• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.5
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• pp.750-756
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• 1994

The effect of onion juice on ethanol -induced lipid peroxidation were studied were studied in rats. The contents of thiobarbituric acid (TBA) -reactants increased significantly in liver thanol(4ml/kg/day) administered -rats. The activities of serum alanine aminotransferase and alkaline phosphatase increased by ethanol administration compared with control group, but alterations of antioxidant enzymes activities in liver of ethanol administered rats were not significant vs control group. The glutathione contents in liver decreased by ethanol , whereas the glutathione level increased in ethanol and onion juice group compared with ethanol group. The contents of hepatic TBA-reactants and serum aminotrasnferase activity in ethanol group were reduced by onion juice administration. In these results, increased hepatic TBA-reactants of liver in ethanol group might be due to decreased glutathione contents in liver. Reduced glutathione (GSH) plays an important roles in the liver in several detoxification and the reduction of lipid peroxides. So the protective effects of onion juice on ethanol-induced increment of TBA-reactants may be due to the increament of lgutathions content. The glutathione depletion by ethanol was an important factor of ethanol-induced cell damage, and the prevention of onion juice to the glutathione depletion reduced by ethanol may be an important factor on the protection from ethanol-induced lipid perpxidation in rats.

• Toxicological Research
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• v.11 no.2
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• pp.253-259
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• 1995

To investigate an effect of ethanol pretreatment on the bromobenzene metabolism, the brornobenzene (400 mg/kg body wt. i. p.) was given 3 times at intervals of one day to the male rats orally pretreated with 5% ethanol throughout 2 months. In the ethanol pretreated rats, liver injuries were not demonstrated on the basis of the liver weight per body weight, serum levels of alanine aminotransferase (ALT) activity and histopathologic findings. By the bromobenzene treatment, ethanol pretreated rats showed the more decreased levels of serum ALT and liver weight/body weight(%), and decreased degree of liver damage on histopathological observation than the control group. The ethanol pretreated rats showed the more increased activities of hepatic aniline hydroxylase, glutathione Stransf erase (GST) and the more decreased contents of glutathione than the control. Concomitantly the ethanol pretreated rats showed the more decreased contents of hepatic glutathione and increased activities of GST by the bromobenzene treatment. Above results indicate that ethanol pretreatment enhance the metabolizing ability of bromobenzene in rats.

• Korean Journal of Environmental Biology
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• v.18 no.1
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• pp.41-45
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• 2000

Which sublethal cadmium pretreatment may prevent from lethal cadmium's killing mice and which cadmium pretreatment-induced protection against cadmium lethality to mice may be related with their hepatic glutathione contents were investigated. When cadmium chloride was subcutaneously injected to mice (ICR strain) at various doses, all mice died, which treated with cadmium at dose of 300 $\mu$moles/kg or more, and none died, which treated with cadmium at dose of 80 $\mu$moles/kg or less. Subcutaneous pretreatment of sublethal cadmium decreased sacrifice of mice which subsequently injected with lethal cadmium, with most effectiveness at pretreatment dose of cadmium of 40 $\mu$moles/kg b.w. and at 48 hours of interval between sublethal cadmium pretreatment and lethal cadmium treatment. Even if a great part of the cadmium-pretreated mice were sacrificed while treated with lethal cadmium, they survived longer than the non-pretreated mice. Sublethal cadmium pretreatment (40 $\mu$moles/kg b.w.) 48 hours before lethal cadmium treatment to mice didn't decrease hepatic glutathione contents of the survived mice, while decreases in the glutathione in livers were observed in the mice just after died. These results indicate that sublethal cadmium pretreatment-induced protection against cadmium lethality to mice may be related to their hepatic glutathione contents. [Cd pretreatment, Cd lethality, Hepatic glutathione contents].

• Preventive Nutrition and Food Science
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• v.5 no.1
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• pp.48-53
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• 2000

Inhibitory effects of the methanol extract, hexane extract, methanol soluble fraction (MSF) and juice from 3 weeks fermented Kimchi on the tumor formation in sarcoma-180 cell transplanted mice were studied. Effects of the solvent extracts and juice of the Kimchi on the levels of lipid peroxide, glutathione, and the enzyme activities of the liver were also investigated in normal and sarcoma-180 cell transplanted mice. At 32 days following trans-plantation, MSF reduced the tumor formation by 54% compared with the control group, resulting in the smallest tumor weight. Lipid peroxided content in liver increased by the transplantation of sarcoma-180 cells. However, it decreased when MSF of Kimchi was treated to the mice. MSF also suppressed xanthine oxidase activity in cytosol of the liver cells in mice transplanted by sarcoma-180 cells. Kimchi extracts had no inhibitory effect on hepatic aminopyrine-N-demethylase activity in sarcoma-180 cell transplanted or normal mice. Methanol extract and hexane extract of Kimchi slightly increased hepatic glutathione contents in sarcoma-180 treated mice. The injection of MSF from Kimchi markedly increased glutathione levels in the liver of sarcoma-180 treated mice. The injection of MSF from Kimchi markedly increased glutathione levels in the liver of sarcoma-180 treated mice compared to the controls. The MSF recovered the activities of hepatic glutathione reductase and glutathione S-transferase that decreased by the injection of sarcoma-180 cells. These results showed that MSF of Kimchi could suppress the growth of tumors, inhibiting lipid peroxide production and xanthine oxidase activity, in mice. We also suggested that Kimchi extract might play an important role in the prevention of cancer by enhancement of the glutathione level itself as well as via glutathione reductase and glutathione S-transferase.

• Journal of the Korean Society of Food Science and Nutrition
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• v.22 no.6
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• pp.678-684
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• 1993

To evaluate the role of xanthine oxidase in liver damage by CCl4, a group of rats were fed tungstate for a month, which suppressed the activities of xanthine oxidase in serum and liver. Control group of rats were fed standard diet without tungstate. Liver damage was induced both in tungstate fed and control groups by two intraperitoneal injections of CCl4 at the level of 0.1ml/100g body weight at intervals of 24 hours. Increases in the levels of serum alanine aminotransferase by CCl4 were significantly smaller in tungstate fed rats than in control rats. Concomitantly, histopathologic changes were less in tungstate fed rats than in control ones. In rats either treated with CCl4 or not, hepatic type O xanthine oxidase activities were remarkably reduced by tungstate feeding. Hepatic aniline hydroxylase activities were higher in rats fed tungstate than control rats when animals were not treated with CCl4, but the enzyme activities were lower in tungstate fed rats than control when they were treated with CCl4. Neither tungstate feeding nor CCl4 treatment caused any significant changes in hepatic glutathione contents, and activities of hepatic glutathione S-transferase, glutathione peroxidase and superoxide dismutase. It is concluded xanthine oxidase reaction augment CCl4 induced liver damage via oxygen free radical system.

• Archives of Pharmacal Research
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• v.13 no.1
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• pp.38-42
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• 1990

The present study was undertaken to determine the inhibitory effects of cholane compounds, unsodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) on the development of morphine-induced tolerance and physical dependence, and also to determine the hepatic glutathione contents. UDCA and CDCA inhibited the development of morphine-induced tolerance and physical dependence significantly. UDCA inhibited the hepatic glutathione decrease induced by morphine multiple injections, while this effect was not observed in CDCA treated mice. It was throught that the inhibitory effects of hepatic glutathione decrease in morphine-treated mice by UDCA and CDCA showed a tendency of inhibitory effects of development of morphine tolerance and dependence.

• Korean Journal of Environmental Biology
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• v.19 no.2
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• pp.147-152
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• 2001

Whether the pretreatment of sublethal arsenic or cadmium may prevent from lethality of arsenic or cadmium to mice, respectively, and also the protection against to lethality of arsenic or cadmium which might be induced by pretreatment of arsenic or cadmium may be related with their hepatic glutathione contents were investigated. When sodium arsenite or cadmium chloride was subcutaneously injected to mice (ICR strain) using lethal doses, all mice of both group were killed. The mortality of mice which were subsequently injected with lethal arsenic 24 hours after pretreatment of sublethal arsenic was decreased, and the same result was obtained in the case of cadmium. Sublethal pretreatment of arsenic or cadmium prior to lethal arsenic or cadmium treatment to mice, respectively, didn't decrease hepatic glutathione contents of the survived mice, while decreases of that contents in liver were observed in the mice just after they died. Cadmium pretreatment decreased mortality of mice which subsequently injected with lethal arsenic, while arsenic pretreatment didn't protect against cadmium lethality. These results indicate that protection against arsenic or cadmium lethality to mice induced by pretreatment of sublethal arsenic or cadmium may be directly related to other factors induced by sublethal camium pretreatment, not to hepatic glutathione contents.

• Toxicological Research
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• v.11 no.2
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• pp.247-252
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• 1995

To evaluate the effect of xanthine oxidase on liver injury by $CCl_4$, liver damage was induced both in allopurinol pretreated rats (500 mg/kg. ip) and control group by twice intraperitoneal injection of $CCl_4$ (0.1 ml/100 g body wt. 50% in olive oil) at interval of one day. Increases in the levels of serum alanine aminotransferase and liver weight/body weight (%) by $CCl_4$ were significantly smaller inallopurinol pretreated rats than in control whereas the hepatic microsomal glucose-6-pholphatase activities were significantly higher in allopurinol pretreated rats than control group by $CCl_4$ treatment. These results indicates that allopurinol pretreatment may reduce the liver damage in $CCl_4$ intoxicated rats. In rats either with $CCl_4$or not, hepatic type O xanthine oxidase activities were significantly reduced by allopurinol pretreatment and the increasing rate of these enzymes to each control was remarkably lower in allopurinol pretreated rats than control. Liver cytosolic protein contents and aniline hydroxylase, aminopyrine demethylase activities were higher in allopurinol pretreated rats than coirol rats when animals were treated with $CCl_4$. On the other hand, neither allopurinol pretreated nor $CCl_4$ treatment caused any significant changes in hepatic superoxide dismutase and catalase activities. Hepatic glutathione contents were higher in $CCl_4$-treated rats than control, but no significant changes were found in both between the allopurinol treated rats and $CCl_4$-treated rats pretreated with allopurinol, and glutathione and glutathione S-transferase activities were significantly reduced in $CCl_4$-treated rats than control whereas these enzyme activities showed on significant change in both between allopurinel treated and $CCl_4$-treated rats pretreated with allopurinol. It is concluded that xanthine oxidase reaction system augment $CCl_4$ induced liver injury via even oxygen free radical system.

• 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.

• Food Science and Biotechnology
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• v.18 no.3
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• pp.739-744
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• 2009

This study aims to evaluate the therapeutic action of administration of Nigella sativa (NS) and Peganum harmala (PH) oils in diabetes and hepatic toxicity. Results show that treatment of diabetic rats with NS oil or PH oil ameliorate hyperglycaemia induced stress oxidative and hepatic dysfunction in diabetic rats. Administration of NS or PH oil to diabetic rats caused an anti-diabetic and antioxidant activities by the decrease in plasmatic glucose level and increase in hepatic superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities, reduced glutathione (GSH) and glycogen contents compared to untreated diabetic rats. Besides, NS and PH oils protect the hepatic function observed by decrease of triglyceride (TG), total cholesterol (TCh), and increase of high density lipoprotein-cholesterol (HDL-Ch) levels in serum and hepatic tissues. Moreover, a diminution in the bilirubin, transaminase glutanic pyruvic (TGP), and transaminase pyruvic oxaloacetic (TPO) contents in serum and the thiobarbituric acid-reactive substances levels (TBARs) in hepatic tissues are also detected.