• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.8 no.2
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• pp.263-268
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• 2005

Erythropoietic protoporphyria is a genetic disorder due to a deficiency of ferrochelatase resulting in excessive accumulation and excretion of protoporphyrin. The predominant clinical feature is photosensitivity. Severe hepatic failure occurs in a small percentage of patients, and neurological symptoms are very rare. We report a case of erythropoietic protoporphyria associated with severe hepatic dysfunction and neurological symptoms. A 9-year-old girl presented with severe abdominal pain, nausea, weakness and pain of extremities, and urinary retention. Ultrasonogram and abdominal CT scanning revealed a diffuse infiltrated and enlarged liver. Liver biopsy showed deposition of dense dark brown pigment within the bile, hepatocytes and Kupffer cells. Plus, dense dark brown deposits gave a red birefringent under polarize light. Porphyrin studies demonstrated markedly elevated serum free erythrocyte protoporphyrin. This girl was diagnosed as erythropoietic protoporphyria with severe liver dysfunction and neurological symptoms.

• Korean Journal of Veterinary Research
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• v.28 no.2
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• pp.371-377
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• 1988

In order to know the effect of dexamethasone on the induction of the rabbit viral hepatitis, the pathological changes were observed in the native rabbits, 2 to 6 months old in age, that were injected by dexamethasone and liver emulsion of Angora rabbit naturally infected with viral hepatitis. The results were summarized as follows: The native rabbits injected by dexamethasone and liver emulsion were infected with viral hepatitis and died between 2 and 7 days after inoculation. Clinical signs and gross lesions were very similar to those of Angora rabbit naturally occurred, In microscopical findings, the hepatic lesions were characterized by peripheral necrosis of the lobules, and peripheral necrosis of the lobules with fatty changes of hepatic cells was occurred in a few cases. Perivascular lymphocytic infiltration in the central nervous system was observed in some cases, The lesions of the other organs were very similar to those of Angora rabbit naturally occurred. On the other hand, the native rabbits that were injected by only liver emulsion of Angora rabbit naturally infected with viral hepatitis were not infected with the disease except very few cases.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.4803-4812
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• 2015

Chronic alcohol and tobacco abuse plays a crucial role in the development of different liver associated disorders. Intake promotes the generation of reactive oxygen species within hepatic cells exposing their DNA to continuous oxidative stress which finally leads to DNA damage. However in response to such damage an entangled protective repair machinery comprising different repair proteins like ATM, ATR, H2AX, MRN complex becomes activated. Under abnormal conditions the excessive reactive oxygen species generation results in genetic predisposition of various genes (as ADH, ALDH, CYP2E1, GSTT1, GSTP1 and GSTM1) involved in xenobiotic metabolic pathways, associated with susceptibility to different liver related diseases such as fibrosis, cirrhosis and hepatocellular carcinoma. There is increasing evidence that the inflammatory process is inherently associated with many different cancer types, including hepatocellular carcinomas. The generated reactive oxygen species can also activate or repress epigenetic elements such as chromatin remodeling, non-coding RNAs (micro-RNAs), DNA (de) methylation and histone modification that affect gene expression, hence leading to various disorders. The present review provides comprehensive knowledge of different molecular mechanisms involved in gene polymorphism and their possible association with alcohol and tobacco consumption. The article also showcases the necessity of identifying novel diagnostic biomarkers for early cancer risk assessment among alcohol and tobacco users.

• Biomedical Science Letters
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• v.7 no.3
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• pp.99-102
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• 2001

Toluene is mainly metabolized in liver by oxidative pathway. Oxigen free radicals occur through the process of toluene metabolism Therefore it causes tissue and cell min by the oxygen free radicals from the metabolism of toluene. Melatonin acts as a highly efficient free radical scavenger that protects cells from damage by oxygen free radicals. To test this hypothesis, toluene hepatotoxicity was induced by an abdominal injection of toluene. To see if the melatonin protects the rat's liver, melatonin was administrated orally, at the time of each toluene injection. Aspartate aminotransferase(AST), alanin aminotransferase(ALT), latic dehydrogenase(LDH) and alkaline phosphatase(ALP) levels in serum were measured to estimate hepatic function. Malondialdehyde(MDA), which gives an indirect index of oxidative injury was also measured. Hippuric acid is the last metabolic Production of toluene was measured by HPLC. There were significantly higher in AST, ALT, LDH, MDA and hippuric acid in toluene group, but there were no significant difference in melatonin group except ALT and hippuric acid. There was significantly lower in ALP level in toluene group, but there was no significant difference melatonin group, suggesting a significant hepatotoxicity due to oxygen free radicals through the process of toluene metabolism Melatonin treatment significantly protected hepatic function and free radical-mediated injury in the liver against toluene-induced changes. Accordingly, this study shows that melatonin is helpful in protecting liver injury by acute toluene intoxication.

• Biomolecules & Therapeutics
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• v.8 no.2
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• pp.119-124
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• 2000

We hypothesized that the extent of hypoxic injury would be involved in reduction of oxygen delivery to the tissue. Livers isolated from 18 hr-fasted rats were subjected to $N_2$-induced hypoxia or low flow hypoxia. Livers were perfused with nitrogen/carbon dioxide gas for 45min or perfused with normoxic Krebs-Henseleit bicarbonate buffer (KHBB) at low flow rates around 1 ml/g liver/min far 45min, which caused cells to become hypoxic because of insufficient delivery of oxygen. When normal flow rates(4 ml/g liver/min) of KHBB (pH 7.4, 37$^{\circ}C$, oxygen/carbon dioxide gas) were restored for 30min reoxygenation injury occurred. Lactate dehydrogenase release gradually increased in $N_2$-induced hypoxia, whereas it rapidly increased in low flow hypoxia. Total glutathione in liver tissue was not changed but oxidized glutathione markedly increased after hypoxia and reoxygenation, expecially in $N_2$-induced hypoxia. Similarly, lipid peroxidation in liver tissue significantly increased after hypoxia and reoxygenation in low flow hypoxia. Hepatic drug metabolizing functions (phase I, II) were suppressed during hypoxia, especially in $N_2$-induced hypoxia but improved by reoxygenation in both models. Our findings suggest that hypoxia results in abnormalities in drug metabolizing function caused by oxidative stress and that this injury is dependent on hypoxic conditions.

• Food Science and Biotechnology
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• v.18 no.1
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• pp.172-178
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• 2009

Fermented ginseng (FG) is an ethanol extract of ginseng radix processed with $\beta$-galactosidase. It was hypothesized that FG may exert anti-hyperlipidemic and anti-diabetic activities through modulating AMP-activated protein kinase (AMPK) in HepG2 human hepatoma cells. In this study, we showed that AMPK phosphorylation was stimulated by FG. These effects were abolished by pretreatment with an AMPK inhibitor, compound C. In addition, FG regulated the expression of genes associated with lipogenesis and lipolysis, thus causing suppression of hepatic triglyceride accumulation. In vivo study using db/db mice, FG reduced fasting plasma glucose, HbAlc, and insulin resistance index, when compared to diabetic control. FG also increased the phospho-AMPK and glucose transporter 4 (GLUT4) expressions in liver and skeletal muscle, respectively. In liver, expressions of lipogenic gene were decreased whereas expressions of lipolytic genes were induced, when compared to diabetic control. Taken together, we may suggest that FG ameliorates hyperglycemia and hyperlipidemia through activation of AMPK and could be developed as a health functional food or therapeutic agent for type 2 diabetic patients.

• Korean Journal of Acupuncture
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• v.27 no.3
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• pp.25-46
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• 2010

Objective & Methods : The purpose of this study is to observe the effects of herbal- acupuncture with Achyranthis Radix(AR-HA) at GB34(Yangleungchean) on hyperlipidemia in rats. The author performed several experimental items to analyze the levels of various components and enzymes in serum and liver, as well as the histological changes of liver and aorta. Results : 1. Achyranthis Radix herbal acupuncture solution increased DPPH radical scavenging activity and HMG-CoA reductase inhibition rate in rat liver cells. 2. AR-HA at GB34 decreased the level of serum total cholesterol, and increased the ratios of HDL-cholesterol to total cholesterol, phospholipid to total cholesterol in hyperlipidemic rat. 3. AR-HA at GB34 decreased the hepatic HMG-CoA reductase activity in hyperlipidemic rat. 4. AR-HA at GB34 increased the hepatic GSH level in hyperlipidemic rat. Conclusion : From the above results, it is suggested that AR-HA at GB34 has a therapeutic effect on hyperlipidemia.

• Journal of Environmental Health Sciences
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• v.22 no.4
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• pp.91-101
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• 1996

Exposure indices are important tools which enable scientists to reliably predict and detect exposures to xenobiotics and resultant cell injury. Since the de novo synthesis of stress proteins can be detected early after exposure to some agents, analysis of toxicant-induced changes in gene expression, i.e. alterations in patterns of protein synthesis, may be useful to develop as biomarkers of exposure and toxicity. The acute and chronic effects of cadmium(Cd, $CdCl_2$ 20 mg/kg) on Wistar male rats were evaluated concerning cadmium contents, tissues enzyme activity, HSP expression. The results of the study were as follows: 1. Less cadmium was absorbed through the digestive tracts, but the ratio of contents in renal to hepatic cadmium was higher at 8 weeks after treatment. 2. ALT(alanine aminotransferase), AST(aspartate aminotransferase), glucose, BUN(blood urea nitrogen), creatinine, the key indices of the clinical changes in hepatic and renal function were significantly changed by the cadmium treatment after 1 week in liver, after 4 weeks in kidney. 3. Enhanced synthesis of 70 KDa relative molecular mass proteins were detected in 2 hours after cadmium exposure, with maximum activity occurring at 8~48 hours. Induction of $HSP_{70}$ was evident at proximal tubules and glomeruli in kidney. Testicular cells produced enough HSP to be detected normally. From the above results, it could be concluded that $HSP_{70}$ induction by the cadmium treatment was a rapid reaction to indicate the exposure of xenobiotics.

• Molecular & Cellular Toxicology
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• v.2 no.1
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• pp.48-53
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• 2006

[ ${\alpha}-Naphthylisothiocyanate$ ] (ANIT) induces intrahepatic cholestasis, involving damage to biliary epitheial cells. This study investigates hepatic gene expression and histopathological alterations in response to ANIT treatment in order to elucidate early time response of ANIT-induced hepatotoxicity. ANIT was treated with single dose (3, 6, and 60 mg/kg) in corn oil by oral gavage. Serum biochemical and histopathological observation were performed for evaluation of hepatotoxicity level. Affymetrix oligo DNA chips were used for gene expression profile by ANIT-induced hetpatoxicity. Hepatic enzyme levels (ALT, AST, and ALP) were increased in 24 hr high dose group. In microscopic observations, moderate hepatocellular necrosis, were confirmed 24 hr high dose groups. We found that gene expression patterns were dependent on time and dose. Our selected genes were related inflammation and immunomodulation. In this study, ANIT-induced hepatotoxicity was involved in acute phase responses and provides evidence for role of neutrophil could be mechanism associated with ANIT-mediated hepatotoxicity.

• Journal of Veterinary Clinics
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• v.40 no.5
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• pp.387-392
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• 2023

A 13-year-old intact male English Springer Spaniel presented with anorexia. Physical examination revealed a palpable abdominal mass without peripheral lymphadenopathy. Ultrasonography revealed hepatosplenomegaly and a markedly enlarged hepatic lymph node. Fine-needle aspiration of the splenic and nodal lesions revealed atypical round cells admixed with numerous histiocytes. The dog was euthanized owing to deteriorating condition despite a month of chemotherapy with lomustine. Histopathology revealed obliteration of the normal architecture of the liver, spleen, kidney, and hepatic and mesenteric lymph nodes by CD3⁺ neoplastic lymphocytes, accompanied by extensive F4/80⁺ histiocytic infiltration. This report describes a rare presentation of T-cell lymphoma with prominent histiocytic infiltration that may initially be misdiagnosed as histiocytic neoplasia in a dog.