Gaballah, Hanaa Hibishy;Zakaria, Soha Said;Ismail, Saber Abdelrahman
Asian Pacific Journal of Cancer Prevention
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v.15
no.16
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pp.6911-6917
/
2014
Background: Hepatocellular carcinoma is a complex and heterogeneous tumor with poor prognosis due to frequent intrahepatic spread and extrahepatic metastasis. The molecular mechanisms underlying HCC pathogenesis still remain obscure. Objectives: We aimed to investigate the abundance and the DNA binding activity of nuclear factor kappa B/p65 subunit in peripheral blood mononuclear cells from patients with HCC and to assess its prognostic significance and association with hypoxia inducible factor one alpha (HIF-$1{\alpha}$) in blood. Subjects and methods: This study was carried out on 40 patients classified equally into liver cirrhosis (group I) and HCC (group II), in addition to 20 healthy volunteers (group III). All groups were subjected to measurement of NF-${\kappa}B$/P65 subunit expression levels by real time-PCR, and DNA binding activity was evaluated by transcription factor binding immunoassay. Serum HIF-$1{\alpha}$ levels were estimated by enzyme-linked immunosorbent assay (ELISA). Significant increase of both the expression level and DNA binding activity of NF-${\kappa}B$/P65 subunit together with serum HIF-1 alpha levels was noted in HCC patients compared to liver cirrhosis and control subjects, with significant positive correlation with parameters for bad prognosis of HCC. In conclusion, NF-${\kappa}B$ signaling is activated in HCC and associated with disease prognosis and with high circulating levels of HIF-1 alpha.
Cho, Young-Eun;Lomeda, Ria-Ann R.;Ryu, Sang-Hoon;Sohn, Ho-Yong;Shin, Hong-In;Beattie, John H.;Kwun, In-Sook
Nutrition Research and Practice
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v.1
no.2
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pp.113-119
/
2007
Zn is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant function, growth, and reproduction. The present study evaluated whether Zn deficiency would negatively affect bone-related enzyme, ALP, and other bone-related minerals (Ca, P and Mg) in rats. Thirty Sprague Dawley rats were assigned to one of the three different Zn dietary groups, such as Zn adequate (ZA, 35 mg/kg), pair fed (PF, 35 mg/kg), Zn deficient (ZD, 1 mg/kg) diet, and fed for 10 weeks. Food intake and body weight were measured daily and weekly, respectively. ALP was measured by spectrophotometry and mineral contents were measured by inductively coupled plasma-mass, spectrophotometer (ICP-MS). Zn deficient rats showed decreased food intake and body weight compared with Zn adequate rats (p<0.05). Zn deficiency reduced ALP activity in blood (RBC, plasma) and the tissues (liver, kidney and small intestine) (p<0.05). Also, Zn deficiency reduced mineral concentrations in rat tissues (Ca for muscle and liver, and Mg for muscle and liver) (p<0.05). The study results imply the requirement of proper Zn nurture for maintaining bone growth and formation.
Park, Jong-Cheol;Kim, Jong-Yeon;Lee, Youn-Ju;Lee, Ji-Seon;Kim, Bo-Geum;Lee, Seung-Ho;Nam, Doo-Hyun
YAKHAK HOEJI
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v.52
no.4
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pp.316-321
/
2008
The hepatoprotection by the methanol extract of Oenanthe javanica DC (water dropwort) (OJME) was investigated in Sprague Dawley rats with inducing liver damage by acetaminophen. After OJME administration for 1 week, the increase of hepatic lipid peroxide level by acetaminophen-induced hepatotoxicity was significantly reduced. In case of phase I microsomal enzyme systems including cytochrome P-450, aminopyrine N-demethylase and aniline hydroxylase, any significant differences between in control and in OJME-pretreated group was observed after acetaminophen treatment. However, the pretreatment of OJME maintained the hepatic glutathione level and the activity of liver cytosolic glutathione S-transferase, which was significantly decreased by the acetaminophen intoxication. Among the glutathione-generating system, glutathione reductase was more responsible for its biosynthesis rather than ${\gamma}-glutamylcystein$ synthetase. OJME itself showed the strong inhibition activity on DPPH radical generation. In conclusion, OJME administration maintains the liver glutathione pool and hepatic glutathione S-transferase activity, in addition with its high anti-oxidative capability, to show hepatoprotective effect from acetaminophen intoxication.
Razis, Ahmad Faizal Abdull;Konsue, Nattaya;Ioannides, Costas
Asian Pacific Journal of Cancer Prevention
/
v.16
no.7
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pp.2679-2683
/
2015
Background: Phenethyl isothiocyanate (PEITC), the most comprehensively studied aromatic isothiocyanate, has been shown to act as an anti-cancer agent mainly through modulation of biotransformation enzymes responsible for metabolizing carcinogens in the human body. Humans are often exposed to carcinogenic factors, some of which through the diet, such as polycyclic aromatic hydrocarbon benzo[a]pyrene via the consumption of over-cooked meats. Inhibition of the enzymes responsible for the bioactivation of this carcinogen, for example CYP1A1, the major enzyme required for polycyclic aromatic hydrocarbons (PAHs) bioactivation, is recognized as a chemoprevention strategy. Objective: To evaluate the inhibitory effects of PEITC against benzo[a]pyrene-induced rise in rat liver CYP1A1 mRNA and apoprotein levels. Materials and Methods: Precision cut rat liver slices were treated with benzo[a]pyrene at 1 and $5{\mu}M$ in the presence of PEITC ($1-25{\mu}M$) for 24 hours, followed by determination of CYP1A1 mRNA and apoprotein levels using quantitative polymerase chain reaction and immunoblotting. Results: Findings revealed that PEITC inhibited benzo[a]pyrene-induced rise in rat liver CYP1A1 mRNA in a dose-dependent manner as well as the apoprotein levels of CYP1A. Conclusions: It was demonstrated that PEITC can directly inhibit the bioactivation of benzo[a]pyrene, indicating chemopreventive potential.
This study is to find out the antioxidative effect and serum lipid composition of wild grape seed powder in vivo. 20 white Sprague Dawley rats of six weeks old were divided into 2 groups and AIN-93 basic diet, high fat and cholesterol were provided. And they were examined to know how wild grape seed powder worked for antioxidative effect and serum lipid composition. For the comparing group, wild grape seed powder consisting 5% of the diet weight was provided and the quantity of protein, fat, carbohydrate, and cellulose was controlled following the analysis of the ingredients. The rats were fed for four weeks with experimental diet. Serum lipid and the antioxidant enzyme activity in blood and liver microsome were measured after 4 weeks of experiment. The results are as follows; There was no difference between the experimental groups in the initial body weight, final body weight, weight gain and FER. Food intake was higher in the group wild grape seed powder was provided than in the control group(p<0.05). Serum total cholesterol in the control group was significantly higher than that in the group wild grape seed powder was provided.(p<0.05). There was no difference serum HDL cholesterol and LDL cholesterol between the groups. Serum triglyceride showed no significant difference between the groups. In blood, glutanthione peroxidase activity was higher in the group supplemented with wild grape seed powder than in the control group. The glutathione reductase activity of blood showed no difference between the groups. In liver, the glutanthione peroxidase activity was higher in the group supplemented with wild grape seed powder than in the control group(p<0.05). Glutathione reductase activity in liver showed no difference in accordance with the supplementation of wild grape seed powder.
Jung, In Ah;Cho, Won Kyoung;Jeon, Yeon Jin;Kim, Shin Hee;Cho, Kyoung Soon;Park, So Hyun;Jung, Min Ho;Suh, Byung-Kyu
Clinical and Experimental Pediatrics
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v.58
no.6
/
pp.234-237
/
2015
Hepatic glycogenosis in type 1 diabetes mellitus (DM) can be caused by poor glycemic control due to insulin deficiency, excessive insulin treatment for diabetic ketoacidosis, or excessive glucose administration to control hypoglycemia. Mauriac syndrome, which is characterized by hepatomegaly due to hepatic glycogenosis, growth retardation, delayed puberty, and Cushingoid features, is a rare diabetic complication. We report a case of hepatic glycogenosis mimicking Mauriac syndrome. A 14-year-old girl with poorly controlled type 1 DM was admitted to The Catholic University of Korea, Seoul St. Mary's Hospital for abdominal pain and distension. Physical examination revealed hepatomegaly and a Cushingoid face. The growth rate of the patient had decreased, and she had not yet experienced menarche. Laboratory findings revealed elevated liver enzyme levels. A liver biopsy confirmed hepatic glycogenosis. Continuous glucose monitoring showed hyperglycemia after meals and frequent hypoglycemia before meals. To control hyperglycemia, we increased insulin dosage by using an insulin pump. In addition, we prescribed uncooked cornstarch to prevent hypoglycemia. After strict blood glucose control, the patient's liver functions and size normalized. The patient subsequently underwent menarche. Hepatic glycogenosis is a complication of type 1 DM that is reversible with appropriate glycemic control.
The present study examined the effects of consumption of Jeju ground water containing vanadium components on oxidative stress in obese (ob/ob) mice. Intake of Jeju ground water decreased the generation of oxidative stress induced-lipid peroxidation in the liver of ob/ob mice It also enhanced the enzymatic antioxidant defense system by increasing the protein expression and activity of superoxide dismutase, catalase, and glutathione peroxidase in liver tissues. Jeju ground water intake also upregulated the intracellular content of reduced glutathione. The induction of antioxidant enzyme expression by consumption of Jeju ground water was mediated by the erythroid transcription factor NF-E2 (Nrf2). Increased nuclear expression of phospho Nrf2 was observed in ob/ob mouse liver cells following ntake of Jeju ground water. These results suggest that consumption of Jeju ground water stimulated the antioxidant defense system in the livers of ob/ob mice via induction of Nrf2.
This study was undertaken to elucidate the effect of DHA-rich fish oil (DHA-rich oil) added to different dietary fats on lipid metabolism. Rats were fed perilla oil, sesame oil and beef tallow with or without DHA-rich oil for 12 weeks. The weight gain was higher in groups with DHA-rich oil than that of groups without DHA-rich oil, with DHA-rich oil, while weight of epididymal fat pad was lower in perilla oil and beef tallow groups with DHA-rich oil. The contents of total lipid and triglyceride in plasma were not affected by dietary fat types, but that of total and HDL cholesterol in plasma were higher in sesame oil group than perilla oil and beef tallow groups without DHA-rich oil. The contents of total lipid, triglyceride, total cholesterol, HDL cholestrol and LDL cholesterol in plasma were decreased by DHL-rich oil addition. The contents of total lipid, total cholesterol and triglyceride in the liver were not affected by dietary fat type. The contents of total cholesterol and triglyceride in the liver were not affected by dietary fat type. The contents of total lipid and TG in liver were not affected by DHA-rich oil addition while hepatic cholesterol increased by DHA-rich oil addition. The activities of glucose 6-phosphate dehydrogenase and malic enzyme were highest in beef tallow group without DHA-rich oil and decreased by DHA-rich oil addition. Peroxisomal ${\beta}$-oxidation had an inverse relationship against the activities of lipogenic enzymes. In conclusion, dietary DHA-rich oil decreased fat accumulation and had hypolipidemic effect, especially in beef tallow group. Also groups with DHA-rich oil showed more hypolipidemic effect than perilla oil group. And DHA-rich oil addition to diets resulted in increasing dietary n-3/n-6 ratio. Therefore increase in n-3/n-6 ratio as well as dietary DHA were considered to be responsible for the hypolipidemic effect resulted from DHA-rich oil addition.
This study was designed to examine the involvement of lead in function of target organ, and the protective effect of selenium in lead-treated guinea pigs for 8 weeks. The effects of exposure to 0.5% lead acetate(lead) and/or 4ppm sodium selenite(selenium) in feed on serveral aspects were evaluated by measuring thyroid stimulating hormone(TSH), triiodothyronine($T_3$), thyroxine($T_4$), serum biochemical activities, organ weights, and serum and organ lead concentrations in growing animals. The many indicators of endocrine function(TSH, $T_3$, and $T_4$ in serum), enzyme and biochemical activities(${\alpha}$-glutamyltranspeptidase, alkaline phosphatase, lactate dehydrogenase, triglyceride, creatinine, $Ca^{2+}$ in serum), and organ weights(kidney, spleen and testis) were correlated with lead exposure or showed significantly different mean values between the exposed and controls. These changes on some aspects were reversed by combination-fed of selenium, but did not statistically significant. The organ(kidney, liver, spleen, testis and brain) and serum lead concentrations of lead-fed group were clearly higher than that of controls. Selenium supplementation resulted in a significant protection against lead accumulation in liver and testis. These results suggest that lead can cause a toxic effect on several organ and that selenium seems to has a protective effect on specific reaction by lead-induced organic function toxicity.
An extract of Allomyrina dichotoma larva (ADL), one of the insects used most frequently in traditional Chinese medicine for the treatment of liver diseases such as hepatocirrhosis and hepatofibrosis, was assessed for antioxidant bioactivity in this study. In the current work, we have investigated the protective effects of ADL extracts on tert-butyl hydroperoxide (t-BHP)-induced hepatotoxicity in cultured hepa1c1c7 cells and in the mouse liver. The treatment of the hepa1c1c7 cells with ADL extracts induced a significant reduction of t-BHP-induced oxidative injuries, as determined by cell cytotoxicity, lipid peroxidation (LPO) and reactive oxygen species contents, in a dose-dependent manner. Moreover, ADL extracts evidenced a protective effect against t-BHPinduced oxidative DNA damage, as revealed by the results of the Comet assay in hepa1c1c7 cells. ADL extracts also protected against hydroxyl radical-induced 2-deoxy-d-ribose degradation by ferric ion-nitrilotriacetic acid and $H_2O_2$. In addition, ADL extracts were shown to be able to quench 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals. Our in vivo study revealed that ADL extracts pretreatment applied prior to t-BHP administration significantly prevented an increase in the serum levels of hepatic enzyme markers and reduced LPO in the mouse liver in a dose-dependent manner. Taken together, these results suggest that the protective effects of ADL extracts against t-BHP-induced hepatotoxicity may be attributable, at least in part, to its ability to scavenge free oxygen radicals, and to protect against DNA damage due to oxidative stress.
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