• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2009.10a
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• pp.252-252
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• 2009

• YAKHAK HOEJI
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• v.36 no.1
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• pp.66-72
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• 1992

In order to test relationships between hepatotoxicity and transmethylation, activities of protein methylases and SAM (S-adenosyl-L-methionine)-synthetase were examined in liver tissues of rats treated with $CCl_4$. Also the concentrations of SAM and SAH were measured by HPLC in rat liver. The results are as follows. (1). Activities of protein methylases were not significantly changed in 24 hours after $CCl_4$ treatment. However, in 48 hours, activities of protein methylases were significantly increased in comparison with that of control. (2). Activity of SAM-synthetase was increased steadily in the time course after $CCl_4$ treatment. (3). S-adenosyl-L-methionine concentration of liver tissues in $CCl_4$-treated group was elevated in 24 hours, and then declined thereafter. But the SAH concentration was slightly decreased in the time course after $CCl_4$ treatment. These results indicate that SAM was very actively used in transmethylation reactions of $CCl_4$ damaged rat liver, suggesting the strong relationships between hepatotoxicity and transmethylation phenomena.

• YAKHAK HOEJI
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• v.37 no.5
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• pp.499-503
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• 1993

Betaine, a major component of Lycii Fructus, was evaluated for its anti-hepatotoxic activity on carbon tetrachloride-induced hepatotoxicity in primary cultured rat hepatocytes. Betaine was found to attenuate carbon tetrachloride-induced hepatotoxicity both morphologically and biochemically. Typical hepatocyte necrosis due to carbon tetrachloride seemed to be reduced by 50 to 500 $\mu{M}$ of betaine under microscopical observation. The value of glutamic pyruvic transaminase released from the hepatocytes into the medium significantly decreased as betaine concentration increased. Betaine also significantly elevated the reduced activities of some enzymes, cytochrome P-450, 7-ethoxycoumarin-0-deethylase and glutathione-S-transferase, involved in xenobiotic metabolism due to carbon tetrachloride-induced hepatotoxicity. These results demonstrate a possible hepato-protective role of betaine against fatty liver that could be easily induced by carbon tetrachloride.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.5
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• pp.617-624
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• 2013

The purpose of this study is to investigate the protective effects of 25 herbal formulas on acetaminophen (APAP) or D-galactosamine (D-GalN)-induced hepatotoxicity in primary rat hepatocytes. Cell viability was measured using by Cell Counting Kit-8. 15 kinds of herbal formulas significantly reversed the cell viabilities of D-GalN-treated rat hepatocytes compared with D-GalN alone (p<0.05). In particular, 9 herbal formulas (Bangpungtongseong-san, Bojungikgi-tang, Galgeun-tang, Gumiganghwal-tang, Guibi-tang, Sagunja-tang, Samsoeum, Pyeongwi-san and Yijin-tang) showed the potent protective effects. However, 8 herbal formula exerted weak protective effects and 2 herbal formula did not exert effects on hepatotoxicity by D-GalN. On APAP-induced hepatotoxicity, 7 kinds of herbal formulas increased the viabilities of hepatocytes compare with APAP alone (p<0.05). These results could be provide a valuable information for the future in vivo or clinical studies to predict the hepatoprotective effects of herbal formulas.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.12
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• pp.5071-5074
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• 2016

Background: Azoxymethane (AOM) is a well-known colon cancer-inducing agent in experimental animals via mechanisms that include oxidative stress in rat colon and liver tissue. Few studies have investigated AOM-induced oxidative stress in rat liver tissue. Red seaweeds of the genera Hypnea Bryodies and Melanothamnus Somalensis are rich in polyphenolic compounds that may suppress cancer through antioxidant properties, yet limited research has been carried out to investigate their anti-carcinogenic and antioxidant influence against AOM-induced oxidative stress in rat liver. Objective: This study aims to determine protective effects of red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts against AOM-induced hepatotoxicity and oxidative stress. Materials and Methods: Sprague-Dawley rats received intraperitoneal injections of AOM, 15 mg/kg body weight, once a week for two consecutive weeks and then orally administered red seaweed (100 mg/kg body-weight) extracts for sixteen weeks. At the end of the experiment all animals were overnight fasted then sacrificed and blood and liver tissues were collected. Results: AOM treatment significantly decreased serum liver markers and induced hepatic oxidative stress as evidenced by increased liver tissue homogenate levels of nitric oxide and malondialdehyde, decreased total antioxidant capacity and glutathione, and inhibition of antioxidant enzymes (catalase, glutathione peroxidase, glutathione S-transferase, glutathione reductase and superoxide dismutase). Both red seaweed extracts abolished the AOM-associated oxidative stress and protected against liver injury as evidenced by increased serum levels of liver function markers. In addition, histological findings confirmed protective effects of the two red seaweed extracts against AOM-induced liver injury. Conclusion: Our findings indicate that red seaweed (Hypnea Bryodies and Melanothamnus Somalensis) extracts counteracted oxidative stress-induced hepatotoxicity in a rat model of colon cancer.

• Toxicological Research
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• v.9 no.2
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• pp.167-175
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• 1993

Protective effects of dithiol malonate derivatives (DMDs), YH-100, YH-150 and YH-439 on carbon tetrachloride-induced hepatotoxicity were investigated in primary rat hepatocytes culture. Treatment of DMDs to hepatocytes culture did not affect total cytochrome P-450 content and ECOD and AHH activities. Protein and RNA synthesis was also similar to control. Meanwhile, DMDs significantly decreased LDH release and in vitro lipid peroxidation induced by $CCI_4$. Accumulation of cellular triglyceride and decreased secretion of VLDL from liver cells by $CCI_4$ treatment were also significantly protected.

• Journal of Ginseng Research
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• v.19 no.2
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• pp.108-113
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• 1995

Effect of ginseng polysaccharide fraction was examined for $CCl_4$-induced hepatotoxicity in vitro and in vivo. In $CCl_4$-injured primary cultured rat hepatocytes, treatment of the polysaccharide fraction (0.1, 0.3, 1.0 mg/ml) significantly Inhibited the release of LDH and GOT into the culture medium in a dose-dependent manner. Oral administration of the polysaccharide fraction (100, 200 mg/kg) inhibited the decrease of body weight and the increase of the ratio of liver to body weight in $CCl_4$-intoxicated rats. Elevation of GOT, GPT and ALP activity in the serum by $CCl_4$-induced hepatotoxicity was suppressed by administration of ginseng polysaccharide fraction. MDA levels increased in the serum as well as in the liver tissue by treatment with $CCl_4$ showed a tendency to be 연w in the rats given to the polysaccharide fraction. These results suggest that the polysaccharide fraction may be active substance responsible for antihepatotoxic effect of Panax ginseng.

• YAKHAK HOEJI
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• v.36 no.1
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• pp.80-86
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• 1992

Streptozotocin (STZ) is a naturally occurring nitrosoamide used extensively to produce diabetes in experimental animals. Our previous study has demonstrated that i.v. administraton of streptozotocin induces significant red blood cell hemolmysis in rats. Since it has been reported that the highest concentration of STZ is found in the liver, the effect of STZ in freshly isolated rat hepatocytes has been investigated. STZ treatment (10 mM) did not cause significant loss of viability throughout 4 hour incubation, while high dose of STZ (300 mM) to hepatocytes resulted in complete cell death within 3 hours. Addition of 40 mM glucose to incubation medium did not potentiate STZ-induced hepatotoxicity, suggesting that STZ-induced hyperglycemia in vivo did not affect its hepatotoxicity. To investigate the mechanixm of the toxicity, intracellular total glutathione level was determined. Tratment with 10 mM STZ which was not toxic to hepatocytes led to complete depletion of intracellular glutathione level within 1 hour incubation. These results suggest that STZ-induced hepatotoxicity may be independent on the intracellular glutathione depletion.

• Biomolecules & Therapeutics
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• v.2 no.1
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• pp.47-53
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• 1994

The methylation response as well as the level of methyl donor substance, 5-adenosyl-L-methionine (SAM) has been suggested to be related to hepatotoxicity including hepatocarcinogenesis. But direct correlation between protein methylation and hepatotoxicity has not been established to the present. To observe relationship between protein methylation and short-term hepatotoxicity induced by chemical substances, the activities of protein methylase I and II (PM I, PM II) were examined in cytosolic fraction of SD rat treated orally with acetaminophen(AA), $\alpha$-naphtyl-isothiocyanate (ANIT) and tetracycline (TC) that was known to produce necrosis, cholestasis and steatosis respectively. To evaluate the degree of hepatotoxicity induced by each chemicals, we observed the serum levels of indicative parameters and histopathological alteration. In AA treated group, the activities of PM I were increased at 6, 12 hours after administration, prior to the appearance of the hepatotoxicity by clinical parameters. It was suggested that the levels of PM I were related with the initial stage of hepatotoxic mechanism induced by AA. In ANIT treated group, though most of clinical parameters were significantly increased at 24, 48 hours after administration, the activity of PM I was not changed, indicating that ANIT induced hepatotoxicity was not coupled to protein methylation.

• Korean Journal of Pharmacognosy
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• v.36 no.2 s.141
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• pp.81-87
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• 2005

The effects of the DWP-04 [DDB:selenium yeast:glutathione (31.1 : 6.8 : 62.1 (w/w%)] on acetaminophen detoxification enzyme system were studied in rats. Treatment with DWP-04 was prevented againt acetaminophen-induiced hepatotoxicity in rat as evidenced by the decreased formation of lipid peroxide. Effect of DWP-04 on the activities of free radical-generating enzymes, free radical scavenging enzymes and glutathione-related enzymes as well as detoxification mechanism of DWP-04 against acetaminophen-treated was investigated in rat. Activities of cytochrome p450, cytochrome b5, aminopyrine demethylase and aniline hydroxylase as free radical-generating enzymes activities were decreased by the treatment with DWP-04 against acetaminophen treated. Although acetaminophen-induced hepatotoxicity results in the significantly decrease in the level of hepatic glutathione and activities of glutathine S-transferase, quinone reductase, glutathione reductase and ${\gamma}-glutamyl-$cysteine synthetase, these decreasing effects were markedly lowered in the DWP-04-treated rat. Therefore, it was concluded that the mechanism for the observed preventive effect of DWP-04 against the acetaminophen-induced hepatotoxicity was associated with the decreased activities in the free radical-generating enzyme system.