研究者データベース


フリーワードで探す

全文検索となっています

菅野 さな枝カンノ サナエ

所属部署医学研究科法医学分野
職名講師
メールアドレス
ホームページURL
生年月日
Last Updated :2020/06/02

研究者基本情報

所属学協会

  • The International Association of Forensic of Toxicology
  • Society of Toxicology
  • 日本薬学会
  • 日本法中毒学会
  • 日本法医学会

経歴

  •   2017年04月 - 現在, 名古屋市立大学 大学院 医学研究科, 法医学分野, 講師
  •   2010年10月 - 2017年03月, 聖マリアンナ医科大学, 法医学, 助教
  •   2008年04月 - 2010年09月, 浜松医科大学, 特任研究員
  •   2004年06月 - 2008年03月, 国立環境研究所, 環境リスク研究センター, Post-doctoral Fellow
  •   2000年06月 - 2004年05月, Science and Technology Agency, CREST, Technical staff
  •   1997年06月 - 2000年05月, Science and Technology Agency, Japan Society for the Promotion Science (JSPS) Fellow

研究活動情報

研究キーワード

    肺表面活性, 法中毒学, ナノ粒子, 環境毒性学

論文

  • An autopsy case of nearly complete ossification of the stylohyoid chain: Eagle syndrome in forensic aspect., Kato H, Kanno S, Ohtaki J, Nakamura Y, Kobayashi K, Aoki Y, Legal medicine (Tokyo, Japan), 32, 19 - 22,   2018年05月, 査読有り
  • A case of transnasal intracranial penetrating injury with skull base fracture caused by a broken golf club shaft., Kato H, Kanno S, Ohtaki J, Nakamura Y, Horita T, Fukuta M, Eguchi K, Hassan Gaballa M, Aoki Y, Legal medicine (Tokyo, Japan), 32, 57 - 60,   2018年05月, 査読有り
  • Differential Regulation of IL-1β and IL-6 Release in Murine Macrophages., Hirano S, Zhou Q, Furuyama A, Kanno S, Inflammation, 40, (6) 1933 - 1943,   2017年12月, 査読有り
  • Inflammatory responses to neutral fat and fatty acids in multiple organs in a rat model of fat embolism syndrome., Takada M, Chiba S, Nagai T, Takeshita H, Kanno S, Ikawa T, Sakamoto K, Sagi M, Ichiba K, Mukai T, Forensic science international, 254, 126 - 132,   2015年09月, 査読有り
  • The role of Rho-kinases in IL-1β release through phagocytosis of fibrous particles in human monocytes., Kanno S, Hirano S, Chiba S, Takeshita H, Nagai T, Takada M, Sakamoto K, Mukai T, Archives of toxicology, 89, (1) 73 - 85,   2015年01月, 査読有り
  • Macrophage Receptor with Collagenous Structure (MARCO) Is Processed by either Macropinocytosis or Endocytosis-Autophagy Pathway., Hirano S, Kanno S, PloS one, 10, (11) ,   2015年, 査読有り
  • Human organic cation transporter 2 (hOCT2): Inhibitor studies using S2-hOCT2 cells, Shoetsu Chiba, Toru Ikawa, Hiroshi Takeshita, Sanae Kanno, Tomonori Nagai, Meri Takada, Toshiji Mukai, Michael F. Wempe, TOXICOLOGY, 310, 98 - 103,   2013年08月, 査読有り, Highly expressed in kidney and located on the basolateral membrane, human organic cation transporter 2 (hOCT2) can transport various compounds (i.e. drugs and toxins) into the proximal tubular cell. Using cultured proximal tubule cells stably expressing hOCT2 (i.e. S2-hOCT2 cells), we sought to probe different compound classes (e.g. analgesics, anti-depressants, anti-psychotics, disinfectant, herbicides, insecticides, local anesthetic, muscarinic acetylcholine receptor antagonist, sedatives, steroid hormone, stimulants and toxins) for their ability to inhibit C-14-TEA uptake, a prototypical OCT2 substrate. Aconitine, amitriptyline, atropine, chlorpyrifos, diazepam, fenitrothion, haloperidol, lidocaine, malathion, mianserin, nicotine and triazolam significantly inhibited 14C-TEA uptake; IC50 values were 59.2, 2.4, 2.0, 20.7,32.3,13.2,32.5, 104.6, 71.1, 17.7, 52.8 and 65.5 mu M, respectively. In addition, aconitine, amitriptyline, atropine, chlorpyrifos, fenitrothion, haloperidol, lidocaine, and nicotine displayed competitive inhibition with K-i values of 145.6, 2.5, 2.4, 24.8, 16.9, 51.6, 86.8 and 57.7 p:M, respectively. These in vitro data support the notion that compounds pertaining to a wide variety of different drug classes have the potential to decrease renal clearance of drugs transported via hOCT2. Consequently, these data warrant additional studies to probe hOCT2 and its role to influence drug pharmacokinetics. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
  • Sulfide induces apoptosis and Rho kinase-dependent cell blebbing in Jurkat cells, Sanae Kanno, Seishiro Hirano, Morihisa Sagi, Shoetsu Chiba, Hiroshi Takeshita, Toru Ikawa, Kazue Ichiba, Tomonori Nagai, Meri Takada, Kana Sakamoto, Toshiji Mukai, ARCHIVES OF TOXICOLOGY, 87, (7) 1245 - 1256,   2013年07月, 査読有り, Hydrogen sulfide (H2S) is a toxic gaseous substance, and accidental exposure to high concentrations of H2S has been reported to be lethal to humans. Inhaled and absorbed H2S is partially dissolved within the circulation and causes toxic effects on lymphocytes. However, the mechanisms involved in H2S toxicity have not been well documented. In this study, we examined the cellular uptake and injury of sulfide-exposed human T lymphocytes (Jurkat). Cells were exposed to a H2S donor, sodium hydroxysulfide (NaHS), at pH 6.0, 7.0, or 8.0 for 1 h at 37 A degrees C in a sealed conical tube to avoid the loss of dissolved H2S gas. Cytotoxicity and cellular sulfide concentrations increased dramatically as the pH of the NaHS solution decreased. Sulfide enhanced the cleavage of caspase-3 and poly (ADP-ribose) polymerase and induced early cellular apoptosis. A pan-caspase inhibitor reduced sulfide-induced apoptosis. These results indicate that sulfide induces pH-dependent and caspase-dependent apoptosis. We also found that blebbing of the plasma membrane occurred in sulfide-exposed cells. Both ROCK-1 and ROCK-2 (Rho kinases) were activated by sulfide, and sulfide-induced cell blebbing was suppressed by a ROCK inhibitor, suggesting that a Rho pathway is involved in sulfide-induced blebbing in lymphocytes.
  • Macrophage receptor with collagenous structure (MARCO) is a dynamic adhesive molecule that enhances uptake of carbon nanotubes by CHO-K1 Cells, Seishiro Hirano, Yuji Fujitani, Akiko Furuyama, Sanae Kanno, TOXICOLOGY AND APPLIED PHARMACOLOGY, 259, (1) 96 - 103,   2012年02月, 査読有り, The toxicity of carbon nanotubes (CNTs), a highly promising nanomaterial, is similar to that of asbestos because both types of particles have a fibrous shape and are biopersistent. Here, we investigated the characteristics of macrophage receptor with collagenous structure (MARCO), a membrane receptor expressed on macrophages that recognizes environmental or unopsonized particles, and we assessed whether and how MARCO was involved in cellular uptake of multi-walled CNTs (MWCNTs). MARCO-transfected Chinese hamster ovary (CHO-K1) cells took up polystyrene beads irrespective of the particle size (20 nm-1 mu m). In the culture of MARCO-transfected CHO-K1 cells dendritic structures were observed on the bottom of culture dishes, and the edges of these dendritic structures were continually renewed as the cell body migrated along the dendritic structures. MWCNTs were first tethered to the dendritic structures and then taken up by the cell body. MWCNTs appeared to be taken up via membrane ruffling like macropinocytosis, rather than phagocytosis. The cytotoxic EC50 value of MWCNTs in MARCO-transfected CHO-K1 cells was calculated to be 6.1 mu g/mL and transmission electron microscopic observation indicated that the toxicity of MWCNTs may be due to the incomplete inclusion of MWCNTs by the membrane structure. (C) 2011 Elsevier Inc. All rights reserved.
  • Simultaneous analysis of cardiac glycosides in blood and urine by thermoresponsive LC-MS-MS, Sanae Kanno, Kanako Watanabe, Itaru Yamagishi, Seishiro Hirano, Kayoko Minakata, Kunio Gonmori, Osamu Suzuki, ANALYTICAL AND BIOANALYTICAL CHEMISTRY, 399, (3) 1141 - 1149,   2011年01月, 査読有り, A new thermoresponsive polymer separation column was applied to simultaneous analysis of four cardiac glycosides (CGs) being widely used for the treatment of arrhythmias and heart failure in human blood and urine. This column is composed of an N-isopropylacrylamide polymer, the surface of which undergoes a reversible alteration from hydrophilic to hydrophobic by changing temperature. The chromatographic separation and retention times can be easily be controlled by adjusting the column temperature. As the column temperature was changed from 50 to 10 degrees C over 8 min, five CGs, including deslanoside, digoxin, methyldigoxin, digitoxin, and digitoxigenin (internal standard) were better resolved. Using these LC conditions, we analyzed four CGs in human whole blood and urine simultaneously by liquid chromatography-tandem mass spectrometry (LC-MS-MS). Validation data as functions of recovery rates, linearity, accuracy, and precision were carefully tested; all were generally satisfactory. The detection limits for the four CGs in both matrices were 0.2-0.3 ng/mL. The method was applied to analysis of methyldigoxin and its main metabolite digoxin in whole blood and urine samples obtained from a deceased person in actual autopsy case. To our knowledge, this is the first report describing an LC-MS-MS method using a thermoresponsive column for analysis of drug(s). The inclusion of the thermoresponsive column in an LC-MS-MS technique seems to extend the possibility for simultaneous analysis of compounds of different properties, such as hydrophobic precursors and their hydrophilic metabolites in biological samples within limited analysis times.
  • Uptake and cytotoxic effects of multi-walled carbon nanotubes in human bronchial epithelial cells, Seishiro Hirano, Yuji Fujitani, Akiko Furuyama, Sanae Kanno, TOXICOLOGY AND APPLIED PHARMACOLOGY, 249, (1) 8 - 15,   2010年11月, 査読有り, Carbon nanotubes (CNT) are cytotoxic to several cell types. However, the mechanism of CNT toxicity has not been fully studied, and dosimetric analyses of CNT in the cell culture system are lacking. Here, we describe a novel, high throughput method to measure cellular uptake of CNT using turbimetry. BEAS-2B, a human bronchial epithelial cell line, was used to investigate cellular uptake, cytotoxicity, and inflammatory effects of multi-walled CNT (MWCNT). The cytotoxicity of MWCNT was higher than that of crocidolite asbestos in BEAS-2B cells. The IC(50) of MWCNT was 12 mu g/ml, whereas that of asbestos (crocidolite) was 678 mu g/ml. Over the course of 5 to 8 h, BEAS-2B cells took up 17-18% of the MWCNT when they were added to the culture medium at a concentration of 10 mu g/ml. BEAS-2B cells were exposed to 2, 5, or 10 mu g/ml of MWCNT, and total RNA was extracted for cytokine cDNA primer array assays. The culture supernatant was collected for cytokine antibody array assays. Cytokines IL-6 and IL-8 increased in a dose dependent manner at both the mRNA and protein levels. Migration inhibitory factor (MIF) also increased in the culture supernatant in response to MWCNT. A phosphokinase array study using lysates from BEAS-2B cells exposed to MWCNT indicated that phosphorylation of p38, ERK1, and HSP27 increased significantly in response to MWCNT. Results from a reporter gene assays using the NF-kappa B or AP-1 promoter linked to the luciferase gene in transiently transfected CHO-KI cells revealed that NF-kappa B was activated following MWCNT exposure, while AP-1 was not changed. Collectively, MWCNT activated NF-kappa B, enhanced phosphorylation of MAP kinase pathway components, and increased production of proinflammatory cytokines in human bronchial epithelial cells. (C) 2010 Elsevier Inc. All rights reserved.
  • Determination of iodide in urine using electrospray ionization tandem mass spectrometry, Kayoko Minakata, Itaru Yamagishi, Sanae Kanno, Hideki Nozawa, Masako Suzuki, Osamu Suzuki, JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES, 878, (20) 1683 - 1686,   2010年06月, 査読有り, A rapid and sensitive electrospray ionization (ESI) tandem mass spectrometry (MS-MS) procedure was developed for the determination of iodide (I(-)) A gold (Au) and I(-) complex was formed Immediately after the addition of the chelating agent NaAuCl(4) to I(-) solution. and was extracted with methyl isobutyl ketone One to five microliters of the extract were injected directly into an ESI-MS-MS instrument I(-) quantification was performed by selecting reaction monitoring of the product ion I(-) at m/z 127 derived from the precursor ion (197)AuI(2)(-) at m/z 451 I(-) concentration was measured in the quantification range from 10(-7) to 10(-5) M using 50 mu L of solution within 10 min Iodate was reduced to I(-) with ascorbic acid and determined I(-) concentration in reference urine 2670a was measured after treatments (C) 2010 Elsevier B V All rights reserved
  • Extrapulmonary translocation of intratracheally instilled fine and ultrafine particles via direct and alveolar macrophage-associated routes, Akiko Furuyama, Sanae Kanno, Takahiro Kobayashi, Seishiro Hirano, ARCHIVES OF TOXICOLOGY, 83, (5) 429 - 437,   2009年05月, 査読有り, Translocation of inhaled ultrafine particles from the lungs into the blood may impair cardiovascular function. We administered ultrafine (20-nm) and fine (200-nm) gold colloid or fluorescein-labeled polystyrene particles to mice intratracheally and examined their localization in the lung and extrapulmonary organs. Fifteen minutes after instillation, dispersed and agglomerated 20-nm gold colloid particles were observed on the surface of endothelial cells, on the alveolar surface, in endocytotic vesicles of alveolar epithelial cells, and in the basement membrane of the lung. A small but noteworthy amount of gold was detected in the liver, kidney, spleen, and heart by inductively coupled plasma-mass spectrometry. After administration of 20- or 200-nm fluorescent particles, free particles were detected infrequently in blood vessels, on the endocardial surface, and in the kidney and liver only in the mice that received 20-nm particles, whereas phagocytes containing 20- or 200-nm particles were found in the extrapulmonary tissues. Fluorescent particle-laden alveolar macrophages administered intratracheally translocated from alveoli to extrapulmonary organs via the blood circulation. Thus, small amounts of ultrafine particles are transported across the alveolar wall into the blood circulation via endocytotic pathways, but particle-laden alveolar macrophages translocate both ultrafine and fine particles from the lungs to the extrapulmonary organs.
  • Effects of eicosane, a component of nanoparticles in diesel exhaust, on surface activity of pulmonary surfactant monolayers., Kanno S, Furuyama A, Hirano S, Archives of toxicology, 82, (11) 841 - 850,   2008年11月, 査読有り
  • Multi-walled carbon nanotubes injure the plasma membrane of macrophages., Hirano S, Kanno S, Furuyama A, Toxicology and applied pharmacology, 232, (2) 244 - 251,   2008年10月, 査読有り
  • A murine scavenger receptor MARCO recognizes polystyrene nanoparticles, Sanae Kanno, Akiko Furuyama, Seishiro Hirano, TOXICOLOGICAL SCIENCES, 97, (2) 398 - 406,   2007年06月, 査読有り, Recent toxicological studies indicate that nanoparticles or ultrafine particles (< 100 nm) are more toxic than fine particles (< 2 mu m) because of their greater surface area. It is well known that alveolar macrophages play an important role in the first defense against various environmental particles and microorganisms. This is accomplished by binding to a macrophage receptor with collagenous structure (MARCO), one of several scavenger-type receptors expressed on the cell surface of macrophages. MARCO has been shown to mediate the ingestion of unopsonized environmental particles such as TiO2 and Fe2O3 (1.3 mu m in diameter). However, very little is known about the cellular uptake of nanoparticles. In the present study, we investigated whether MARCO mediates the uptake of nanoparticles by using fluorescent-tagged polystyrene particles (20 nm, 200 nm, and 1 mu m in diameter). COS-7 cells were transfected with either MARCO cDNA or an empty vector, and the association of the particles with the cells were observed by fluorescence microscopy and atomic force microscopy. MARCO-transfected cells associated with all three sizes of particles in a time-dependent manner, while no obvious binding of particles occurred after 5 h to the empty vector-transfected cells. The uptake of particles by MARCO-transfected cells was partially inhibited by polyG. These results suggest that macrophages associate with nanoparticles (20 nm) at least in part through MARCO and that MARCO plays a role in clearing nanoparticles which can deposit in the alveolar region.
  • Accumulation and toxicity of monophenyl arsenicals in rat endothelial cells, S Hirano, Y Kobayashi, T Hayakawa, Cui, X, M Yamamoto, S Kanno, A Shraim, ARCHIVES OF TOXICOLOGY, 79, (1) 54 - 61,   2005年01月, 査読有り, Clark 1 (diphenylarsine chloride) and Clark 2 ( diphenylarsine cyanide) were used as chemical weapon agents (CWA), and the soil contamination by these CWA and their degraded products, diphenyl and phenyl arsenicals, has been one of the most serious environmental issues. In a series of comparisons in toxicity between trivalent and pentavalent arsenicals we investigated differences in the accumulation and toxicity of phenylarsine oxide (PAO(3+)) and phenylarsonic acid (PAA(5+)) in rat heart microvascular endothelial cells. Both the cellular association and toxicity of PAO(3+) were much higher than those of PAA(5+), and LC50 values of PAO(3+) and PAA(5+) were calculated to be 0.295 muM and 1.93 mM, respectively. Buthionine sulfoximine, a glutathione depleter, enhanced the cytotoxicity of both PAO(3+) and PAA(5+). N-Acetyl-L-cysteine (NAC) reduced the cytotoxicity and induction of heme oxygenase-1 (HO-1) mRNA in PAO(3+)-exposed cells, while NAC affected neither the cytotoxicity nor the HO-1 mRNA level in PAA(5+)-exposed cells. The effect of NAC may be due to a strong affinity of PAO(3+) to thiol groups because both NAC and GSH inhibited the cellular accumulation of PAO(3+), but PAA(3+) increased tyrosine phosphorylation levels of cellular proteins. These results indicate that the inhibition of protein phosphatases as well as the high affinity to cellular components may confer PAO(3+) the high toxicity.
  • Effects of the phytoestrogen coumestrol on RANK-ligand-induced differentiation of osteoclasts, S Kanno, S Hirano, F Kayama, TOXICOLOGY, 203, (1-3) 211 - 220,   2004年10月, 査読有り, Phytoestrogens. which have structural similarity to 17beta-estradiol, have been reported to act as agonists/antagonists of estrogen in animals and humans. Estrogen is known to have an important role in maintaining bone mass, because the concentration of serum estrogen decreases after menopause and the estrogen deficiency causes bone loss. In this study, we investigated the effects of coumestrol and other phytoestrogens on osteoclast differentiation using estrogen receptor alpha-transfected RAW264.7 (RAW264.7-ERalpha) cells. When the cells were cultured with the receptor activator of nuclear factor kappa B-ligand (RANKL), both formation of tartrate-resistant acid phosphatase (TRAP) positive multinucleated cells and TRAP activity were increased compared with control cells that were Cultured in the absence of RANKL. Coumestrol decreased RANKL-induced formation of TRAP-positive multinucleated cells and TRAP activity dose-dependently. RANKL-stimulated RAW264.7-ERalpha cells formed resorption pits on calcium phosphate films and the pit formation was inhibited by coumestrol in a dose-dependent manner. RT-PCR analyses revealed that coumestrol (10 muM) decreased mRNA levels of calcitonin receptor (CTR) and matrix metalloproteinase-9 (MMP9) in RANKL-treated cells. In addition, pretreatment of coumestrol decreased RANKL-induced phosphorylation of extracellular signal-regulated kinases/p44/42 (ERK1/2). These results suggest that coumestrol has an inhibitory effect on the differentiation of osteoclasts, at least partially via ERK1/2 pathway. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
  • The accumulation and toxicity of methylated arsenicals in endothelial cells: important roles of thiol compounds, S Hirano, Y Kobayashi, Cui, X, S Kanno, T Hayakawa, A Shraim, TOXICOLOGY AND APPLIED PHARMACOLOGY, 198, (3) 458 - 467,   2004年08月, 査読有り, Excess intake of arsenic is known to cause vascular diseases as welt as skin lesions and cancer in humans. Recent reports suggest that trivalent methylated arsenicals, which are intermediate metabolites in the methylation process of inorganic arsenic, are responsible for the toxicity and carcinogenicity of environmental arsenic. We investigated acute toxicity and accumulation of monomethylarsonic acid (MMA(V)), dimethylarsinic acid (DMA(V)), trimethylarsine oxide (TMAO), and monomethylarsonous acid diglutathione (MMA(III) (GS)(2)) in rat heart microvessel endothelial (RHMVE) cells. MMA(V) (LC50 = 36.6 mM) and DMA(V) (LC50 = 2.54 mM) were less toxic than inorganic arsenicals (cf. LC50 values for inorganic arsenite (iAs(III)), and inorganic arsenate (iAs(V)) was reported to be 36 and 220 muM, respectively, in RHMVE cells. TMAO was essentially not toxic. However, MMA(III) (GS)(2) was highly toxic (LC50 = 4.1 muM). The order of cellular arsenic accumulation of those four organic arsenic compounds was MMA(III) (GS)(2) much greater than MMA(V) > DMA(V) > TMAO. MMA(III) (GS)(2) was efficiently taken up by the cells and cellular arsenic content increased with the concentration of MMA(III) (GS)(2) in culture medium. N-acetyl-L-cysteine (NAC) reduced cellular arsenic content in DMA(V)-exposed cells and also decreased the cytotoxicity of DMA(V), whereas it changed neither cellular arsenic content nor the viability in MMA(V)-exposed cells. mRNA levels of heme oxygenase-1 (HO-1) were decreased by NAC in DMA(V)-exposed, but MMA(V)-exposed cells. Buthionine sulfoximine (BSO), a cellular glutathione (GSH) depleting agent, enhanced the cytotoxicity of MMA(V). However, BSO reduced, rather than enhanced, the cytotoxicity of DMA(V). These results suggest that intracellular GSH modulated the toxic effects of arsenic in opposite ways for MMA(V) and DMA(V). Even though intracellular GSH decreased the cytotoxicity of MMA(V), extracellularly added GSH enhanced the cytotoxicity of MMA(V). The use of high-performance liquid chromatography (HPLC)-inductively coupled plasma mass spectrometric analyses suggested that a small amount of MMA(V) was converted to MMA(III) (GS)(2) in the presence of GSH. These results suggest that MMA(III) (GS)(2) is highly toxic compared to other arsenic compounds because of faster accumulation of this species by cells, in addition to having the toxic nature of methylated trivalent organic arsenics. (C) 2004 Elsevier Inc. All rights reserved.
  • Effects of phytoestrogens and environmental estrogens on osteoblastic differentiation in MC3T3-E1 cells, S Kanno, S Hirano, F Kayama, TOXICOLOGY, 196, (1-2) 137 - 145,   2004年03月, 査読有り, Phytoestrogens and environmental estrogens, which have in part some structural similarity to 17beta-estradiol, are reported to act as agonists/antagonists of estrogen in animals and humans. Estrogen is known to play an important role in maintaining bone mass, since the concentration of serum estrogen decreases after menopause and the estrogen deficiency results in bone loss. In this study, we report the effects of phytoestrogens (genistein, daidzein, and coumestrol) and environmental estrogens (bisphenol A (BPA), p-n-nonylphenol (NP) and bis(2-ethylhexyl)phthalate (DEHP)) on osteoblast differentiation using MC3T3-E1 cells, a mouse calvaria osteoblast-like cell line. Coumestrol (10(-10) to 10(-6) M) slightly enhanced cell proliferation, while neither the other phytoestrogens (daidzein, genistein) nor environmental estrogens increased cell proliferation. Alkaline phosphatase (ALP) activity and cellular calcium (Ca) and phosphorus (P) contents were increased by phytoestrogens and BPA; however, neither NP nor DEHP affected those osteoblastic indicators. The effects of estrogenic potency, using the cell proliferation of MCF-7 cells, an estrogen receptor (ER)-positive human breast cancer cell line, indicate that coumestrol has the highest estrogenic potency among those phytoestrogens and environmental estrogens. The estrogenic potency of NP and DEHP were lower than the others. In conclusion, phytoestrogens, such as coumestrol, genistein and daidzein, and BPA increased ALP activity and enhanced bone mineralization in MC3T3-E1 cells, suggesting that not only phytoestrogen but also BPA, an environmental estrogen, is implicated in bone metabolism. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
  • Subchronic exposure to arsenic through drinking water alters expression of cancer-related genes in rat liver, Cui, X, S Li, A Shraim, Y Kobayashi, T Hayakawa, S Kanno, M Yamamoto, S Hirano, TOXICOLOGIC PATHOLOGY, 32, (1) 64 - 72,   2004年01月, 査読有り, Although arsenic exposure causes liver disease and/or hepatoma, little is known about molecular mechanisms of arsenic-induced liver toxicity or carcinogenesis. We investigated the effects of arsenic on expression of cancer-related genes in a rat liver following subchronic exposure to sodium arsenate (1, 10, 100 ppm in drinking water), by using real-time quantitative RT-PCR and immunohistochemical analyses. Arsenic accumulated in the rat liver dose-dependently and caused hepatic histopathological changes, such as disruption of hepatic cords, sinusoidal dilation, and fatty infiltration. A 1-month exposure to arsenic significantly increased hepatic mRNA levels of cyclin D1 (10 ppm), ILK (1 ppm), and p27(Kip1) (10 ppm), whereas it reduced mRNA levels of PTEN (1 ppm) and beta-catenin (100 ppm). In contrast, a 4-month arsenic exposure showed increased mRNA expression of cyclin D1 (100 ppm), ILK (1 ppm), and p27(Kip1) (1 and 10 ppm), and decreased expression of both PTEN and beta-catenin at all 3 doses. An immunohistochemical study revealed that each protein expression accords closely with each gene expression of mRNA level. In conclusion, subchronic exposure to inorganic arsenate caused pathological changes and altered expression of cyclin D1, p27(Kip1), ILK, PTEN, and beta-catenin in the liver. This implies that arsenic liver toxicity involves disturbances of some cancer-related molecules.
  • PCR-based subtraction analyses for upregulated gene transcription in cadmium-exposed rat lung type 2 epithelial cells, S Hirano, H Kitajima, T Hayakawa, Cui, X, S Kanno, Y Kobayashi, M Yamamoto, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 308, (1) 133 - 138,   2003年08月, 査読有り, The aim of this study was to gain insight into early events in the lung epithelial cells following acute Cd exposure. We adopted the polymerase chain reaction (PCR)-based subtraction technique and found several genes that were upregulated in immortalized rat lung type 2 epithelial cells (SV40T2). The upregulation of those genes was confirmed by Northern blot analysis and categorized into three groups (highly, moderately, and weakly inducible genes). Heme oxygenase-1 (HO-1), HSP 72, hepatic steroid hydroxylase/ CYPIIA2, and Cd-inducible gene 1 (cdig1, a new gene, Accession Nos. AB086233 and AB086234) were highly inducible genes, testosterone-repressed prostate message 2 mRNA was moderately inducible, and collagen-binding protein and cdig2 (another new gene, Accession No. AB086193) mRNAs were weakly inducible. The expression of cdig1 increased linearly with time up to 9 h, while that of HO-1 reached the maximum value at 4 h in response to 10 muM Cd. (C) 2003 Elsevier Inc. All rights reserved.
  • Difference in uptake and toxicity of trivalent and pentavalent inorganic arsenic in rat heart microvessel endothelial cells, S Hirano, Cui, X, S Li, S Kanno, Y Kobayashi, T Hayakawa, A Shraim, ARCHIVES OF TOXICOLOGY, 77, (6) 305 - 312,   2003年06月, 査読有り, Intake of inorganic arsenic is known to cause vascular diseases as well as skin lesions and cancer in humans. We investigated the differences in cytotoxicity, uptake rate of arsenic, and gene expression of antioxidative enzymes between arsenite (As3+)- and arsenate (As5+)-exposed rat heart microvessel endothelial cells. As3+ was more cytotoxic than As5+, and LC50 values were calculated to be 36 and 220 muM, respectively. As3+ (1-25 muM) increased mRNA levels of antioxidant enzymes such as heme oxygenase-1 (HO-1), thioredoxin peroxidase 2, NADPH dehydrogenase, and glutathione S-transferase P subunit. HO-1 mRNA levels showed the most remarkable increase in response to As3+, cDNA microarray analysis indicated that there was no prominent difference in arsenic-induced transcriptional changes between As3+- and As5+-exposed cells, when the cells were exposed to one-fourth the LC50 concentration of arsenic (9 and 55 muM for As3+ and As5+, respectively). N-acetyl-L-cysteine (NAC) reduced both the cytotoxicity of inorganic arsenic and the HO-1 mRNA level, and buthionine sulfoximine enhanced cytotoxicity of inorganic arsenic. As3+ was taken up by the endothelial cells 6-7 times faster than As5+, and the presence of NAC in the culture medium did not change the uptake rate of As3+. These results suggest that the effects of NAC on arsenic-induced cytotoxicity and oxidative stress were due to the antioxidative role of non-protein thiols and not to chelation of arsenic in the culture medium. The difference in cellular uptake of arsenic between As3+ and As5+ appeared not to be due to the ionic charge on arsenic (at physiological pH, trivalent arsenic is neutral whereas pentavalent arsenic is negatively charged). These results suggest that the higher toxicity of As3+ compared with that of As5+ is probably due to the faster uptake of As3+ by endothelial cells, and inorganic arsenic exerts its toxicity at least in part via intracellular oxidative stress.
  • krox-20/egr-2 is up-regulated following non-specific and homophilic adhesion in rat macrophages, S Hirano, CD Anuradha, S Kanno, IMMUNOLOGY, 107, (1) 86 - 92,   2002年09月, 査読有り, Macrophages are known to adhere to a plastic dish via beta(2) integrin (CR3) and scavenger receptors. Although their functions such as phagocytosis, endocytosis, and nitric oxide production have been investigated on adherent macrophages in vitro , very little is known about intracellular signals triggered by adhesion to a plastic dish. Recently we reported that the mRNA level of krox-20/egr-2 was significantly increased in rat alveolar macrophages following exposure to fibrous titanium dioxide particles. In the present study we report that up-regulation of krox-20/egr-2 gene expression following adhesion to a plastic dish and homophilic adhesion in rat alveolar macrophages and rat macrophage cell line, NR8383. The mRNA level of krox-20/egr-2 increased with a peak 1 hr after adhesion to a plastic dish in both cell types. Piceatannol inhibited tyrosine-phosphorylation of Syk and decreased both adhesion and krox-20/egr-2 mRNA level. In contrast staurosporine, a serine/threonine kinase inhibitor, increased adherence of macrophages and yet prohibited the adhesion-dependent increase in krox-20/egr-2 gene expression. When NR8383 cells are cultured in suspension, the cells aggregated naturally and produced cell clumps. The mRNA level of krox-20/egr-2 also increased in response to the homophilic intercellular adhesion. The increased mRNA level of krox-20/egr-2 was not caused by inflammatory stimuli, because lipopolysaccharide did not affect the aggregation-dependent up-regulation of krox-20/egr-2 gene. The up-regulation of krox-20/egr-2 gene due to the homophilic cell aggregation was also inhibited either by piceatannol or staurosporine. Those results suggest that krox-20/egr-2 gene expression is triggered by sensing non-specific and homophilic cellular adhesion and the following phosphorylation of signal transducing proteins including Syk and staurosporine-inhibitable kinases.
  • Chemotactic responces of osteoblastic MC3T3-E1 cells toward zinc chloride., S. Kanno, C.D. Anuradha, S. Hirano, Biol. Trace Ele. Res., 83, 49 - 55,   2001年, 査読有り
  • Localization of zinc after in vitro mineralization in osteoblastic cells., S. Kanno, C.D. Anuradha, S. Hirano, Biol. Trace Ele. Res., 83, 39 - 47,   2001年, 査読有り
  • Oxidative damage to mitochondria is a preliminary step to caspese-3 activation in fluoride-induced apoptosis in HL-60 cells., C.D. Anuradha, S. Kanno, S. Hirano, Free Radic. Biol. Med., 31, 367 - 373,   2001年, 査読有り
  • luoride induced apoptosis by caspase-3 activation in human leukemia cells., C.D. Anuradha, S. Kanno, S. Hirano, Arch. Toxicol., 74, 226 - 230,   2000年, 査読有り
  • Transcription of krox-20/egr-2 is upregulated after exposure to fibrous particles and adhesion in rat alveolar macrophages., S. Hirano, C.D. Anuradha, S. Kanno, Am. J. Respir. Cell Mol. Biol., 23, 313 - 324,   2000年, 査読有り
  • RGD peptide-induced apoptosis in human leukemia HL-60 cells requires caspase-3 activation, CD Anuradha, S Kanno, S Hirano, CELL BIOLOGY AND TOXICOLOGY, 16, (5) 275 - 283,   2000年, 査読有り, RGD motif-containing peptides have been used in various studies of cell adhesion and growth. We report that RGD triggered apoptosis at a concentration of 1 mmol/L, whereas RAD-containing peptides failed to induce apoptosis in HL-60 cells. RGD-treated cells revealed internucleosomal DNA fragmentation. Western blot reveals caspase-3 activation in RGD peptide-treated cells. A caspase-3 inhibitor z-VAD-FMK completely blocked the apoptosis, but a caspase-1 inhibitor (Ac-YVAD-CMK) and caspase-2 inhibitor (z-VDVAD-FMK) did not block the apoptosis, suggesting that caspase-3 might have a critical role in the execution process of apoptosis induced by RGD. RGD peptides have been used extensively to inhibit tumor metastasis. Our results should help in further understanding the RGD peptide-induced apoptosis, which is important since RGD peptides have a potential role in therapies of the future.
  • Inflammatory responses of rat alveolar macrophages following exposure to fluoride, S Hirano, M Ando, S Kanno, ARCHIVES OF TOXICOLOGY, 73, (6) 310 - 315,   1999年08月, 査読有り, Inhalation exposure to fluoride compounds has been associated with respiratory failure. We have addressed effects of fluoride on alveolar macrophages and lung responses to intratracheally (i.t.) instilled fluoride in rats. I.t. instillation of fluoride at doses of 200 and 400 mu g F/rat caused significant polymorphonuclear leukocyte (PMN) infiltration in the rat lung at 20 h postadministration. while 100 mu g fluoride did not recruit a significant number of PMNs in the alveolar space. Total RNA was extracted from the lung lavage cells obtained from 5 h post i.t. instillation and mRNA levels of chemokines and proinflammatory cytokines were semiquantitatively evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). I.t. instillation of fluoride significantly enhanced mRNA expression of cytokines such as interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha. cytokine-induced neutrophil chemoattractant, and macrophage inflammatory proteins-1 alpha and -2. Fluoride-induced augmentation in IL-1 beta mRNA expression was also examined by Northern hybridization following in vitro exposure of alveolar macrophages to fluoride. However, the enhancement of IL-1 beta mRNA expression following in vitro exposure to fluoride was observed only at 500 mu M, a dose higher than the 50% lethal concentration (LC50). Non-specific adhesion of alveolar macrophages to the plastic dish was significantly increased following in vitro exposure to fluoride. The fluoride-induced non-specific adhesion was significantly reduced by anti-CD18, suggesting that beta(2) integrin played a role in the increase of adherence. Those results suggest that fluoride activates alveolar macrophages, enhances the production of chemokines and proinflammatory cytokines, and causes PMN infiltration in the lung.
  • Syk and paxillin are differentially phosphorylated following adhesion to the plastic substrate in rat alveolar macrophages, S Hirano, S Kanno, IMMUNOLOGY, 97, (3) 414 - 419,   1999年07月, 査読有り, Adhesion is associated with tyrosine phosphorylation in many types of cells. Although macrophages are known to adhere and phagocytose foreign particles, the signal transduction pathway of macrophages in response to adhesion to the foreign substrate has not been fully investigated. In the present study we investigated tyrosine-phosphorylated proteins and phosphorylation of paxillin in alveolar macrophages (AMs) following adhesion to a plastic substrate. Adhesion to a plastic dish resulted in tyrosine phosphorylation of a 68 000 MW protein, which was shown, by immunoprecipitation and immunoblotting in the present study, to be a rat Syk kinase. Treatment with erbstatin reduced both tyrosine phosphorylation of Syk and adherence of AMs, while treatment with cytochalasin B inhibited spreading of AMs but did not inhibit tyrosine phosphorylation of Syk. These results suggest that tyrosine phosphorylation of Syk plays an important role in adhesion of AMs to the plastic substrate, but not in AM spreading. Paxillin is known to be tyrosine phosphorylated following adhesion to the extracellular matrix in many types of cells. However, paxillin appeared to be serine/threonine phosphorylated rather than tyrosine phosphorylated following adhesion of AMs to the plastic substrate. Treatment with A23187 (a calcium ionophore), but not phorbol 12-myristate 13-acetate (PMA; a protein kinase C stimulator), induced tyrosine phosphorylation of Syk in non-adherent AMs. Treatment with either A23187 or PMA caused electromobility changes of paxillin that were mainly a result of serine/threonine phosphorylation. These results suggest that adhesion to the plastic substrate leads to two differently regulated events in AMs: tyrosine phosphorylation of Syk and serine/threonine phosphorylation of paxillin, both of which are probably mediated by an increase in intracellular calcium.
  • Changes in element concentrations following calcification in an osteoblastic cell line (UMR-106)., S. Kanno, S. Hirano, M. Ando, Biomed. Res. Trace Elements, 8, (3) 205 - 206,   1997年, 査読有り
  • COPPER-METABOLISM LEADING TO AND FOLLOWING ACUTE HEPATITIS IN LEC RATS, KT SUZUKI, S KANNO, S MISAWA, Y AOKI, TOXICOLOGY, 97, (1-3) 81 - 92,   1995年03月, 査読有り, The accumulation process of copper (Cu) in the liver and the following metabolic disorder of Cu were examined in LEC rats, a mutant strain which accumulates Cu with age and shows spontaneous acute hepatitis and/or hepatoma. Cu concentration in the liver of female rats was similar to 220 mu g/g liver at 2 weeks of age, decreased to 100 mu g/g liver at 4-6 weeks, and then started to increase with age linearly to the highest concentration of 250 mu g/g liver at 16 weeks. Although the Cu level expressed by concentration (mu g/g liver) decreased during weaning, it increased linearly with age when it was expressed by content (mg/liver), indicating a constant and preferential accumulation of Cu in the liver. Cu concentration stopped increasing at 16 weeks in the liver, followed by a sudden decrease to 1/2 the highest level. Biological markers (serum lactate dehydrogenase and glutamic-oxaloacetic transaminase activities) for liver damage started to increase, together with the appearance of signs of jaundice, when Cu attained the highest concentration. Distributions of Cu and zinc (Zn) in the supernatant fraction of the liver indicated that both metals were mostly distributed to metallothionein (MT) and, to a small extent, to superoxide dismutase on a gel filtration column throughout the course of the experiments. Serum Cu concentration started to increase in a form of ceruloplasmin, together with serum marker enzyme activities for liver damage, Cu concentration in the kidneys also started to increase after the increase of serum Cu. The results indicate that Cu accumulates in the form of MT in the liver of LEC rats to a maximum level of similar to 250 mu g/g liver, and then decreases suddenly with the onset of acute hepatitis. The maximum level seems to be related to the capacity of MT synthesis, and acute hepatitis is assumed to occur when Cu accumulates beyond the capacity. Serum Cu started to increase, from the abnormally low level, when the metal accumulated beyond the capacity of MT synthesis in the liver, and it was partly reabsorbed by the kidneys and the rest was excreted into urine. Changes in iron and zinc levels were determined and discussed in relation to those of Cu.
  • ENHANCED SYNTHESIS OF METALLOTHIONEIN AS A POSSIBLE CAUSE OF ABNORMAL COPPER ACCUMULATION IN LEC RATS, S KANNO, Y AOKI, JS SUZUKI, N TAKEICHI, S MISAWA, KT SUZUKI, JOURNAL OF INORGANIC BIOCHEMISTRY, 56, (2) 117 - 125,   1994年11月, 査読有り, Long-Evans rats with a cinnamon-like coat color (LEC) is an inbred strain accumulating copper (Cu) in the liver abnormally and showing spontaneous hepatitis and hepatoma. The present study was intended to clarify how Cu accumulates in the LEC rat liver. For this purpose, the distribution profiles of Cu and zinc (Zn) and the inducibility of metallothionein (MT) synthesis were examined in the liver between Cu-loaded Long Evans agouti (LEA, the original strain of LEC) rats and were compared with those in control LEC rats. LEA rats (female, five weeks old) were injected subcutaneously with CuCl2 daily at a dose of 3 mg Cu/kg body weight for 2, 4, 6, and 9 days. The concentration of Cu (124 mu g/g) accumulated in the LEA rat liver after four injections was comparable to that in control LEC rats. Only 20% of Cu in the liver of LEA rats was recovered in the supernatant fraction in the form of MT, while Cu in the LEC rat liver (113 mu g/g) was recovered mostly in the supernatant fraction, and was bound to MT. Although the increased concentration of Cu in the LEA rat liver was further elevated after additional injections of Cu, the amount of MT did not increase further. The MT mRNA content in the LEA rat liver remained lower than that of LEC rats even after further injections of Cu. Therefore, the present results suggest that LEC rats can accumulate Cu at a high concentration in the liver because of their extremely high inducibility of MT.
  • SELECTIVE ENHANCEMENT OF METALLOTHIONEIN MESSENGER-RNA EXPRESSION BY COPPER IN PRIMARY CULTURED LIVER PARENCHYMAL-CELLS OF LEC RATS, S KANNO, JS SUZUKI, Y AOKI, KT SUZUKI, RESEARCH COMMUNICATIONS IN CHEMICAL PATHOLOGY AND PHARMACOLOGY, 84, (2) 153 - 162,   1994年05月, 査読有り, Mechanisms for the abnormal copper (Cu) accumulation in the liver of LEC rats were examined using primary cultured liver parenchymal cells prepared from mutant LEC rats and those from control LEA rats (original strain). The Cu and metallothionein (MT) mRNA levels in the liver of LEC rats were caused to decrease to the same levels as those of LEA rats by removing Cu in vivo selectively with tetrathiomolybdate. Cu was taken up by LEC rat cells to the same extent as LEA rat cells by exposure to low medium Cu and to a higher extent by exposure to high medium Cu, while the MT mRNA level in LEC rat cells increased dose-dependently at a much higher rate than that in LEA rats. MT mRNA levels in both cells were comparable by exposure to cadmium, zinc and dexamethazone. The results indicate that expression of MT mRNA is selectively enhanced by Cu in LEC cells despite the fact that uptake of Cu is comparable with normal cells.
  • Mechanisms for accumulation of copper in the liver of LEC rats and removal by tetrathiomolybdate., Y. Ogra, K.Yamamoto, S. Kanno, Y. Aoki, K.T. Suzuki, Jap. J. Toxicol. Environ. Health, 40, 23 - 23,   1994年, 査読有り
  • SELECTIVE REMOVAL OF COPPER BOUND TO METALLOTHIONEIN IN THE LIVER OF LEC RATS BY TETRATHIOMOLYBDATE, KT SUZUKI, K YAMAMOTO, S KANNO, Y AOKI, N TAKEICHI, TOXICOLOGY, 83, (1-3) 149 - 158,   1993年10月, 査読有り, LEC rats (Long-Evans with a cinnamon-like coat color) have a genetical defect in Cu metabolism. Male LEC rats aged 10 weeks were injected ip with TTM at a dose of 5 or 10 mg/kg body weight for 8 consecutive days and killed one day after the last injection. Cu that had accumulated in the liver at a concentration of 251 mu g/g liver was decreased to 82.7 or 74.3 mu g/g liver respectively, by the treatment. Although most of Cu was bound to MT as a soluble form before TTM treatment, the metal remaining in the liver after the treatment was present almost exclusively in the non-soluble fraction. Zinc (Zn) present, bound to MT before the treatment, was also partly removed from the liver by TTM, and the Zn remaining in the liver after the treatment was revealed to be bound to MT (Zn-MT) by high performance liquid chromatography-atomic absorption spectrophotometry. Iron (Fe) in the liver was not affected by TTM treatment. Cu in the kidneys and spleen increased by TTM treatment, while Zn and iron were not affected. Treatment of LEC rats with severe jaundice effectively cured the animals from otherwise lethal signs by only two ip injections of TTM at a dose of 10 mg/kg body weight.
  • Mechanisms for selective removal of copper from metallothionein in the liver of LEC rats., K.T. Suzuki, K. Yamamoto, Y. Ogra, S. Kanno, Y. Aoki, Biomed. Res. Trace Elements, 4, (2) 147 - 148,   1993年, 査読有り
  • Changes of copper distributions in plasma and kidneys of LEC rats following acute hepatitis., K.T. Suzuki, S. Kanno, S. Misawa, Y. Sumi, Res. Commun. Chem. Pathol. Pharmacol., 82, 225 - 232,   1993年, 査読有り
  • Changes of hepatic copper distributions leading to hepatitis in LEC rats., K.T. Suzuki, S. Kanno, S. Misawa, Y. Sumi, Res. Commun. Chem. Pathol. Pharmacol., 82, 217 - 224,   1993年, 査読有り
  • Mechanisms for removal of copper from metallothionein by tetrathiomolybdate., K.T. Suzuki, K. Yamamoto, Y. Ogra, S. Kanno, Y. Aoki, J. Inorg. Biochem., 54, 157 - 165,   1993年, 査読有り
  • HISTOCHEMICAL AND IMMUNOHISTOCHEMICAL LOCALIZATION OF COPPER, IRON AND METALLOTHIONEIN IN THE LIVER AND KIDNEY OF LEC RATS, Y SUMI, S KAWAHARA, Y KIKUCHI, J SAWADA, T SUZUKI, KT SUZUKI, ACTA HISTOCHEMICA ET CYTOCHEMICA, 26, (1) 5 - 9,   1993年, 査読有り, In LEC (Long-Evans, with a cinnamon-like coat color) rats, intense staining for copper and iron was limited to Kupffer cells in the liver, and no staining was seen in hepatocytes, even though they appeared to be in various stages of degeneration. In the kidney, copper and iron reaction products were localized in the epithelial cells of urinary tubules. Intense staining for metallothionein was observed in Kupffer cells and hepatocytes, and also in epithelial cells of urinary tubules. These results suggest that hepatitis in the LEC rat may be associated with abnormal deposition of both iron and copper.
  • Distribution of cadmium, copper and zinc between blood plasma and liver soluble proteins- An in vitro study for the discriminatory uptake mechanism, S. Kawahara, S. Misawa, K.T. Suzuki, Jpn. J. Toxicol. Environ. Health, 38, 9 - 9,   1992年, 査読有り
  • Intracellular cadmium sequestration by the heavy metal-tolerant green algae Chlorella vulgaris and Uronema confervicolum, A.T. Wilczok, M.M. Watanabe, S. Kawahara, K.T. Suzuki, K. Sugawara, Jpn. J. phycol., 40, 229 - 238,   1992年, 査読有り
  • EFFLUX OF ENDOGENOUS ZINC LIBERATED FROM METALLOTHIONEIN AND ALCOHOL-DEHYDROGENASE IN THE LIVER BY REPLACEMENT WITH CADMIUM, KT SUZUKI, S KAWAHARA, H SUNAGA, N SHIMOJO, TOXICOLOGY AND APPLIED PHARMACOLOGY, 105, (3) 413 - 421,   1990年09月, 査読有り
  • Effects of pretreatment with cadmium on the discriminative uptake of subsequent cadmium, copper and zinc., K.T. Suzuki, S. Kawahara, H. Sunaga, N. Shimojo, Comp. Biochem. Physiol., 95C, 285 - 290,   1990年, 査読有り
  • Discriminative uptake of metals by the liver and its relation to induction of metallothionein by cadmium, copper and zinc., K.T. Suzuki, S. Kawahara, H. Sunaga, E. Kobayashi, N. Shimojo, Comp. Biochem. Physiol., 95C, 279 - 284,   1990年, 査読有り

MISC

  • 変死体中薬物分析と質量分析-精神作用薬服用症例 愛知県2大学における法医解剖薬毒物分析に関する考察, 小川 匡之, 大瀧 純, 鈴木 隆佳, 岩井 雅枝, 近藤 文雄, 菅野 さな枝, 福田 真未, 加藤 秀章, 青木 康博, 妹尾 洋, JSBMS Letters, 43, (Suppl.) 57 - 57,   2018年08月
  • 骨芽細胞分化に伴うメタンフェタミンの細胞内蓄積と分化指標への影響, 菅野 さな枝, 千葉 正悦, 呂 彩子, 鷺 盛久, 井川 亨, 大出 透乃, 向井 敏二, 日本法医学雑誌, 71, (1) 98 - 98,   2017年05月
  • 乳幼児の心臓性突然死2剖検例, 竹下 裕史, 坂本 圭菜, 井川 亨, 高田 女里, 菅野 さな枝, 千葉 正悦, 一場 一江, 鷺 盛久, 向井 敏二, 日本法医学雑誌, 70, (2) 144 - 144,   2016年12月
  • 植物性エストロジェンが骨芽細胞の分化及びIL-6産生に及ぼす影響, 菅野 さな枝, 平野 靖史郎, 日本薬学会年会要旨集, 120年会, (4) 189 - 189,   2000年03月
  • 肺胞マクロファージにおける接着応答性krox-20/egr-2の発現, 平野 靖史郎, 菅野 さな枝, 日本免疫学会総会・学術集会記録, 29,   1999年10月
  • 繊維状酸化チタン粒子状物質を貪食した肺胞マクロファージにおけるimmediate-early gene krox-20の発現, 平野 靖史郎, 菅野 さな枝, 日本臨床免疫学会会誌, (26回抄録集) 301 - 301,   1998年10月
  • 骨芽細胞の亜鉛に対する走化応答性, 菅野 さな枝, 平野 靖史郎, 安藤 満, 日本薬学会年会要旨集, 118年会, (3) 23 - 23,   1998年03月
  • 骨形成に伴う細胞内微量金属濃度の変化, 菅野 さな枝, Biomedical Research on Trace Elements, 8, (3) 205 - 206,   1997年12月

書籍等出版物

  • NLRP3 inflammasome-mediated toxicity of fibrous particles. In Biological Effects of Fibrous and Particulate Substances, 菅野 さな枝, 共著, p27-50, Springer Japan. Tokyo,   2015年
  • Effects of arsenite on macropinocytotic and autophagic activities in CHO-K1 cells. In Understanding the Geological and Medical Interface of Arsenic, 菅野 さな枝, 分担執筆, p196-198, CRC Press. Boca Raton,   2012年
  • Accumulation of copper in the liver as the cause acute hepatitis in LEC rats. In Metal Ions in Biology and Medicine, 菅野 さな枝, 分担執筆, p187-192, John Libbey Eurotext, Paris,   1994年
  • Discriminative uptake of cadmium, copper and zinc by the liver. In Metallothionein in Biology and Medicine, 菅野, 河原, さな枝, 分担執筆, p197-208, CRC Press. Boca Raton,   1991年

講演・口頭発表等

  • Cytotoxicity of cationic disinfectants through apoptosis in human alveolar epithelial cells., S. Kanno, S. Hirano, J. Otaki, H.Kato, M. Fukuta, Y. Nakamura, T. Horita, Y. Aoki, The International Association of Forensic Toxicologists,   2019年09月02日

競争的資金

  • 陽イオン界面活性剤使用による健康被害の実態解明に関する基礎研究, 日本学術振興会, 科学研究費,   2018年04月 - 2022年03月
  • 薬毒物が骨リモデリングの与える影響―骨形成と骨吸収の両側面からの検討, 日本学術振興会, 科学研究費,   2017年04月 - 2019年03月
  • ナノマテリアル・ナノ粒子のアクシデンタルな曝露による生体影響, 日本学術振興会, 科学研究費,   2012年04月 - 2014年03月
  • 違法ドラッグの新分析法の開発:超高速型HPLCとTOF-MSとの結合, 日本学術振興会, 科学研究費,   2008年04月 - 2010年03月
  • 高感度ラマン分光による重金属毒物検出法の開発, 日本学術振興会, 科学研究費,   2007年04月 - 2009年03月
  • 原子間力顕微鏡を用いたナノ粒子の細胞への取り込みに関する研究, 日本学術振興会, 科学研究費,   2005年04月 - 2006年03月


Copyright © MEDIA FUSION Co.,Ltd. All rights reserved.