• Toxicological Research
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• v.13 no.4
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• pp.377-383
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• 1997

To investigate the circadian variation in the bromobenzene metabolism, bromobenzene(400 mg/kg 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. Each group of animals was sacrificed at 8hr after last injection of bromobenzene. The contents of hepatic CYP were more increased in control rats of night phase than those of day phase but in case of bromobenzene treatment there were no differences in hepatic CYP between rats of the night phase and those of day phase and the injection of prednisolon inhibited the hepatic CYP content in rats. Furthermore, the decreasing rate of hepatic glutathione contents to the control was higher in rats of day phase than those of night phase by the bromobenzene treatment. And the hepatic glutathione S-transferase activities were increased both in control and bromobenzene treated rats of the night phase than those of day phase. On the other hand, liver weight per body weight(%), hepatic lipid peroxide content, serum levels of alanine aminotransferase were more increased both in bromobenzene-treated and control rats of the night phase than those in the day phase. These results indicate that the rats of night phase may induce more accelerated formation of bromobenzene 3,4-oxide from bromobezene than those of day phase in rats.

• Journal of Nutrition and Health
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• v.35 no.6
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• pp.643-649
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• 2002

This study was done to investigate effects of ${\gamma}$-irradiated pork feeding on the formation of glutathione S-transferase placental form positive (GST-P$^{+}$) foci, lipid peroxidation, cytochrome P450 system and microsomal glucose 6-phosphatase activity in diethylnitrosamine (DEN)-initiated rat hepatocarcinogenesis. Weaning Sprague-Dawley male rats were fed the diet containing ${\gamma}$-irradiated ground pork at the dose of 0, 3, 10, 30 kGy as a 20％ of protein source for 8 weeks. One week after feeding, rats were intraperitoneally injected twice with a dose of DEN (50 mg/kg BW). As a promote.,0.05％phenobarbital was fed in drinking water from one week after DEN treatment until the end of experiment. At the end of 8th week, rats were sacrificed and hepatic GST-P$^{+}$ foci, microsomal malondialdehyde (MDA) and conjugated diene contents were determined. In addition, cytochrome P450 content and the activities of NADPH cytochrome P450 reductase and glucose 6-phosphatase were also measured. There was no significant effect by gamma irradiation on microsomal MDA content, conjugated diene, cytochrome P450 content and activities of NADPH cytochrome P450 reductase and glucose 6-phosphatase. However with DEN treatment, microsomal MDA content showed a increasing tendency. Cytochrome P450 content was also significantly increased while microsomal glucose 6-phophatase activity was significantly decreased with DEN treatment. However the activity of NADPH cytochrome P450 reductase was not affected. An interesting finding in this study was that the number and area of hepatic GST-P$^{+}$ foci of rats fed gamma irradiated pork were tended to be decreased by high dose of irradiation, but were not significantly different. These results might imply that the consumption of low dose of gamma irradiated pork does not affect the formation of hepatic GST-P$^{+}$ foci and lipid peroxide and membrane stability.ability.

• Journal of the Korean Society of Food Science and Nutrition
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• v.17 no.4
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• pp.376-383
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• 1988

The effect of dietary methionine level on lipid peroxidation of rats was studied. Rats were fed vitamin E- selenium- deficient diet or diet supplemented with various levels (0.3, 0.6, 0.9%) of methionine. In rat fed MF diet, body weight gain and feed efficiency ratio were decreased compared with those of control rats, but reversed by supplementation with 0.3 and 0.6% methionine. Lipid peroxide levels in plasma and hepatic mitochondrial fraction of MF group rats were significantly higher than those of control rats. However, supplementation with 0.6% methionine modified this increment. GSH-Px activity was decrased to varying degrees in erythrocyte and hepatic mitochondrial fraction from rats fed MF diet. Methionine supplementation did not affect induction of this enzyme activity. Examination of hepatocytes by electronmicroscopy showed that Influence of vitamin E, selenium, and methionine deficiency was mainly characterized by lipid droplets, swollen mitochondria and microvilli destruction. Supplementation with various levels of dietary methionine modified these changes to some extent. The results of this experiment indicated that MF diet causes significant change in lipid peroxide level, GSH-Px activity and morphology of rats which these changes may lessen by supplementation with 0.6% methionine.

• Herbal Formula Science
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• v.10 no.2
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• pp.127-141
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• 2002

Objectives: Haeganjeon(HGJ) has been used for the treatment of liver disease in traditional medicine. The present study was carried out to evaluate the antioxidant and protective effects of HGJ extract on oxidative damage of hepatocytes by tert-butyl hydroperoxide(t-BHP). Methods: In the linoleic acid water-alcohol system, the levels of lipid peroxide(LPO) were determined by TBA method. The scavenging effect of HGJ on ${\alpha},{\alpha}-diphenyl-{\beta}-picrylhydrazyl$(DPPH) radical was determined according to the method of Hatano. In the Fenton system(ferrous ion reaction with hydrogen peroxide), the levels of hydroxyl radical induced LPO in rat liver homogenate were determined according to the method of TBA. Inhibitory effect of HGJ on superoxide generation was measured by xanthine-xanthine oxidase system. In order to evaluate antioxidative activity of HGJ in the liver cell, cultured normal rat liver cells(Ac2F) were prepared and incubated with or without HGJ. After 18hr, cells placed in DMEM medium without serum, and then incubated with 1mM tert-butyl hydroperoxide(t-BHP) for 2hrs. Viable cells were detected by MTT assay. Conclusions: In the linoleic acid autoxidation system, HGJ extract significantly inhibited the time course of the lipid peroxidation. These effects were similar to those of BHA HGJ extracts showed about 70% scavenging effect on DPPH radical. And HGJ extract inhibited the lipid peroxide formation in rat liver homogenate induced by hydroxyl radical derived from Fenton system. In addition, HGJ extract protected the cell death induced by t-BHP and significantly increased cell viability in the normal rat liver cell. These result indicated that HGJ extract might playa protective role against oxidative hepatic cell injury by means of free radical scavenger.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.4
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• pp.901-906
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• 1999

This study was designed to investigate the effect of Pueraria radix extract on lipid peroxidation in ethanol administered rats. Male sprague dawley rats were given 25% ethanol(2.5g per Kg body weight; E), 10% pueraria radix extract(CP), 25% ethanol and 10% pueraria radix extract(EP). The activity of hepatic superoxide dismutase was increased by ethanol and was lower in the EP group than in the E group. Hepatic catalase activity was increased by ethanol, but decreased by Pueraria radix extract. E group rats had significantly higher liver glutathione peroxidase activity. Activity of hepatic glutathione S transferase was higher in the CP group than in the other groups. No significant dif ferences was found in liver glutathione and lipid peroxide contents between control and EP group. These data indicate that the peroxidative damage associated with chronic ethanol consumption might be decreased by Pueraria radix extract.

• Journal of the East Asian Society of Dietary Life
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• v.5 no.3
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• pp.215-221
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• 1995

This study was undertaken to investigate the effect of Taraxacum herba extract on the hepatic xanthine oxidase activity as a oxygen free radical generating enzyme in vitro and in vivo. It was observed that partial purified hepatic xanthine oxidase (type O) activity was strongly inhibited by the addition of Taraxacum herba n-butanol extract in vitro. The Km value of xanthine oxidase without affecting the Vmax value for xanthine was significantly increased by the addition of ta-dase (type O) activity was significantly inhibited by the treatment of Taraxacum gerba n-butanol ex-tract for 5days(over 40mg/kg, i.p), whereas, xanthine oxidase (type D) activity was not changed by the injection of Taracacum herba n-butanol extract. Meanwhile, liver weight / body weight(%), serum alanine aminotransferase activity and hepatic lipid peroxide content in Taraxacum herba n-buta-nol extract-treated rat were not changed. These findings led us to conclude that Taraxacum herba n-butanol extract may regulate the hepatic xanthine oxidase type O activity to prevent toxic effect of oxidative stress by the oxygen free radicals.

• Journal of Nutrition and Health
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• v.32 no.3
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• pp.221-229
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• 1999

Certain indigestible oligosaccharides may benefit gastrointestinal tract via fermentation and proliferation of desirable bacterial species. The purose of this study was to elucidate the effect of selected oligosaccharides, such as fructooligosaccharides(FOS), soybean oliosaccharides(SOE), and highly concentrated branched oligosaccharides(HiBOS), on fecal micorflora proliferation, lipid concentration, lipid peroxide formation and antioxidant enzymes acitivies in plasma and liver of the rats. Thirty two male Sprague-Dawley rats were randomly assigned to one of four treatments ; 1) control diet(AIN-93G diet); 2) control diet +5% FOS ; 3) control diet + 5% SOE ; 4) control diet + 5% HiBOS. The duration of the study was 4 weeks. Fecal bifidobacteria concentration were significantly higher (p<0.05) in the HiBOS group compared with the control after 4 weeks of dietary treatment. FOS and SOE groups also had higher fecal bifidobacteria levels than control, but statistical significance was not found. The concentration of plasma total lipid was decreased by oligosaccharide consumption, especially in HiBOS group(p<0.05). The concentration of plasma total triglyceride was significantly lower in all of the oligosaccharide containing groups compared with the control(p<0.05). The plasma total cholesterol concentration tended to be lower in the oligosaccharide consuming groups than control. The concentrations of hepatic total lipid, triglyceride and total cholesterol were not affected by consumption of oligosaccharides. Thiobarbituric acid reactive substance(TBARS) concentrations and antioxidant enzyme activities in plasma and liver were not affected much by experimental diets. There results suggest that dietary oligosaccharides may be beneficial for increasing intestinal bifidobacteria and lowering plasma lipid levels.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.1
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• pp.81-86
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• 2002

The present study was conducted to investigate the effect of dietary supplementation of vitamin A or $\beta$-carotene on oxidative damage induced by acute ethanol administration. Sprague-Dawley rats were fed on the experimental diets supplemented with retinyl acetate (2.86 mg/kg diet) or $\beta$-carotene (15.2 mg/kg diet) for 5 weeks. After fed the diet, rats were administered 20% ethanol solution (3g/kg B.W.) acutely. Lipid peroxide values in hepatic tissue, hepatic antioxidative enzyme activities and contents of antioxidative nutrient such as vitamins A and E in serum and hepatic tissue were measured. Hepatic level of malondialdehyde decreased in $\beta$-carotene group compared to the control group. However, there was no significant difference between retinal acetate and $\beta$-carotene groups. Superoxide dismutase activity was higher in retinal acetate group than in the control group. Hepatic glutathione-S-transferase activity of retinal acetate and $\beta$-carotene groups significantly decreased as compared with that of control group. The hepatic content of retinol increased in retinal acetate and $\beta$-carotene groups, especially, in retinyl acetate group. But there was no significant difference in serum content of retinol among the groups. Hepatic content of $\alpha$-tocopherol was significantly increased in retinyl acetate and $\beta$-carotene groups. In conclusion, acute ethanol administration might induce lipid peroxidation, and the dietary supplementation of retinyl acetate or $\beta$-carotene improve partly the antioxidative system through activation of superoxide dismutase and retention of hepatic $\alpha$-tocopherol in ethanol-treated rats.

• Preventive Nutrition and Food Science
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• v.16 no.2
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• pp.95-103
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• 2011

This study was performed to investigate the antioxidant mechanism of tomato wine with varying lycopene content in rats fed a high fat diet (HFD). Male Sprague-Dawley rats were randomly divided into five groups (n=10 per group) and fed an HFD (35% of total energy from fat) plus ethanol (7.2% of total energy from alcohol), tomato wine with varying lycopene content (0.425 mg%, 1.140 mg% or 2.045 mg% lycopene) or an isocaloric control diet for 6 weeks. Mice fed HFD plus ethanol significantly increased erythrocyte hydrogen peroxide and thiobarbituric acid reactive substances (TBARS) levels with increases in activities of erythrocyte antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) compared to pair-fed rats. Supplementation of tomato wine with varying lycopene content decreased ethanol-mediated increases of erythrocyte lipid peroxidation and antioxidant enzyme activities in HFD-fed rats, and tomato wine with higher lycopene appeared to be more effective. Tomato wine also dose-dependently lowered TBARS levels with decreased pro-oxidant enzyme, xanthine oxidase (XOD) activity in plasma of HFD-fed rats. In contrast to erythrocytes, the inhibitory effects of tomato wine on hepatic lipid peroxidation were linked to increased hepatic antioxidant enzymes (SOD and CAT) and alcohol metabolizing enzyme (alcohol dehydrogenase and aldehyde dehydrogenase) activities. There were no significant differences in hepatic XOD and cytochrome P450-2E1 activities among the groups. Together, our data suggest that tomato wine fortified with lycopene has the potential to protect against ethanol-induced oxidative stress via regulation of antioxidant or pro-oxidant enzymes and alcohol metabolizing enzyme activities in plasma, erythrocyte and liver.

• Nutrition Research and Practice
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• v.10 no.4
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• pp.386-392
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• 2016

BACKGROUND/OBJECTIVES: Changes in nutritional status during gestation and lactation have detrimental effects on offspring metabolism. Several animal studies have shown that maternal high-fat diet (HFD) can predispose the offspring to development of obesity and metabolic diseases, however the mechanisms underlying these transgenerational effects are poorly understood. Therefore, we examined the effect of maternal HFD consumption on metabolic phenotype and hepatic expression of involved genes in dams to determine whether any of these parameters were associated with the metabolic outcomes in the offspring. MATERIALS/METHODS: Female C57BL/6 mice were fed a low-fat diet (LFD: 10% calories from fat) or a high-fat diet (HFD: 45% calories from fat) for three weeks before mating, and during pregnancy and lactation. Dams and their male offspring were studied at weaning. RESULTS: Dams fed an HFD had significantly higher body and adipose tissue weights and higher serum triglyceride and cholesterol levels than dams fed an LFD. Hepatic lipid levels and mRNA levels of genes involved in lipid metabolism, including $LXR{\alpha}$, SREBP-2, FXR, LDLR, and ABCG8 were significantly changed by maternal HFD intake. Significantly lower total liver DNA and protein contents were observed in dams fed an HFD, implicating the disturbed liver adaptation in the pregnancy-related metabolic demand. HFD feeding also induced significant oxidative stress in serum and liver of dams. Offspring of dams fed an HFD had significantly higher serum cholesterol levels, which were negatively correlated with liver weights of dams and positively correlated with hepatic lipid peroxide levels in dams. CONCLUSIONS: Maternal HFD consumption induced metabolic dysfunction, including altered liver growth and oxidative stress in dams, which may contribute to the disturbed cholesterol homeostasis in the early life of male mice offspring.