• The Korean Journal of Food And Nutrition
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• v.25 no.4
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• pp.1016-1022
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• 2012

In order to investigate the effects of 70% EtOH extract obtained from Hovenia dulcis Thunberg on enzymes relating reactive oxygen intermediate, cancer-stricken animals induced by DEN (N,N-diethylnitrosamine) were recovered by administering the extract of Hovenia dulcis Thunberg. It showed that there was no effect on the generation of superoxide radical by the extract of Hovenia dulcis Thunberg. However, considering the increase of the activity of Cu, Zn-SOD and Mn-SOD in the tested animal class, the extract of Hovenia dulcis Thunberg could participate directly in removing of superoxides. The experimented-animals treated with the extract of Hovenia dulcis Thunberg showed an increase in the activity of the enzymes, catalase and glutathione peroxidase, which can eliminate hydrogen peroxide pertained in liver tissue. The extract of Hovenia dulcis Thunberg seemed to have some factors that accelerate the oxidation. Also, the extract of Hovenia dulcis Thunberg showed effects on the enzymes relating to the active oxygen toxicity which could be an indicator of aging and body toxicity.

• Korean Journal of Clinical Laboratory Science
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• v.49 no.3
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• pp.248-255
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• 2017

Increased hepatic enzymes are associated with insulin resistance, metabolic complications, and type 2 diabetes mellitus. Metabolically healthy obese (MHO) phenotype is not accompanied by metabolic complications and maintains insulin sensitivity, despite excessive body fat. The purpose of this study was to evaluate the clinical implications of hepatic enzymes in MHO men. The diagnostic criteria for MHO were based on NCEP-ATP III and obesity in adults was defined using WHO Asian-Pacific criteria. We used the data from 9,683 obese men aged between 20 and 70 years. The subjects were divided into three groups according to the diagnostic criteria: The metabolically healthy non-obese (MHNO, N=2,878), metabolically healthy obese (MHO, N=5,427), and metabolically abnormal obese (MAO, N=1,378). Obesity criteria were classified according to the standards set forth by WHO Asia-Pacific Criteria. AST, ALT, and GGT were significantly lower in the MHO group than in the MAO group (p<0.001, respectively). However, the hepatic enzyme levels were higher in the MHO group than in the MHNO group (p<0.001). Liver enzymes were associated with metabolic syndrome risk factors. Waist circumference, fasting glucose, total cholesterol, triglyceride, and HDL-C were risk factors for metabolic syndrome affecting liver enzymes. In conclusion, hepatic enzymes were found to predict metabolic abnormalities in metabolically healthy obese men.

• The Korea Journal of Herbology
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• v.27 no.2
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• pp.53-59
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• 2012

Objectives : This study was undertaken to investigate the effects of the GGEx18 ethyl acetate fraction (EF) on lipid accumulation and gene expression of fatty acid-oxidizing enzymes using 3T3-L1 adipocytes, C2C12 skeletal muscle cells, and NMu2Li liver cells. Methods : PPAR${\alpha}$, AMPK and UCPs transactivation was examined in NMu2Li hepatocytes, C2C12 myocytes, and 3T3-L1 preadipocytes using transient transfection assays. Results : 1. Compared with control, EF significantly increased the mRNA expression of VLCAD in 3T3-L1 adipocytes. 2. Compared with control, EF (0.1 ${\mu}g/ml$) significantly inhibited lipid accumulation in 3T3-L1 adipocytes. 3. EF significantly increased the mRNA expression of AMPK${\alpha}$1, AMPK${\alpha}$2 and PPAR${\alpha}$ in C2C12 skeletal muscle cells compared with control. 4. EF significantly increased the mRNA expression of genes involved in fatty acid ${\beta}$-oxidation, such as thiolase, MCAD, and CPT-1 in C2C12 skeletal muscle cells compared with control. 5. EF significantly increased the mRNA expression of UCP2 involved in energy expenditure in C2C12 skeletal muscle cells compared with control. 6. Compared with control, EF (10 ${\mu}g/ml$) significantly inhibited lipid accumulation in C2C12 skeletal muscle cells. 7. EF (10 ${\mu}g/ml$) significantly increased the mRNA expression of ACOX, HD, VLCAD and MCAD in NMu2Li liver cells compared with control. Conclusions : These results suggest that EF may prevent obesity by increasing the mRNA expression of mitochondrial fatty acid ${\beta}$-oxidizing enzymes in 3T3-L1 adipocytes, by not only regulating the fatty acid oxidation through activation of AMPK and PPAR${\alpha}$, but also increasing the UCP2 mRNA expression in C2C12 skeletal muscle cells, and by stimulating the mRNA expression of fatty acid-oxidizing enzymes in NMu2Li liver cells.

• Parasites, Hosts and Diseases
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• v.38 no.1
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• pp.45-48
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• 2000

An enzyme analysis of the liver fluke, Clonorchis sinensis from Kimhae, Korea and from Shenyang, China was conducted using a horizontal. starch gel electrophoresis in order to elucidate their genetic relationships. A total of eight enzymes was employed from two different kinds of buffer systems. Two loci from each enzyme of aconitase and esterase (${\alpha}-Na{\;}and{\;}{\beta}-Na$) : and only one locus each from six enzymes, gluucose-6-phosphate dehydrogenase (G6PD), ${\alpha}-glycerophosphate$ dehydrogenase (GPD), 3-hydroxybutyrate dehydrogenase (HBDH), malate dehydrogenase (MDH), phosphoglucose isomerase (PGI), and phosphoglucomutase (PGM) were detected. Most of loci in two populations of C. sinensis showed homozygous monomorphic banding patterns and one of them, GPD was specific as genetic markers between two different populations. However, esterase (${\alpha}-Na$), GPD, HBDH and PGI loci showed polymorphic banding patterns. Two populations of C. sinensis were more closely clustered within the range of genetic identity value of 0.998-1.0. In summarizing the above results, two populations of C. sinensis employed in this study showed mostly monomorphic enzyme protein banding patterns, and genetic differences specific between two populations.

• Journal of Korean Academy of Nursing
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• v.19 no.3
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• pp.299-306
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• 1989

In order to evaluate the effect of fish oil on lipid drogenase(G6PDH), malic enzyme(ME), glucose-6-phosphatase(G6Pase) activities were measured in liver and adipose tissue of rats fed 13 days supplemented fish oil at the level of 10% (W/W). Two other groups of rats were fed 10% soybean oil or lard to compare with the effect of fish oil. In all groups, activities of hepatic G6PDH and ME were depressed from the beginning of feeding. This effect was greatest (50%) in fish oil group. Hepatic G6Pase was highest in rats fed lard. When the level of fish oil was reduced to half, as total fat content was maintained at the level of 10% by complementary lard, lipogenic enzyme depressing effect of fish oil was as significant as shown in 10% fish oil diet. Hepatic G6PDH was depressed significantly(14%) in rats fed fish oil as low as 2％. On the other hand, changes in adipose tissue G6PDH and ME activities were small. Adipose tissue G6Page activity increased slightly in rats fed with increasing fish oil(above 0.5%). It is suggested that fish oil alter, more markedly than either soybean oil or lard, cellular lipid metabolism by reducing activities of hepatic lipogenic enzymes.

• Journal of Nutrition and Health
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• v.34 no.8
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• pp.858-864
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• 2001

The study was designed to observe an antioxidant activities of conjugated linoleic acid(CLA) in rat liver by determining the activities of antioxidative enzymes(superoxide dismutase, glutathione peroxidase, catalase) and the levels of tocopherol and thiobarbituric acid reactive substance(TBARS). Male Sprague Dawley rats at weeks-old were divided into groups according to the types of dietary fat(beef tallow and fish oil) and then each group was subdivided into groups depending on CLA supplement. All rats were fed experimental diet containing 12% total fat including 1% CLA by weight for 30 weeks. CLA supplemented to beef tallow diet did not have significant effect on the level of TBARS and tocopherol. The level of TBARS was significantly increased in fish oil diet(highly unsaturated fat diet), but its level was significantly reduced by increasing SOD and GSH-Px activities when CLA was supplemented to fish oil diet so that CLA showed a sparing action of tocopherol in tissue. CLA did not have significant effect on peroxisomal catalase activities, but its activity was significantly increased when TBARS production was high in the fish oil diet. CLA could be incorporated into phospholipid of microsomal membrane, and interfered the conversions of C18 : 0 into C18 : 1 and C18 : 2 into C20 : 4 in liver. In conclusion, CLA had an antioxidant activities depending on the type of fat in diet. Therefore, it could be recommended to use CLA when highly unsaturated fat was used in meal preparation.

• Journal of Ginseng Research
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• v.8 no.1
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• pp.15-21
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• 1984

It has been known that ethyl acetate fraction and petroleum ether fraction prepared from ginseng are inhibitory to the L5178Y and sarcoma 180 cell at the concentrations o! 0.Imgfml or 0.2mg/ml. The shiny was carried out to examine effects of the two fractions on the activities of RNA polymerase, succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) present in normal rabbit liver. The ethyl acetate fraction did not show any inhibitory effect on the RNA polymerase and SDH activity at the concentrations of 0.Imgfml and 0.2mglml, but inhibited malate dehydrogenase activity by 12.3% and 15.5%, at the same concentrations, respectively. The fraction also inhibited all the three enzymes at higher concentrations tested, but stimulated the succinate dehydrogenase activity at 0.024mg/ml to increase the enzyme activity by 14.6%. The petroleum ether fraction activated the SDH activity by 12.9% and 20.8%, at the concentration of 0.1mg/ml and 0.2mg/ml respectively. But the fraction did not affect the MDH activity at the same concentration. The fraction, however, inhibited the MDH activity and activated the SDH activity by 13.5% and 18.2%, at the concentration of 0.8mg/ml respectively.

• Korean Journal of Pharmacognosy
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• v.34 no.4 s.135
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• pp.297-302
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• 2003

Cnidii Rhizoma water extract (CRW) was tested for liver cancer chemopreventive potential by measuring the inhibition of phase I enzyme and benzo[a]pyrene-DNA adduct formation and induction of phase II detoxification enzymes. There was 17.0% inhibition in the activity of cytochrome P450 1A1 enzyme with the treatment of 150 mg/ml CRW. At concentration of 30 mg/ml CRW, the binding of $[^3H]B[a]P$ metablites to DNA of NCTC-clone 1469 cell was inhibited by 33.3%. CRW was potent inducer of quinone reductase (QR) and glutathione S-transferase (GST) activities in cultured murine hepatoma Hepalc1c7 cells. However, hepatic glutathione (GSH) level was not influenced by CRW. These findings suggest that CRW has chemopreventive potential of liver cancer by inhibiting cytochrome P450 1A1 activity and benzo[a]pyrene-DNA adduct formation and inducing QR and GST activities.

• YAKHAK HOEJI
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• v.44 no.3
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• pp.237-244
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• 2000

Liver isolated from 18 hours fasted rats was subjected to $N_2$hypoxia (for 45 min) followed by reoxygenation (for 30 min). The perfusion medium used was Krebs-Henseleit bicarbonate buffer (pH 7.4, $37^{\circ}C$). Vitamin C (0.5 mM) and trolox C (0.5 mM), soluble vitamin E analog, were added to perfusate. Lactate dehydrogenase (LDH), total glutathione, oxidized glutathione, lipid peroxide and drug-metabolizing enzymes were measured. After hypoxia LDH significantly increased but this increase was attenuated by vitamin C and combination of vitamin C and E. Total glutathione and oxidized glutathione in perfusate markedly increased during hypoxia and this increase was inhibited by vitamins C, E and its combination. Similarly; oxidized glutathione and lipid peroxide in liver tissue increased after hypoxia and reoxygenation and this increase was inhibited by vitamin I and combination of vitamin C and E. Hepatic drug metabolizing function (phase I, II) were suppressed during hypoxia but improved during reoxygenation. While vitamins C and E only increased glucuronidation, the combination of vitamin C and E increased the oxidation, glucuronidation and sulfation. Our findings suggest that vitamins C and E synergistically ameliorates hepatocellular damage as indicated by abnormalities in drug metabolizing function during hypoxia/reoxygenation and that this protection is in major part, caused by decreased oxidative stress.

• Proceedings of the Ginseng society Conference
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• 1987.06a
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• pp.47-58
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• 1987

Ethanol exerts different effects on hepatic cellular metabolism, depending mainly on the duration of its intake. In the presence of ethanol following an acute load, a number of hepatic functions are inhibited, including lipid oxidation and microsomal drug metabolism. In its early stages, chronic ethanol consumption produces adaptive metabolic changes in the endoplasmic reticulum which result in increased metabolism of ethanol and drugs and accelerated lipoprotein production. Prolongation of ethanol intake may result in injurious hepatic lesions such as alcoholic hepatitis and cirrhosis A number of such metabolic effects of ethanol are directly linked to the two major products of its oxidation; hydrogen and acetaldehyde. The excess hydrogen from ethanol unbalances the liver cell's chemistry. In the presence of excess hydrogen ions the process is turned in a different direction. In this study, it was attempted to observe the effect of ginseng saponins on alcohol Oehydrogenase(ADH), aldehyde dehydrogenase(ALDH) and microsomal ethanol oxidizing system(MEOS) in vivo as well as in vitro. Furthermore, the effect of ginseng saponin on the hydrogen balance in the liver and the hepatic cellular distribution of (1-14C) ethanol, its incorporation into acetaldehyde and lipids was also investigated. It seemed that ginseng saponin stimulated the above enzymes and other related enzymes in ethanol metabolism, resulting in a rapid removal of acetaldehyde and excess hydrogen from the animal body,