• Toxicological Research
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• v.13 no.3
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• pp.183-186
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• 1997

Acute toxicity of pectenotoxin 2 (PTX2) was examined in mice. Treatment of mice with a toxic dose of PTX2 resulted in clinical signs such as ataxia, cyanosis and an abrupt decrease in body temperature. Histopathological studies revealed that the liver is the major target organ for PTX2. Activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and sorbitol dehydrogenase (SDH) were significantly elevated by PTX2 administration. Glucose-6-phosphatase activities were not changed by the treatment. The PTX2 treatment decreased relative liver weight without changing the body weight. The effect of PTX2 on hepatic drug metabolizing enzyme system was determined. An ip dose of PTX2 (200 $\mu$g/kg) induced a significant decrease in the hepatic microsomal protein content. Cytochrome P-450 content, cytochrome b$_5$ content, NADPH cytochrome c reductase, aminopyrine N-demethylase activities, or hepatic glutathione content were not altered by PTX2 treatment.

• Journal of Environmental Health Sciences
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• v.19 no.3
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• pp.58-63
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• 1993

In order to elucidate the alteration of drug-metabolizing enzymes and mechanism in the animal with hepatic injury and ketosis, the regulation of P450IIE was studied in the rats with heaptic injury caused by CCl$_4$ and with ketosis caused by streptozotocin and high-fat diet. P450IIE expression in liver was examined by the combination of enzyme activities, Western immunoblot, and mRNA Northern blot analyses using specific polyclonal antibody and cDNA probe for P450IIE. Enzyme activity and amounts of immunoreactive P450IIE were rapidly decreased in a time-dependent manner after a single dose of CCl$_4$ . However, the decreases in P450IIE enzyme activity and immunoreactive protein by CCl$_4$ were not accompanied by a decline in its mRNA level. The data thus suggested a post-translational reduction of P450IIE by CCl$_4$. The enzyme activities (aniline hydroxylase) in hepatic microsomes were elevated about 2-3-fold by streptozotocin and feeding with a high fat diet. This increases in enzyme activities were also accompanied by 3-fold increases in immunoreactive P450IIE protein and its mRNA. Our data thus indicated that P450IIE induction during the ketosis appears to be due to pretranslational activation.

• Journal of Environmental Health Sciences
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• v.28 no.2
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• pp.81-88
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• 2002

Effect of cyclohexanone treatment on the activities oxygen free radical and cyclohexanone metabolizing enzyme in acute liver damaged rats, was investigated. Acute liver damage was induced in rats with pretreatment of 50% $CCl_4$ in olive oil(0.1ml/100g body wt) intraperitoneally 3 times every other day. Cyclohexanone(1.56g/kg body wt, i.p.) was administered to the animals 24 hours after the last Pretreatment of CC1$_4$. Rats were sacrificed at 4 hours after injection of cyclohexanone. On the basis of liver weight/body weight(％), serum levels alanine aminotransferase activity and hepatic protein content, cyclohexanone treatment to acute liver damaged animals led to the more enhanced liver damage. On the other hand, injection of cyclohexanone to the rats led to the increased activities of hepatic cytochrome P-450 dependent aniline hydroxylase and xanthine oxidase. Furthermore, by treatment of cyclohexanone to the acute liver damaged rats hepatic xanthine oxidase activity was more increased than the $CCl_4$ treated rats. In case of oxygen free radical scavenging system, the hepatic glutathione content and the activities of hepatic glutathione S-transferase, catalase, superoxide dismutase were generally increased by injection of cyclohexanone to rats, and the hepatic glutathione content, catalase and alcohol dehydrogenase activities were more decreased in liver damaged rats by the treatment of cyclohexanone. In conclusion, the cyclohexanone treatment to acute liver damaged rats led to enhancement of liver damage that may be due to oxygen free radical together with cyclohexanone.

• Nutritional Sciences
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• v.9 no.1
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• pp.14-19
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• 2006

Breast cancer may be the consequence of free radical damage, which is partially caused by the excessive intake of dietary fat and imbalances in antioxidant scavenger system;. In this experiment, we examined! the effects of dietary peroxidizability index (PI) values on hepatic thiobmbituric acid reaction substances (TBARS) and antioxidant enzyme activities in rats treated with 7,12-dimethylbenz[$\alpha$]anthracene (DMBA). Female Sprague-Dawley rats were used and 7,12-DMBA (20 mg/kg body weight) was gastrically intubated at seven weeks of age in order to induce mammary tumors (MT). The levels of dietary PI were 36, 81, 126 and 217 (LPI, MLPI, MHPI and HPI), while dietary polyunsaturated/saturated fatty acids ratio was maintained at the same level (1.0). Fat used in the experiment was mixed with soybean oil, com oil, palm oil, perilla oil, sesame oil, fish oil, and beef tallow. Experimental diets were given for the following 20 weeks. We measured tumor numbers and weights, and then assayed the hepatic TBARS levels and antioxidant enzyme activities such as superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione-S-transferase (GST) and glutathione reductase (GR). The incidence of Mr was the lowest in the MHPI group. The hepatic TBARS level was significantly raised with increasing dietary PI value. The hepatic SOD and GR activities were differed significantly by dietary PI value. The hepatic SOD activity was negatively correlated with dietary PI value and GR activity was the highest in the rats fed the MHPI diet. When the dietary P/S ratio is kept at 1.0, adequate dietary PI value (PI value of 126) may reduce the incidence and growth of Mr, but this benefit may be lost with higher dietary PI value. These results suggest that the awareness of dietary PI values may help to decrease breast cancer incidence and growth.

• Korean Journal of Environmental Biology
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• v.22 no.4
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• pp.559-564
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• 2004

The effects of intra-peritoneal injection of inorganic mercury on haemato-logical parameters and hepatic oxidative stress enzyme activities were studied in common carp, Cyprinus carpio. The fish were injected thrice intra-peritoneally with mercuric chloride TEX>$(5,\;10mg\;Hg\;kg\;b.W.^{-1})$. After exposure of three different mercury concentrations a physiological stress response was exerted on C. carpio by causing changes in the blood status such as erythropenia in blood and oxidative stress in liver. Red blood cell counts, hemoglobin concentration and hematocrit level were reduced in most cases by inorganic mercury. Remarkable low level of serum chloride, calcium and osmolality were also observed in the mercury- exposed fish. However, serum magnesium and phosphate were not altered by exposure to mercury. An increased activity of hepatic glutathione peroxidase was observed in the lowest treatment group of carp $(1mg\;Hg\;mg\;b.w.^{-1})$, hence, hepatic catalase and glutathione peroxidase of carp exposed to higher concentration of mercury $(5,\;10mg\;Hg\;kg\;b.W.^{-1})$ showed significant reduction in such activities.

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.1
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• pp.149-156
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• 1998

The purpose of this study was to investigate the effects of vitamin E supplementation on the activities of antioxidative enzymes in liver of KK mice of various ages and various duration of diabetes. Diabetes was induced by feeding high fat diet containing 20% corn oil(wt/wt). Weaned KK mice were fed high fat diet containing 51 IU or 2080 IU vitamin E per kg diet. Animals were sacrificed at 4, 6, and 9 months of age. In nondiabetic group, we found the decrease of antionxidative enzyme activities with aging. In diabetic group, antioxidative enzyme activities were decreased, and the change of hepatic vitamin E was related to glutathione peroxidase activity (r=0.71, p<0.001). Treatment with vitamin E did not modify the level of fasting blood glucose. However, it was observered that glutathione reductase and glutathione peroxidase activities as well as hepatic glutathione levels were increased by vitamie E supplementation, whereas catalase activity did not changed. The present result suggest that high vitamin E supplementation protects against lipid peroxidative damage in diabetic KK mice.

• Preventive Nutrition and Food Science
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• v.11 no.4
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• pp.289-297
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• 2006

This study examined the effect of hesperidin supplementation with an ethanol diet on lipid and antioxidant metabolism in rats. Male Sprague-Dawley rats were divided into two groups (n=10), and were assigned to one of two dietary categories: $E_8$, ethanol diet (50 g/L) for 8 wks; $E_8H_4$, ethanol diet for the first 4 wks and hesperidin (0.02%, w/w) supplemented ethanol diet for the last 4 wks. The plasma and hepatic lipids, hepatic cholesterol regulating enzyme activity, hepatic antioxidant enzyme activity and lipid peroxidation were determined. Supplementation with hesperidin for the last 4 wks during the 8 wks period of the ethanol diet, significantly increased the ADH activity. In conjunction with the chronic administration of ethanol, hesperidin supplementation resulted in a significant decrease in the hepatic cholesterol and triglyceride concentrations compared to the $E_8$ group. The hepatic HMG-CoA reductase and ACAT activities were significantly lower in the hesperidin-supplemented group. When comparing hepatic antioxidant enzyme activities, SOD, GSH-Px, and G6PD activities and GSH level were significantly higher in the $E_8H_4$ group than in the E8 group. Plasma TBARS levels were significantly lower in rats fed ethanol with hesperidin compared to the rats fed only ethanol; however, the hepatic TBARS levels were not significantly different between the groups. Accordingly, the additional hesperidin supplement with an ethanol diet might be effective for improving the hepatic lipid metabolism and antioxidant defense system.

• 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.40 no.8
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• pp.693-700
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• 2007

This study was performed to investigate the effects of genistein, a kind of soy isoflavones, on fatty liver and lipid metabolism in rats fed high fat diet. Twenty four male Sprague-Dawley rats were divided into four groups by dietary fat and genistein contents then raised for six weeks. The rats(n=6/group) were fed normal fat diet(NOR), high fat diet (HF), high fat with 0.1% genistein(HF+0.1%G) or high fat with 0.2% genistein(HF+0.2%G). Hepatic total lipid, triglyceride, total cholesterol and Serum GPT, as a marker for fatty liver, were significantly increased by high fat diet. Also, serum total lipid, triglyceride, total cholesterol, glucose and insulin concentration, hepatic lipogenic enzyme (fatty acid synthase and malic enzyme) activities were significantly increased by high fat diet. However, hepatic total lipid, triglyceride, total cholesterol and Serum GPT were significantly decreased by genistein intake. Also, genistein supplementation decreased serum total lipid, triglyceride, glucose and insulin concentration, hepatic lipogenic enzyme (fatty acid synthase and malic enzyme) activities. There were no differences by genistein level except for serum insulin. These results suggest that fatty liver induced by high fat diet was caused by increased serum lipid profiles and hepatic lipogenesis, whereas, genistein may be useful in inhibiting of fatty liver by reducing serum lipid profiles and hepatic lipogenesis.

• Journal of Environmental Health Sciences
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• v.27 no.2
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• pp.10-16
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• 2001

To evaluate an effect of circadian variation on the xylene metabolizing enzyme activities, 50% m-xylene in olive oil(0.25 $m\ell$/100g body weight) was intraperitoneally administered to the rats every other day for 6 days both in the night; 24:00 and the day; 12:00. Then animals were sacrigiced at 8hr after last injection of m-xylene. Hepatic microsomal cytochrome p450 contents were more increased both in control and xylene treated rats of night phase than those of day phase. But the activity of hepatic alcohol dehydrogenase(ADH) in control of night phase showed the similar value with that in those of day phase and xylene treated rats of day phase showed an increasing tendency of hepatic ADH activity as those of night phase showing similar activity. Furthermore, control rats of night phase than those of day phase. And by xylene treatment, enzyme activities of rats of day phase were higher tendency in rats of control but those of night phase were somewhat inhibited. Besides, xylene-treated animals of night phase showed increasing tendency of urinary methylhippuric acid concentration compared with those of day phase. On the other hand, liver weight per body weight(%), hepatic lipid peroxide content and serum xanthine oxidase activity were higher in night phase. And the activities of hepatic oxygen free radical metabolizing enzymes such as xanthine oxidase, gluthathione S-transferase, and xylene-treated rats of night phase than those of day phase. In conclusion, it can be hypothesized on the basis of the results that the accumulation rate of m-xylene intermediate metabolite, i.e. m-methylbenzaldehyde in liver tissus may be higher in night phase than in day phase and it may be responsible for higher liver toxicity in bight phase than in day phase.