• Korean Journal of Biological Psychiatry
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• v.5 no.2
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• pp.235-242
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• 1998

Objectives : Alcohol-induced oxidative stress has been known to injure various tissues or organs. This stress is related with free radicals which are produced as the result of long-term alcohol consumption. Malonyldialdehyde(MDA) is produced by the interaction of free radicals and cell membrane lipids, and indicates the degree of lipid peroxidation indirectly. The purpose of this study was to investigate the relationship between red blood cell(RBC) membrane lipid peroxidation by free radicals, and associated hepatic injuries and hematologic changes. Methods : Thirty-three subjects diagnosed as alcohol dependence according to DSM-IV diagnostic criteria were evaluated within 72 hours after discontinuing alcohol drinking. Clinical characteristics were evaluated by CAGE questionnaire and Korean Michigan Alcoholism Screening Test(MAST). RBC membrane MDA level was measured as the marker of RBC membrane lipid peroxidation. Aspartate aminotransferase(AST), alanine aminotransferase(ALT) and gamma-glutamyltransferase(GGT) were used as the biochemical markers of liver damage due to alcohol ingestion. The alcohol-induced hematologic change was assessed by mean corpuscular volume(MCV). Results : The results were as follows. Clinical characteristics were not different between two groups having normal and abnormal levels of AST, ALT, GGT or MCV. The levels of MDA were not correlated with the clinical characteristics and serum levels of AST, ALT and GGT. However, there was a significant correlation between the levels of MDA and the value of MCV(p=0.017). Conclusions : These findings suggest that oxidative stress in alcohol dependence may not be reflected in liver enzyme markers such as AST, ALT and GGT, but may be reflected in MCV.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.6
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• pp.525-530
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• 2013

Multidrug resistance 3 (MDR3) is expressed on the canalicular membrane of the hepatocytes and plays an important role in protecting the liver from bile acids. Altered ABCB4 gene expression can lead to a rare hepatic disease, low phospholipid-associated cholelithiasis (LPAC). In this study, we characterized 3 ABCB4 mutations in LPAC patients using various in vitro assay systems. We first measured the ability of each mutant to transport paclitaxel and then the mechanisms by which these mutations might change MDR3 transport activity were determined using immunoblotting, cell surface protein biotinylation, and immunofluorescence. Through a membrane vesicular transport assay, we observed that the uptake of paclitaxel was significantly reduced in membrane vesicles expressing 2 ABCB4 mutations, F165I and S320F. Both mutants showed significantly decreased total and cell surface MDR3 expression. These data suggest two missense mutations of ABCB4 may alter function of MDR3 and ultimately can be determined as LPAC-causing mutations.

• Applied Microscopy
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• v.26 no.1
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• pp.1-9
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• 1996

This paper aims to probe the effect of SQ in the rat liver which pretreated with CP was examined by transmission electron microscope. In the A group, the difference between the normal and the treated groups were not detected at 24 hours, but the few mitochondria were expanded at the 72 hours. In the B group, the cisternae of rough-surfaced endoplasmic reticulum were partially destructed and attached ribosomes were remarkably decreased at 24 hours. A number of the mitochondria were dilated and increased in number, the filamentous materials also detected at 72 hours. These results suggest that SQ is not only concerned with construction of the membrane of the cell organelles but also decreased the cellular toxicity in the hepatic cells.

• Journal of Korean Biological Nursing Science
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• v.2 no.1
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• pp.49-63
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• 2000

Aflatoxin $B_1(AFB_1)$ is a potent hepatotoxic and hepatocarcinogenic mycotoxin in human beings. It is accumulated in animal tissues and injured cell through variable metabolic pathway. This study was conducted to determine the effect of antioxidant vitamins on liver function enzymes and hepatic damage of $AFB_1$ treated mice. The 6 weeks old male ICR mice were randomly separated 6 groups, vehicle solvent or vitamin C(10 mg/kg/day) and vitamin E(63.8 mg/kg/day) were administered by intraperitoneal(i.p.) injection and 1 hr later, vehicle solution(DMSO) or $AFB_1$(0.4 mg/kg) were injected. The results obtained as follow ; The levels of liver function enzymes such as GOT, GPT, LDH, and alkaline phosphatase, in sera of mice were remarkably elevated by treatment with $AFB_1$ only. However, those enzymes were significantly alleviated by co-treatment with antioxidant vitamins(p<0.01). Especially the levels of LDH and ALK phosphatase were similar to those of control groups(p<0.01). The transmission electron microscopy(TEM) image of intracellular microrganelles on the liver cell of mice was also degenerated extremely by treatment with $AFB_1$, but vitamin C and vitamin E gave good effects on cellular deformation. The intracellular microrganelles such as mitochondria, endoplasmic reticulum, nucleus and nucleic membrane were nearly disappeared the cellular deformation by antioxidant vitamins co-administration. With above results, we could estimated that antioxidant vitamins blocked AFB1 induced hepatic cell damage.

• Biomedical Science Letters
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• v.13 no.2
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• pp.135-140
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• 2007

The possible mechanism of decreased catechol-O-methyltransferase (COMT) activity in cholestatic rat liver was studied. Hepatic and serum COMT activities were determined from the experimental rats with choledocho-caval shunt (CCS). The Michaelis-Menten constants in this hepatic enzyme was also measured. The activities of cytosolic, mitochondrial and mircosomal COMT as well as their $V_{max}$ values were found to be decreased significantly in CCS plus taurocholic acid (TCA) injected group than in the control group, such as CCS alone groups. However, their $K_m$ values in the experimental groups did not vary. Seru4m COMT activity increased slightly in the CCS plus TCA injerted group than in the control group. The above results suggest that TCA represses biosynthesis of the COMT in the liver, The elevated activity of the serum COMT is believed to be caused by the increment of membrane permeability of hepatocytes upon TCA mediated liver cell necrosis.

• Korean Journal of Veterinary Research
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• v.16 no.2
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• pp.141-150
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• 1976

In order to know the morphological changes of liver in nitrate poisoning, the ultrastructural studies were carried out on the rabbit liver after potassium nitrate was administered orally at lethal dose, in single treatment, as acute case and at two different levels. 1.0 and 0.5g/kg of body weight daily for 43 and 60 days as chronic case, respectively, The results were summarized as followings: 1. In the hepatic cells of acute case, mitochondria were swollen, disappearance of cristae and variable in shape. Dilatation of rough endoplasmic reticulum and vacuoles containing degenerated cell organells were observed. Glyogen particles were decreased in number. Degenerated Kupffer cells were often seen in acute case. 2. In the hepatic cells of chronic case, there were increase of smooth endoplasmic reticulum, marked enlargement of rough endcplasmic reticulum, detachment of membrane bound ribosome and some rough endoplasmic reticulum changed into smooth endoplasmic reticulum. Secondary lysosome, abundant glycogen paricles and myelin-figure structures were also observed in the cytoplasm of the hepatic cells. The endothelial cells were proliferated in the area of the necrotic cells.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.13-21
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• 1989

The present study was designed to investigate i) the action of various nucleotides on membrane permeability of rat red blood cell and hepatocyte for $Na^{+}$ and $Rb^{+}$ ii) the characteristics of purinoceptors on these cell membranes. Blood from Sprague-Dawley rats was obtained by carotid arterial cannulation. Red blood cells were then washed 3 times with saline at $4{\circ}C$. Hepatic parenchymal cells were isolated from rat livers by using a modification of the Berry and Friend (1969) method. For the $Na^{+}$ influx studies, isolated RBC and hepatocyte were incubated in incubation medium containing $^{22}Na^{+}0.2\;{\mu}Ci/ml$ at $37^{\circ}C$. After various time intervals samples were removed from the incubation flask and washed out 3 times with ice-cold washing solutions. Cells were destroyed by adding Triton X-100 and TCA solution. After centrifugation, the supernatants were assayed for $^{22}Na^{+}$ by gamma counter. $^{86}Rb^{+}$ was used to simulate $K^{+}$ in these $K^{+}efflux$ studies. Isolated hepatocytes were incubated for 60 min in the loading solution containing $^{86}Rb^{+}\;10\;{\mu}Ci/ml$ at $37^{\circ}C$. After loading, the cells washed out 3 times by centrifugation with washing solution. The cells were incubated in buffer solution at $37^{\circ}C$. At intervals thereafter, samples were removed and centrifuged. The supernatants were analyzed for $^{86}Rb^{+}$ by liquid scintillation counter. The main results of the experiments were: 1) ATP and ATPP increased in both $^{22}Na^{+}$ influx and $^{86}Rb^{+}$ efflux in the red blood cell. Although ADP showed a tendency to increase in RBC membrane permeability for $^{22}Na^{+}$ and $^{86}Rb^{+}$, the changes were not significantly different from the control. 2) The Significant changes in $^{22}Na^{+}$ and $^{86}Rb^{+}$ flux by ATP were also demonstrated in hepatocyte. ATPP and ADP showed a tendency to increase in hepatocyte membrane permeability for both ions. 3) Other nucleoside triphosphates-ITP, GTP and CTP-did not change in membrane permeability for $^{22}Na^{+}$ and $^{86}Rb^{+}$ in RBC and hepatocyte. In conclusion, not only ATP but also ATPP activate purinoceptors and change in membrane permeability for $Na^{+}$ and $K^{+}$. In order to activate purinoceptors on the cell membrane, the nucleotides have to possess intact adenine moiety and three phosphates or more in its molecule.

• Journal of Acupuncture Research
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• v.20 no.1
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• pp.159-176
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• 2003

Objective : The purpose of this study is to investigate the antioxidant activities of Alismatis Rhizoma herbal acupuncture by experimental methods. Methods : For this purpose, first, we put an emphasis in the control of enzymes of the antioxidant system in various changes inside the cell; these changes caused by the proliferation or the activation of the cell which were brought about by the handling of PMA and $TNF-{\alpha}$ into the THP-1 monocyte cell of the body each other. After that, we caused the acute oxidant symptom by the injection of AAPH into the mouse' abdominal cavity, and then applied the herbal acupuncture on S36 point(足三里), and finally, we measured the change of blood ingredient and the resistance against the activated oxygen of the red blood cell membrane, MDA, SOD, and catalase. Results : In vitro the revelation of $IL-1{\beta}$, IL-8, $TNF-{\alpha}$, NOS II and IL-6 were decreased and the revelation of IL-10, $TGF-{\beta}$, GM-CSFIL-12, GM-CSF and SOD were increased. The DNA-binding of $NF-{\kappa}B$ and AP-1 were activated and the formation of ROS in the THP-1 cell line was decreased. In vivo $IL-1{\beta}$ among producing the cytokine inside the plasma was meaningfully dwindled and the $INF-{\gamma}$ was meaningfully increased. The resistance of red blood cell membrane against the activated oxygen was meaningfully increased and the MDA formation was meaningfully dwindled, In the activation of hepatic antioxidase, the SOD was meaningfully increased. Conclusion : Alismatis Rhizoma herbal acupuncture by experimental methods has effected on the antioxidant activities.

• Journal of Nutrition and Health
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• v.33 no.2
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• pp.124-133
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• 2000

This study evaluated the effects of chronic ethanol consumption and/or taurine supplementation on hepatic total, phospholipid fatty acid composition and the metabolism of rats fed one of three purified liquid diets for 8 weeks. the rats followed either the control diet (CD, ethanol-free and taurine-free diet); ethanol diet (ED, CD+ 50g ethanol/L) or ethanol-taurine diet (ETD, ED+3.75g taurne/L). Chronic ethanol consumption and/or dietary taurine supplementation were associated with altered hepatic total and phospholipid fatty acid composition. compared to the values for the control rats, ED or ETD significantly decreased the percentage of total monounsaturated fatty acids ($\Sigma$MUFA), and increased the percentage of total polyunsaturated fatty acids ($\Sigma$PUFA) of hepatic total lipids(p〈0.01). Percentages of 14:0(P〈0.01) and 16:0(p〈0.001) were sigificantly lower, and those of 18:0(p〈0.01), 20:0(p〈0.001), 20:3$\omega$6(p〈0.01) and 22:4$\omega$6(p〈0.01) in hepatic total fatty acid compositions were oserved in rats fed ETD versus those fed ED or ETD. No significant differences in hepatic total fatty acid compositions were observed in rats fed ETD versus those fed ED. Percentages of 24:0(p〈0.01), 16:1(p〈0.05), 20:1(p〈0.01), 18:2$\omega$6(p〈0.01) and 18:3$\omega$3(p〈0.05) in hepati phospholipids were significantly higher, and those of 14:0(p〈0.01), 16:0(p〈0.001), 20:3$\omega$3(p〈0.05) in hepatic phospholipids were significantly higher, and those of 14:0(p〈0.01), 16:0(p〈0.001), 20:3$\omega$3(p〈0.001), 22:6$\omega$3(p〈0.001) and $\Sigma$$\omega$3(P〈0.001) were significantly lower in rats fed ED or ETD compared to the values for the control rats. The Δ5 desaturation index(20:3$\omega$6⇒20:4$\omega$6) and elongation index (20:5$\omega$3⇒22:5$\omega$3) of hepatic phospholipid index (20:3$\omega$6⇒20:4$\omega$6) and decreased Δ4 desaturation index (22:5$\omega$3⇒22:6$\omega$3) compared to the values for the ED rats. These changes in hepatic fatty acid composition induced by chronic ethanol consumption and/or taurine supplementation might be associated with the modulations of physical properties of the hepatic cell membrane and its sensitivity to peroxidation damage.

• Biomedical Science Letters
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• v.12 no.2
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• pp.91-97
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• 2006

The effects of intravenous administration of high concentration of taurocholic acid (TCA) on monoamine oxidase (MAO) A and B activities in rat liver mitochondria and microsomes were studied. These liver subcellular organelles and serum MAO activities were determined from the experimental rats with choledocho-caval shunt (CCS). The Michaelis-Menten constants in these hepatic enzymes were also measured. The activities of mitochondrial MAO A and B, and microsomal MAO B as well as their $V_{max}$ values were found to be decreased significantly in CCS plus TCA injected group then in the control group, such as CCS alone groups. However their $K_m$ values in the experimental groups did not vary. MAO of serum appeared in the CCS plus TCA injected groups only. The above results suggest that TCA represses biosynthesis of the MAO in the liver. The MAO of serum is believed to be caused by the increment of membrane permeability of hepatocytes upon TCA mediated liver cell necrosis.