• Applied Microscopy
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• v.31 no.1
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• pp.37-47
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• 2001

In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total burn surface area $20\sim25\%$) except for inhalated injury. At 5 and 24 h after scald burn, biochemical assay and morphological changes in serum and liver tissue were examined. Skin burn increased liver weight (% of body weight, p<0.05) and the activity of serum aniline amino-transferase (ALT, p<0.05), in addition, the activity of xanthine oxidase (XO), an enzyme of oxygen free radical generating system, was elevated (p<0.01) in serum, but not in skin and in liver. Postburn treatment of allopurinol intraperitoneally decreased liver weight, serum ALT activity and serum XO activity. Scald burn induced ultrastructurally swelling of endoplasmic reticulum, ribosome detachment, accumulation of lipid, dilatation of bile canaliculi and intercellular space, neutrophil infiltration, activation of Kupffer's cells and degeneration of hepatocytic microvilli. Futhermore , thermal injury decreased not only the protein concentration in plasma but also the number of intravascular leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. However allopurinol injection after burn inhibited post burn ultrastructural changes. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.

• Journal of Life Science
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• v.25 no.5
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• pp.539-547
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• 2015

This study aimed to investigate the protective effect of Semisulcospira libertina extract on liver injury induced by D-galactosamine in rats. After the administration of S. libertina extract, the local fat degeneration and infiltration of inflammatory cells in liver tissues were significantly decreased and peripheral hemorrhages around portal triads and central necrosis around central veins were found to be protective. The elevated levels of plasma ALT, AST, and LDH, the ALP activation lipid peroxidation, and the lipid contents of a damaged liver were recovered in experimental rats administrated with S. libertina extract, suggesting its role in blood enzyme activation and lipid content restoration within damaged rat liver tissues. Moreover, the expression rate of TNF-α, which accelerates inflammation and induces tissue damage and necrosis, was significantly decreased. In addition, the activities of antioxidant enzymes were more effectively upregulated compared to those of the control group induced hepatotoxicity. All data showed that S. libertina extract has a preventive role against liver damages, such as inflammation and tissue necrosis, as instigated with D-galactosamine by improving the activities of blood enzymes and antioxidant enzymes and modulating the expression of inflammation factor, suggest S. libertina extract is an effective medicinal resource for the restoration of hepatotoxicity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.4
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• pp.320-328
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• 1991

The present study was designed to evaluate the effects of dietary vitamin E and coenzyme $Q_{10}$ supplementation on adriamycin (ADR) -induced lipid petoxidation in rats. After feeding the experimental diets for e weeks. Ann treatment significantly decreased growth performance of rats. But this decrement was not modified by supplementation of vitamin E or coenzyme $Q_{10}$ . Lipid peroxide values of plasma and heart mitochondria were elevated by Ann treatment. But these values were significantly decreased according to vitamin E or coenzyme $Q_{10}$ supplementation. Adriamycin treatment elevated glutathione peroxidase (GSH-Px) activity of rats, but this increment was modified by vitamin E supplementation. There was a tendency of higher superoxide dismutase (SOD) activity in ADR-treated rats. However, vitamin E or coenzyme $Q_{10}$ administration reduced this enzyme activity. With ADR treatment, arachidonic acid (20 : 4) was greatly increased, but docosahexaenoic acid (22 : 6) was not detected. Arachidonic acid was decreased and docosahexaenoic acid increased by supplementation of higher level of vitamin E or coenzyme $Q_{10}$ . Present data showed that dietary vitamin E and coenzyme $Q_{10}$ influenced on ADR-induced lipid peroxidation in rats, and also the degree of antioxidative effect was greater in vitamin E-supplemented rats.

• Korean Journal of Food Science and Technology
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• v.41 no.1
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• pp.93-99
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• 2009

This study aimed to determine whether or not glycoprotein isolated from Cudrania tricuspidata Bureau fruit(CTB glycoprotein) exerts a hepatoprotective effect on liver injury induced by the administration of carbon tetrachloride($CCl_4$, 1.0mL/kg) to A/J mice. Following the administration of CTB glycoprotein(0-20mg/kg), the activities of antioxidant enzymes (superoxide dismutase(SOD), catalase(CAT), and glutathione peroxidase(GPx)), and the quantities of measured thiobarbituric acid reactive substances(TBARS), lactate dehydrogenase(LDH), and nitric oxide(NO) were evaluated from the murine liver tissues and plasma. Additionally, the activity of nuclear factor-kappa B(NF-${\kappa}B$) was assessed after pretreatment with $CCl_4$. When the mice were treated with $CCl_4$ alone, the activities of antioxidative enzymes reduced but amounts of TBARS, LDH, and NO increased. However, the results of treatment with CTB glycoprotein(10 and 20 mg/kg) revealed significantly increased activities of antioxidant enzymes(SOD, CAT, and GPx), as compared with $CCl_4$ alone. On the other hand, the result showed significant diminutions of the quantities of TBARS, LDH, and NO after treatment with CTB glycoprotein(10 and 20 mg/kg), as compared to $CCl_4$ alone. The activity of NF-${\kappa}B$ also declined after pretreatment with CTB glycoprotein, as compared with $CCl_4$ treatment alone. Thus, it is suggested that the CTB glycoprotein exerts a protective effect against $CCl_4$-induced liver injury in A/J mice.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.3 no.1
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• pp.86-93
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• 2003

Background : The SCL began screening of newborns and high risk group blood spots with tandem mass spectrometry (MS/MS) in April 2001. Our goal was to determine approximate prevalence of metabolic disorders, optimization of decision criteria for estimation of preventive effect with early diagnosis. This report describes the ongoing effort to identify more than 30 metabolic disorders by MS/MS in South Korea. Methods : Blood spot was collected from day 2 to 30 (mostly from day 2 to 10) after birth for newborn. Blood spot of high risk group was from the pediatric patients in NICU, developmental delay, mental retardation, strong family history of metabolic disorders. One punch (3.2 mm ID) of dried blood spots was extracted with $150{\mu}L$ of methanol containing isotopically labelled amino acids (AA) and acylcarnitines (AC) internal standards. Butanolic HCl was added and incubated at $65^{\circ}C$ for 15 min. The butylated extract was introduced into the inlet of MS/MS. Neutral loss of m/z 102 and parent ion mode of m/z 85 were set for the analyses of AA and AC, respectively. Diagnosis was confirmed by repeating acylcarnitine profile, urine organic acid and plasma amino acid analysis, direct enzyme assay, or molecular testing. Results : Approximately 31,000 neonates and children were screened and the estimated prevalence (newborn/high risk group), sensitivity, specificity and recall rate amounted to 1:2384/1:2066, 96.55%, 99.98%, and 0.73%, respectively. Confirmed 28 (0.09%) multiple metabolic disorders (newborn/high risk) were as follows; 13 amino acid disorders [classical PKU (3/4), BH4 deficient-hyperphenylalaninemia (0/1), Citrullinemia (1/0), Homocystinuria (0/2), Hypermethioninemia (0/1), Tyrosinemia (1/0)], 8 organic acidurias [Propionic aciduria (2/1), Methylmalonic aciduria (0/1), Isovaleric aciduria (1/1), 3-methylcrotonylglycineuria (1/0), Glutaric aciduria type1 (1/0)], 7 fatty acid oxidation disorders [LCHAD def. (2/2), Mitochondrial TFP def. (0/1), VLCAD def. (1/0), LC3KT def. (0/1). Conclnsion : The relatively normal development of 10 patients with metabolic disorders among newborns (except for the expired) demonstrates the usefulness of newborn screening by MS/MS for early diagnosis and medical intervention. However, close coordination between the MS/MS screening laboratory and the metabolic clinic/biochmical geneticists is needed to determine proper decision of screening parameters, confirmation diagnosis, follow-up scheme and additional tests.

• Allergy, Asthma & Immunology Research
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• v.10 no.6
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• pp.698-715
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• 2018

Purpose: Hrd1 has recently emerged as a critical regulator of B-cells in autoimmune diseases. However, its role in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) remains largely unexplored. This study aimed to examine Hrd1 expression and B-cell accumulation and their possible roles in CRSwNP. Methods: Quantitative real-time polymerase chain reaction, immunohistochemistry, enzyme-linked immunosorbent assay and Western blotting were used to assess gene and protein expression in nasal tissue extracts. Cells isolated from nasal tissues and peripheral blood mononuclear cells were characterized by flow cytometry. Local antibody production was measured in tissue extracts with a Bio-Plex assay. Additionally, changes in Hrd1 expression in response to specific inflammatory stimuli were measured in cultured dispersed polyp cells. Results: Nasal polyps (NPs) from patients with eosinophilic CRSwNP (ECRS) had increased levels of Hrd1, B-cells and plasma cells compared with NPs from patients with non-eosinophilic CRSwNP (non-ECRS) or other control subjects (P < 0.05). The average Hrd1 levels in B-cells in NPs from ECRS patients were significantly higher than those from non-ECRS patients and control subjects (P < 0.05). NPs also contained significantly increased levels of several antibody isotypes compared with normal controls (P < 0.05). Interestingly, Hrd1 expression in cultured polyp cells from ECRS patients, but not non-ECRS patients, was significantly increased by interleukin-$1{\beta}$, lipopolysaccharide and Poly(I:C) stimulation, and inhibited by dexamethasone treatment (P < 0.05). Conclusions: Differential Hrd1 expression and B-cell accumulation between the ECRS and non-ECRS subsets suggests that they can exhibit distinct pathogenic mechanisms and play important roles in NP.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.21 no.1
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• pp.22-27
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• 2021

Propionic acidemia (PA) is an inherited autosomal recessive disorder, due to the deficiency of propionyl-CoA carboxylase (PCC). PCC is the enzyme which catalyzes the conversion of propionyl-CoA to D-methylmalonyl-CoA, and it is critical for the metabolism of amino acids, odd-chain fatty acids, and side chains of cholesterol. The clinical manifestations present mostly at the neonatal period with life-threatening metabolic acidosis and hyperammonemia. Here, we described a case of a 16-year-old Korean boy with late-onset PA who presented with embolic cerebral infarction due to dilated cardiomyopathy (DCMP) with left ventricular noncompaction. And he has family history of sudden cardiac death, so we performed metabolic screening and genetic tests. Elevated levels of 3-hydroxypropionic acid, methylcitric acid and propionylglycerine were detected in urine. Plasma acylcarnitine profile showed elevated propionylcarnitine (C3). Diagnosis of PA was confirmed by genetic analysis, which revealed compound heterozygous mutations, c.[1151T>G] (p.[Phe384Cys]) and c.[1228C>T] (p.[Arg410Trp]) in PCCB gene. His heart function is in improving state and the results of biochemical analysis are stable with heart failure medication and metabolic managements. We present a case of patient without episodes of metabolic decompensation who manifests DCMP as the first symptom of PA.

• Annals of Occupational and Environmental Medicine
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• v.35
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• pp.27.1-27.12
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• 2023

Background: Environmental exposure is characterized by low concentration, chronic, and complex exposure. Traditional epidemiological studies show limitations in reflecting these characteristics since they usually focus on a single or very limited number of exposure factors at a time. In this study, we adopted the methodology of environment-wide association study (EWAS) to figure out the association of human liver function with various environmentally hazardous substances. Methods: We analyzed 2,961 participants from the Korean National Environmental Health Survey Cycle 4 (2018-2020). Using generalized linear model (GLM) analysis, we analyzed the association of 72 variables with 3 liver function indices (aspartate aminotransferase [AST], alanine aminotransferase [ALT], and gamma glutamyl transferase [GGT]). Finally, we visualized our results with Manhattan plot. Results: In GLM analysis, perfluorooctanesulfonate were positively associated with ALT (odds ratio [OR]: 2.2; 95% confidence interval [CI]: 1.39-3.46; p_adjusted = 0.0147) and perfluorodecanoic acid showed positive association with GGT (OR: 2.73; 95% CI: 1.36-5.5; p_adjusted = 0.0256). Plasma mercury showed positive association with GGT (OR: 1.45; 95% CI: 1.14-1.84; p_adjusted = 0.0315). Using a plastic container while keeping food in the refrigerator was associated with elevated GGT compared to using a glass container (OR: 1.51; 95% CI: 1.16-1.95; p_adjusted = 0.0153). 2-ethyl-5-oxohexyl phthalate, showed a negative trend with all 3 indices, with AST (OR: 0.54; 95% CI: 0.39-0.73; p_adjusted = 0.00357), ALT (OR: 0.5; 95% CI: 0.34-0.75; p_adjusted = 0.036), GGT (OR: 0.55; 95% CI: 0.4-0.76; p_adjusted = 0.00697). Bisphenol S and frequent use of sunblock cream showed negative association with ALT (OR: 0.77; 95% CI: 0.66-0.89), and GGT (OR: 0.25; 95% CI: 0.11-0.55), respectively. Conclusions: We conducted an exploratory study on environmental exposure and human liver function. By using EWAS methodology, we identified 7 factors that could have potential association with liver function.

• Journal of Nutrition and Health
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• v.24 no.3
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• pp.166-178
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• 1991

This present study was designed to evaluate whether supplementaion of dietary coenzyme $Q_{10}$ protects the lipid peroxidation damage in adriamycin (ADR)-treated rats. Two experiments were conducted in this study. Experiment I was undertaken under the condition of simultaneous administration of ADR and coenzyme $Q_{10}$ for 4 weeks. Experiment 2 was undertaken under the same condition as experiment I after feeding the experimetal diets alone without administration of ADR for 4 weeks. Results obtained from the present study were as follows. Lipid peroxide value of plasma and heart mitochondria was elevated by ADR treatment. but decreased according to dietary coenzyme $Q_{10}$ supplementation. Pretreatment with dietary coenzyme $Q_{10}$ was more efficient in reducing ADR-induced lipid peroxide value. The simultaneous use of ADR and coenzyme $Q_{10}$ enhanced the heart glutathione peroxidase (GSH-Px) activity. particularly at higher level of coenzyme $Q_{10.}$ The change of superoxide dismutase(SOD) activity was similar to that of GSH-Px activity. In case of pretreatment with coenzyme $Q_{10, }$ these enzyme activities were more enhanced by dietary coenzyme $Q_{10.}$ However, there was little difference in catalase activity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.11
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• pp.1556-1561
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• 2011

The purpose of this study was to investigate antioxidant enzyme activity and vitamin E concentrationin in Sprague-Dawley rat after being fed various extracts of Hizikia fusiforme. There were six experimental groups: control group (C), H. fusiforme ethanol extract group (EtOH), H. fusiforme dichloromethane fraction group ($CH_2Cl_2$), H. fusiforme ethylacetate fraction group (EtOAc), H. fusiforme butanol fraction group (n-BuOH), H. fusiforme water fraction group ($H_2O$). H. fusiforme extracts (400 mg/kg B.W) were orally administrated to the rats every day for 4 weeks. The activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), and concentrations of malondialdehyde (MDA) and vitamin E in the liver and blood were measured. The activity of SOD in the liver was significantly higher in the $CH_2Cl_2$ and $H_2O$ groups (p<0.05) than in the control and other extract groups. The SOD activity in serum increased significantly in all H. fusiforme groups (p<0.05) compared to the control group and it was also significantly higher in the EtOH and $H_2O$ groups (p<0.05) than in other extract groups. The serum catalase activity increased significantly in the n-BuOH group (p<0.05) compared to the control and other extract groups. The plasma MDA concentration decreased significantly in the n-BuOH and $H_2O$ group (p<0.05) compared to the control group. Serum concentration of ${\alpha}$-tocopherol showed no significant differences in most of the experimental groups, but it was significantly higher in the EtOAc group (p<0.05). The ${\alpha}$-tocopherol concentrations in the liver showed a significant increase in the $CH_2Cl_2$ and $H_2O$ groups (p<0.05) compared to the control and other extract groups. The liver ${\gamma}$-tocopherol concentrations in H. fusiforme extract groups showed a tendency to increase compared to the control group and it was significantly higher in the $H_2O$ group (p<0.05) than in other extract groups. These results suggest that supplementation of water extracts of H. fusiforme extract could be effective in improving the antioxidant system.