY-ACID-BINDING PROTEIN 査読有り国際誌

UCHIDA K, FUKUDA A, KAWAKISHI S, TOYOKUNI S, HIAI H, IKEDA S, HORIO F

FEBS LETTERS 357 巻 ( 2 ) 頁： 165 - 167 1995年1月

Acute nephrotoxicity of a carcinogenic iron chelate Selective inhibition of a proteolytic conversion of α<inf>2U</inf>-globulin to the kidney fatty acid-binding protein

Uchida K., Fukuda A., Kawakishi S., Toyokuni S., Hiai H., Ikeda S., Horio F.

FEBS Letters 357 巻 ( 2 ) 頁： 165 - 167 1995年1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

The mechanism of acute nephrotoxicity of an iron chelate in vivo has been investigated. Administration of a renal carcinogen ferric nitrolotriacetate (Fe-NTA) (15 mg Fe/kg body weight, intraperitoneally) led to selective loss of a renal protein with an apparent molecular mass of 17 kDa. Analysis of the 17 kDa protein by NH2-terminal sequence demonstrated its identity over 16 NH2-terminal residues as a kidney fatty acid-binding protein (k-FABP) that is a proteolytically modified form of α2U-globulin, a major urinary protein of adult male rats. An immunochemical study using anti-α2U-globulin polyclonal antibodies confirmed that a single injection of Fe-NTA led to a decrease in k-FABP levels. However, a 19-kDa protein identical to the α2U-globulin progressively appeared in the kidney, suggesting that the proteolytic processing of α2U-globulin in the renal proximal tubules was suppressed by the treatment with Fe-NTA. By monitoring k-FABP and its precursor α2U-globulin, it was determined that repeated exposure to Fe-NTA caused suppression of both proteolytic and endocytotic activity of the kidney. The implications of these data in relation to the nephrotoxicity of Fe-NTA are discussed. © 1995.

DOI： 10.1016/0014-5793(94)01330-4

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4-Hydroxy-2-nonenal-trapping elisa: Direct evidence for the release of a cytotoxic aldehyde from oxidized low density lipoproteins

Uchida K., Osawa T., Hiai H., Toyokuni S.

Biochemical and Biophysical Research Communications 212 巻 ( 3 ) 頁： 1068 - 1073 1995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：Biochemical and Biophysical Research Communications

Among the aldehydes that originate from the peroxidation of cellular membrane lipids, 4-hydroxy-2-nonenal (HNE) is thought to be largely responsible for cytopathological effects observed during oxidative stress. Taking advantage of the fact that HNE is very reactive with proteins and forms stable Michael addition-type adducts, a novel immunochemical procedure for quantifying “free” HNE has been developed. The method designated as “HNE-trapping ELISA” is based on the detection of HNE trapped by a protein that has been coated in the immunoplate. The HNE-derived epitopes generated in the coating protein are then detected by the ELISA using a monoclonal antibody (mAbHNEJ-2) specific to the haptenic groups of the HNE-protein conjugates. Using this method, we determined that a considerable amount of HNE was released from human plasma low density lipoproteins (LDL) treated with copper ions or endothelial cells. © 1995 by Academic Press, Inc.

DOI： 10.1006/bbrc.1995.2078

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MICHAEL ADDITION-TYPE 4-HYDROXY-2-NONENAL ADDUCTS IN MODIFIED LOW-DENSITY LIPOPROTEINS - MARKERS FOR ATHEROSCLEROSIS 査読有り国際誌

UCHIDA K, TOYOKUNI S, NISHIKAWA K, KAWAKISHI S, ODA H, HIAI H, STADTMAN ER

BIOCHEMISTRY 33 巻 ( 41 ) 頁： 12487 - 12494 1994年10月

MICHAEL ADDITION-TYPE 4-HYDROXY-2-NONENAL ADDUCTS IN MODIFIED LOW-DENSITY LIPOPROTEINS - MARKERS FOR ATHEROSCLEROSIS 査読有り国際誌

UCHIDA K, TOYOKUNI S, NISHIKAWA K, KAWAKISHI S, ODA H, HIAI H, STADTMAN ER

BIOCHEMISTRY 33 巻 ( 41 ) 頁： 12487 - 12494 1994年10月

Michael Addition-Type 4-Hydroxy-2-nonenal Adducts in Modified Low-Density Lipoproteins: Markers for Atherosclerosis

Uchida K., Toyokuni S., Nishikawa K., Kawakishi S., Oda H., Hiai H., Stadtman E.

Biochemistry 33 巻 ( 41 ) 頁： 12487 - 12494 1994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：Biochemistry

It has been proposed that plasma low-density lipoprotein (Lall-trans-bRDL) undergoes oxidative modification before it can give rise to foam cells in atherosclerosis. Oxidation of LDL generates a variety of reactive aldehyde products including 4-hydroxy-2-nonenal (HNE), which may covalently attach to the LDL apolipoproteins. We here present direct evidence that HNE derivatization of LDL forms Michael additiontype adducts of HNE with histidine and lysine residues of apolipoprotein B-100 (apo B) and also demonstrate the utility of an antibody specific to the HNE adducts generated in the LDL treated with HNE or oxidatively modified by Cu2+ or cultured endothelial cells. HNE adducts present in the LDL that had been treated with HNE were attested to be Michael addition-type adducts on the basis of the fact that incubation of LDL with 1 mM HNE (2 h, 37 °C) resulted primarily in the formation of Michael addition-type HNE-histidine (39.9 mol/mol of LDL) and HNE-lysine (19.3 mol/mol of LDL) adducts. An enzyme-linked immunosorbent assay (ELISA) and an SDS-polyacrylamide gel electrophoresis (SDS-PAGE)/immunoblot analysis of HNE-modified LDL demonstrated that these HNE adducts were detectable with the HNE-specific antibody affinity-purified with the Michael adduct (HNE-histidine) as a ligand. The following lines of evidence indicated the presence of Michael addition-type HNE adducts in the oxidatively modified LDL in vitro: (i) Amino acid analysis of LDL that had been treated with Cu2+ (24 h, 37 °C) demonstrated the presence of a Michael addition-type HNE-histidine adduct (7-9 mol/mol of LDL). (ii) Competitive ELISA demonstrated the inhibition of antibody binding to HNE-modified LDL by the addition of Cu2+- oxidized LDL. (iii) SDS-PAGE/immunoblot analysis of the Cu2+-oxidized LDL demonstrated the appearance of HNE adducts, which were abolished by the addition of a HNE-modified histidyl peptide. Furthermore, HNE adducts were detected in the LDL that had been treated with cultured bovine aortic endothelial cells (24 h, 37 °C). Taken together, this evidence suggests that the Michael addition-type HNE adducts may be reliable markers for atherosclerosis. © 1994, American Chemical Society. All rights reserved.

DOI： 10.1021/bi00207a016

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