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Dive into the research topics where Soohee Kim is active.

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Featured researches published by Soohee Kim.


Toxicology in Vitro | 2009

Oxidative stress-dependent toxicity of silver nanoparticles in human hepatoma cells

Soohee Kim; Ji Eun Choi; Jinhee Choi; Kyu-Hyuck Chung; Kwangsik Park; Jongheop Yi; Doug-Young Ryu

Cytotoxicity induced by silver nanoparticles (AgNPs) and the role that oxidative stress plays in this process were demonstrated in human hepatoma cells. Toxicity induced by silver (Ag(+)) ions was studied in parallel using AgNO(3) as the Ag(+) ion source. Using cation exchange treatment, we confirmed that the AgNP solution contained a negligible amount of free Ag(+) ions. Metal-responsive metallothionein 1b (MT1b) mRNA expression was not induced in AgNP-treated cells, while it was induced in AgNO(3)-treated cells. These results indicate that AgNP-treated cells have limited exposure to Ag(+) ions, despite the potential release of Ag(+) ions from AgNPs in cell culture. AgNPs agglomerated in the cytoplasm and nuclei of treated cells, and induced intracellular oxidative stress. AgNPs exhibited cytotoxicity with a potency comparable to that of Ag(+) ions in in vitro cytotoxicity assays. However, the toxicity of AgNPs was prevented by use of the antioxidant N-acetylcysteine, and AgNP-induced DNA damage was also prevented by N-acetylcysteine. AgNO(3) treatment induced oxidative stress-related glutathione peroxidase 1 (GPx1) and catalase expression to a greater extent than AgNP exposure, but treatment with AgNO(3) and AgNPs induced comparable superoxide dismutase 1 (SOD1) expression levels. Our findings suggest that AgNP cytotoxicity is primarily the result of oxidative stress and is independent of the toxicity of Ag(+) ions.


Aquatic Toxicology | 2010

Induction of oxidative stress and apoptosis by silver nanoparticles in the liver of adult zebrafish.

Ji Eun Choi; Soohee Kim; Jin Hee Ahn; Pilju Youn; Jin Seok Kang; Kwangsik Park; Jongheop Yi; Doug-Young Ryu

Silver nanoparticles (AgNPs) may induce deleterious effects in aquatic life on environmental release. The hepatotoxicity of AgNPs was assessed in the liver of adult zebrafish, with the aim of studying the roles of oxidative damage and apoptosis. Zebrafish were exposed to an AgNP solution in which free Ag+ ions were absent at the time of treatment. However, the metal-sensitive metallothionein 2 (MT2) mRNA was induced in the liver tissues of AgNP-treated zebrafish, suggesting that Ag+ ions were released from AgNPs after treatment. It is also possible that MT2 mRNA was induced in the liver tissues by AgNP-generated free radicals. A number of cellular alterations including disruption of hepatic cell cords and apoptotic changes were observed in histological analysis of the liver tissues. The levels of malondialdehyde, a byproduct of cellular lipid peroxidation, and total glutathione were increased in the tissues after treatment with AgNPs. The mRNA levels of the oxyradical-scavenging enzymes catalase and glutathione peroxidase 1a were reduced in the tissues. AgNP treatment induced DNA damage, as demonstrated by analysis with the double-strand break marker γ-H2AX and the expression of p53 protein in liver tissues. In addition, the p53-related pro-apoptotic genes Bax, Noxa, and p21 were upregulated after treatment with AgNPs. These data suggest that oxidative stress and apoptosis are associated with AgNP toxicity in the liver of adult zebrafish.


Journal of Applied Toxicology | 2013

Silver nanoparticle-induced oxidative stress, genotoxicity and apoptosis in cultured cells and animal tissues

Soohee Kim; Doug-Young Ryu

Silver nanoparticles (AgNPs) have emerged as an important class of nanomaterials for a wide range of industrial and medical applications. However, the unique properties of AgNPs could potentially lead to unexpected hazards to both human health and the well being of the environment. Possible mechanisms of AgNP‐induced toxicity include the stimulation of oxidative stress, genotoxicity and apoptosis. In this study, a number of previous studies are therefore summarized that demonstrate oxidative stress‐, genotoxicity‐ and apoptosis‐related changes brought about by AgNPs in cultured cells and animal tissues. The physicochemical properties of AgNPs that are involved in encouraging such changes are also discussed. Copyright


Journal of Applied Toxicology | 1996

Effect of a single administration of benzene, toluene or m-xylene on carboxyhaemoglobin elevation and metabolism of dichloromethane in rats.

Soohee Kim; Young Chul Kim

The effect of a single administration of aromatic hydrocarbons (AHCs) on the metabolic activity responsible for the biotransformation of dichloromethane (DCM) to carbon monoxide (CO) was investigated using adult female rats. In rats treated orally with benzene (1.5 ml kg−1), toluene (2.0 ml kg−1) or m‐xylene (2.0 ml kg−1) 16–24 h prior to DCM (3 mmol kg−1, i.p.), the carboxyhaemoglobin (COHb) level was elevated, reaching peaks in blood at 21%, 16% and 23%, respectively, compared to the peak of ca. 10% in rats treated with DCM only. Their effects on COHb generation were highly dependent on the time interval between each AHC and DCM treatment, since an early administration of m‐xylene or toluene decreased the COHb elevation. The half‐life of DCM in blood was shortened significantly, indicating that the metabolic degradation of DCM was enhanced by the AHCs. Disulfiram (3.4 mmol kg−1, p.o.) blocked COHb elevation completely, suggesting that the metabolic conversion of DCM to CO is mediated by cytochrome P‐450 2E1 (P4502E1). Corresponding increases in the concentration and half‐life of DCM in blood were also observed. A single administration of the AHCs did not alter the hepatic glutathione level, suggesting that the increase in DCM‐induced COHb elevation was not due to hepatic glutathione depletion. In vitro studies showed that the hepatic microsomal metabolism of nitrosodimethylamine and p‐nitrophenol was significantly increased by a single dose of each AHC. Total cytochrome P‐450 content and p‐nitroanisole demethylase activity were also increased; however, only toluene and m‐xylene were effective inducers for aminopyrine N‐demethylase. Therefore, benzene appears to be a selective inducer for P4502E1 compared to other alkylbenzenes. The results indicate that even a single dose of benzene, toluene or m‐xylene may induce the activity of P4502E1 significantly, which is responsible for the increased generation of COHb from DCM, as demonstrated in the present study.


Virchows Archiv | 2011

Gene expression profiling of human hepatoblastoma using archived formalin-fixed and paraffin-embedded tissues

Eun Shin; Kyoungbun Lee; Sooyoung Park; Soohee Kim; Han-Suk Ryu; Young-Nyun Park; Eunsil Yu; Ja-June Jang

We elucidated the genetic profile of hepatoblastomas (HBLs) to identify diagnostic and prognostic markers. RNA was extracted from 32 formalin-fixed, paraffin-embedded HBLs and corresponding nonneoplastic liver (NNL) tissues, and cDNA-mediated annealing, selection, extension, and ligation (DASL) chip assays were performed. Immunohistochemistry was performed to confirm the expression of Yin Yang 1 (YY1) protein in HBL. Twenty-four genes that were associated with signal transduction, cell–cell adhesion, cell cycle regulation, and apoptosis were differentially expressed in HBL and NNL tissues. Two apoptosis-associated genes, MYCN and BIRC5, were highly upregulated in HBL. Eight genes, including YY1 and IGF1, were upregulated in HBL cases that had a poor prognosis. Thirty-eight genes, including YY1, were differentially expressed according to histologic differentiation of HBL, and the immunohistochemical expression of YY1 was correlated with poor HBL differentiation. Thus, using DASL chip assays, we report the gene expression profiles of HBL, which suggest new candidate prognostic and diagnostic genetic markers and putative therapeutic targets for HBL.


Toxicology Letters | 2009

Regulation of iron metabolism-related genes in diethylnitrosamine-induced mouse liver tumors.

Pilju Youn; Soohee Kim; Jin Hee Ahn; Yongbaek Kim; Jung-Duck Park; Doug Young Ryu

BACKGROUND It has been suggested that the altered iron metabolism in liver tumors, characterized by the iron-deficient phenotype, is of importance for tumor growth. AIM This study was performed to elucidate the mechanisms underlying iron deficiency in liver tumors by examining how the liver tumor development affects the expression of iron metabolism-related genes. METHODS Iron metabolism reference values were analyzed in the sera of diethylnitrosamine-induced hepatocellular adenoma-bearing mice. Expression of iron metabolism-related genes was analyzed in adenomas and surrounding non-tumor tissues, and a subgroup of adenoma-bearing mice loaded with iron 72h before sacrifice. RESULTS Iron content of the adenoma tissues was 2.0-2.5-fold lower compared to surrounding and age-matched control tissues. There was no significant difference in serum iron levels between the adenoma-bearing and control mice, while the adenoma-bearing mice exhibited a 2.4-fold lower level of serum transferrin saturation. Expression of iron metabolism-related genes was dysregulated in the adenomas. Iron loading affected protein expression similarly in the adenomas and surrounding tissues suggesting that iron-responsive regulation of the proteins was not impaired. However, the mRNA expression for ceruloplasmin and divalent metal transporter 1 (DMT1) IRE(+) in the adenomas was altered independently of iron status, and the dysregulation may contribute to diminished iron content. CONCLUSION These findings suggest that diethylnitrosamine-induced liver adenoma-bearing mice have abnormal iron metabolism and that dysregulation of iron metabolism-related genes contributes to iron deficiency in the adenomas.


Oncotarget | 2017

Dysregulated expression of proteins associated with ER stress, autophagy and apoptosis in tissues from nonalcoholic fatty liver disease

Seung-Woo Lee; Soohee Kim; Seungwoo Hwang; Nathan J. Cherrington; Doug Young Ryu

Nonalcoholic fatty liver disease (NAFLD) is categorized into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH) and has emerged as a risk factor for more critical clinical conditions. However, the underlying mechanisms of NAFLD pathogenesis are not fully understood. In this study, expression of proteins associated with endoplasmic reticulum (ER) stress, apoptosis and autophagy were analyzed in normal, NAFL and NASH human livers by western blotting. Levels of some ER stress-transducing transcription factors, including cleaved activating transcription factor 6, were higher in NASH than in the normal tissues. However, the expression of a majority of the ER chaperones and foldases analyzed, including glucose-regulated protein 78 and ER protein 44, was lower in NASH than in the normal tissues. Levels of apoptosis markers, such as cleaved poly (ADP-ribose) polymerase, were also lower in NASH tissues, in which expression of some B-cell lymphoma-2 family proteins was up- or down-regulated compared to the normal tissues. The level of the autophagy substrate p62 was not different in NASH and normal tissues, although some autophagy regulators were up- or down-regulated in the NASH tissues compared to the normal tissues. Levels of most of the proteins analyzed in NAFL tissues were either similar to those in one of the other two types, NASH and normal, or were somewhere in between. Together, these findings suggest that regulation of certain important tissues processes involved in protein quality control and cell survival were broadly compromised in the NAFLD tissues.Nonalcoholic fatty liver disease (NAFLD) is categorized into nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH) and has emerged as a risk factor for more critical clinical conditions. However, the underlying mechanisms of NAFLD pathogenesis are not fully understood. In this study, expression of proteins associated with endoplasmic reticulum (ER) stress, apoptosis and autophagy were analyzed in normal, NAFL and NASH human livers by western blotting. Levels of some ER stress-transducing transcription factors, including cleaved activating transcription factor 6, were higher in NASH than in the normal tissues. However, the expression of a majority of the ER chaperones and foldases analyzed, including glucose-regulated protein 78 and ER protein 44, was lower in NASH than in the normal tissues. Levels of apoptosis markers, such as cleaved poly (ADP-ribose) polymerase, were also lower in NASH tissues, in which expression of some B-cell lymphoma-2 family proteins was up- or down-regulated compared to the normal tissues. The level of the autophagy substrate p62 was not different in NASH and normal tissues, although some autophagy regulators were up- or down-regulated in the NASH tissues compared to the normal tissues. Levels of most of the proteins analyzed in NAFL tissues were either similar to those in one of the other two types, NASH and normal, or were somewhere in between. Together, these findings suggest that regulation of certain important tissues processes involved in protein quality control and cell survival were broadly compromised in the NAFLD tissues.


Food Science and Biotechnology | 2016

Physicochemical properties and oxidative stabilities of mealworm (Tenebrio molitor) oils under different roasting conditions

Yu-Ho Jeon; Yang-Ju Son; Soohee Kim; Eun-Young Yun; HeeJin Kang; In-Kyeong Hwang

Physicochemical properties and oxidative stabilities of mealworm (Tenebrio molitor) oils under different roasting conditions were investigated. Oils were extracted using n-hexane from mealworms roasted at 200°C for 0, 5, 10, and 15 min and physicochemical properties and oxidative stabilities of oils were analyzed. Roasting increased the color intensity and the oleic acid and δ-tocopherol contents, but decreased linoleic acid, and α- and γ-tocopherol contents. An improvement in oxidative stability was observed in roasted mealworm oils, demonstrated by induction time and peroxide values. Mealworm oil contained abundant essential fatty acids and exhibited a superior oxidative stability.


American Journal of Veterinary Research | 2013

Experimental determination of a subantimicrobial dosage of doxycycline hyclate for treatment of periodontitis in Beagles

Se Eun Kim; Soohee Kim; Manbok Jeong; Jeong Taek Ahn; Young Woo Park; Jae Sang Ahn; Euiri Lee; Doug-Young Ryu; Kangmoon Seo

OBJECTIVE To identify a subantimicrobial dose of doxycycline hyclate (SDD) and for the treatment of periodontitis in dogs. ANIMALS 20 healthy Beagles for measurement of serum doxycycline concentration and 15 Beagles with periodontitis for evaluation of the efficacy of the SDD. PROCEDURES 5 dogs each received doxycycline hyclate PO at a dose of 1, 2, 3, or 5 mg/kg. Blood samples were collected before and after administration, and serum concentrations of doxycycline were measured via high-performance liquid chromatography. Mean serum doxycycline concentrations were calculated, and SDDs were identified. In a separate trial, the identified SDDs (1 or 2 mg/kg) were administered PO once a day for 1 month to dogs with periodontitis (n = 5/group) and a control group (5) was fed vehicle only during the same period. Degree of gingival attachment and bleeding on probing (present or absent) were recorded. Gingival samples were collected before and after the 1-month period from the same anatomic sites. Degree of matrix metalloproteinase inhibition in gingival samples was determined via gelatin zymography and compared among treatment groups. RESULTS Mean serum doxycycline concentrations in healthy dogs that received 1 or 2 mg of doxycycline/kg were consistently significantly lower than the minimal inhibitory doxycycline concentration for treatment of periodontitis throughout the 24-hour posttreatment period. Zymographic intensities were lower in dogs given 1 and 2 mg/kg than in the control dogs, and the degree of gingival attachment and bleeding significantly improved in dogs given 2 mg/kg, compared with in the control dogs and dogs given 1 mg of doxycycline/kg. CONCLUSIONS AND CLINICAL RELEVANCE A doxycycline dosage of 2 mg/kg daily appeared to be an appropriate subantimicrobial regimen for dogs with periodontitis. Furthermore, this dosage may be suitable for long-term treatment of gelatinolytic inflammatory diseases such as periodontitis in this species.


Apmis | 2012

Nuclear expression of S-phase kinase–associated protein 2 predicts poor prognosis of hepatocellular carcinoma

Eun Shin; Soohee Kim; Hae‐Yeon Jeong; Ja-June Jang; K.-W. Lee

Shin E, Kim S‐H, Jeong H‐Y, Jang J‐J, Lee K. Nuclear expression of S‐phase kinase–associated protein 2 predicts poor prognosis of hepatocellular carcinoma. APMIS 2012; 120: 349–57.

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Doug-Young Ryu

Seoul National University

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In-Kyeong Hwang

Seoul National University

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Seung Heon Lee

Seoul National University

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Seung-Woo Lee

Seoul National University

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Eun Shin

Seoul National University

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Ja-June Jang

Seoul National University

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Yang-Ju Son

Seoul National University

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Doug Young Ryu

Seoul National University

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Ji Eun Choi

Seoul National University

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