• 한국어병학회지
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• 제25권2호
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• pp.95-101
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• 2012

설파디메톡신(sulfadimethoxine, SDM)을 넙치(평균 체중 $100{\pm}20$ g, $20{\pm}1.0^{\circ}C$)에 대하여 400 mg/kg의 농도로 1회 경구 투여한 다음, 혈장과 간에서 시간 경과에 따른 잔류량을 HPLC로써 분석하였다. SDM을 넙치의 조직에 2~50 ppm의 농도가 되도록 첨가한 결과, 평균 회수율은 혈장에서 92.24~93.62%, 간에서 88.34~91.90%의 범위로 나타났으며, 이 분석법의 검출한계는 0.05 ppm이었다. SDM은 투여한 후, 1시간 째에 혈액($402.64{\pm}59.66{\mu}g/ml$)과 간($238.18{\pm}54.00{\mu}g/ml$)에서 모두 최고농도로 분포하였다. 이후 SDM은 빠른 속도로 배설되었으며, 480시간째는 혈장과 간에서 검출되지 않았다.

• 한국식품과학회지
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• 제37권5호
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• pp.822-826
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• 2005

본 연구에서는 천년초 줄기 물추출물의 전처치가 사염화탄소로 유발한 흰쥐의 간 손상에 대해 보호효과를 나타내는지 알아보고자 하였다. 천년초 추출액은 건조 고형분량을 측정하고 1g/kg 및 0.5g/kg 체중이 되는 양을 일정시간에 1일 1회 14일동안 경구투여 하였다. $CCl_4$는 올리브유로 희석하여(1:4) 0.5ml/kg체중이 되도록 시료 마지막 투여 종료 3시간 후에 대조군을 제외한 모든 군에 복강주사하였다. 사염화탄소 처치에 의해 혈청 AST, ALT 및 ALP 활성이 대조군과 비교하여 각각 4.3, 4.7 및 1.2배 증가하였다. 반면, 천년초 줄기 추출물을 1g/kg 투여한 군의 AST, ALT 및 ALP의 활성은 $CCl_4$군과 비교하여 각각 약 36%, 41% 및 22% 감소하였다. 사염화탄소에 의해 간의 지질과산화 반응이 증가하였으며 SOD 및 GST활성이 감소하였다. 1g/kg의 천년초 줄기 추출물의 투여는 간의 지질과산화 반응을 감소시키고 SOD 및 GST의 활성을 회복시키는 결과를 보였다. 또한, 천년초 줄기 추출물은 $132.2{\mu}mol$ vit. C eq/g의 OH 라디칼 소거활성을 나타내었으며 페놀화합물의 함량이 6.52mg/g이다. 이러한 결과는 천년초 줄기 추출물의 항산화 활성 및 사염화탄소로 부터 간손상을 예방하는 효과가 있음을 보여주고 있다.

• 대한본초학회지
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• 제25권3호
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• pp.149-157
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• 2010

Objective：Gagam-Gongjin-dan (GGD) is an oriental medicinal prescription composited with Cervi parvum Cornu, Corni Fructus, Angelica Gigantis Radix, Lycii Fructus, Dioscoreae Rhizoma, Citri Pericarpium, Gastrodiae Rihzoma, Agastachis Herba, Cassiae cortex, Scutellariae Radix and Schisandrae Fructus. The purpose of this study was to investigate the effects of GGD extract against acetaminophen (APAP)-induced liver injury in mice. Methods：GGD extract was prepared by extracting with methanol for 7 days. The extract was freeze-dried following filtration through vacuum distillation system. The first, we investigated the antioxidant effects of GGD extract on electronic donating ability (DPPH), nitrite (NO) scavenging and superoxide dismutase (SOD)-like activity. The next, we investigated the possible hepatoprotective effect of GGD extract administration against acetaminophen-induced liver injury in mice. Mice were orally administrated with or without GGD extract of different doses (25-100 mg/kg/day) one times per day for 6 days. After 3 days, APAP was orally applied with a single dose (400 mg/kg). Results：GGD extract increased DPPH, NO and SOD-like activities in dose dependant. APAP treatment significantly increased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities in plasma. Also, APAP treatment significantly evaluated lipid peroxidation product thiobarbituric reacting substances (TBARS) and depleted some antioxidant enzymes (superoxide dismutase, catalase, d-aminolevulinate dehydratase and gluthathione peroxidase activities) in liver homogenates compared to the control group. However, the orally administration of GGD extract was able to counteract these effects. Histological studies provided supportive evidence for biochemical analysis Conclusions：These results suggest that GGD extract has a potential antioxidant and hepatoprotective effect against APAP-induced liver injury, these properties may contribute to liver disease care.

• Journal of Preventive Medicine and Public Health
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• 제24권3호
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• pp.287-304
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• 1991

Tolerance to several toxic effects of cadmium, including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicityandrenaltoxicity. Three groups of rats (A, B, C), each consisting of 16 rats, were studied and each group was divided into four subgroups (1, 2, 3, 4), 4 rats for each subgroup. Rats were subcutaneously pretreated with saline (A), $CdCl_2$ (0.5 mg/kg, B), and $ZnCl_2$ (13.0 mg/kg, C) during time periods of $1{\sim}6$ weeks. At the end of the period, rats were challenged with $CdCl_2$ (3.0, 6.0 and 9.0 mg/kg, ip). After giving the challenge dose, cadmium and metallothionein (MT) concentrations were determined and also observed the histologic change in liver and kidney. The concentration of cadmium in liver and kidney increased dose-dependently to the challenge dosage. These da indicate the kidney is a major target organ of chronic cadmium poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity observed in response to long-term exposure to cadmium. In addition, histologic examination of group $A_2,\;A_3\;and\;A_4$ revealed moderate to severe cadmium toxicity, evidenced by infiltration of inflammatory cells, cell swelling, pyknosis, enlarged sinusoids and necrosis in liver, and tubule cell necrosis and degeneration in kidney. However, MT concentrations in liver and kidney were increased by the pretreatment of $CdCl_2$ and $ZnCl_2$, and their morphological findings were not significantly changed, comparing with control group. Higher MT concentration in liver and kidney observed in the pretreated groups constitutes a plausible explanation of the protective effects of pretreatment against the cadmium toxicity after challenge dosing.

• 한국식품저장유통학회지
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• 제24권1호
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• pp.107-115
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• 2017

동물실험에서 실크단백질 산 가수분해물을 투여하고 t-BHP투여한 군의 혈액 생화학적 검사 결과 t-BHP만 투여한 군과 비교하였을 때 AST, ALT 그리고 LDH가 실크단백질 산 가수분해물의 투여 농도가 높아질수록 수치가 감소하는 것으로 나타났고 세포가 손상할 시에 증가하는 MDA를 간 조직을 대상으로 측정한 결과 실크단백질 산 가수분해물의 농도가 높아질수록 수치가 대조군과 유사한 정도로 감소하는 것으로 보아 간 손상에 관여하는 효소의 누출 억제효과가 있는 것으로 사료된다. HPLC로 간 조직에서의 GSH 측정결과 t-BHP만 투여한 군과 비교하였을 때 유의적으로 증가하였고 조직학적 검사 결과 t-BHP만 투여한 군과 비교하였을 때 실크단백질 산 가수분해물을 투여한 군이 대조군과 가까운 모습을 보이는 것으로 관찰되어 실크단백질 산 가수분해물이 산화적 스트레스로부터의 간 보호 효과가 있는 것으로 사료된다. 따라서 실크단백질 산 가수분해물의 기능적 소재로서의 이용가능성이 확대될 것으로 사료된다.

• Asian-Australasian Journal of Animal Sciences
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• 제13권10호
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• pp.1433-1439
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• 2000

An experiment was carried out with 48 IVRI 2CQ rats 6-8 week old, weighing 50-100 g, to study the effect of lead exposure on antioxidant defense, lipid peroxide level, status of thiol groups and concentration of lead in the liver and kidneys at the end of the exposure and also after withdrawal of lead administration. Twenty four rats were given lead at a daily dose rate of 1 mg lead/2 ml of distilled water/kg body weight as lead acetate solution intraperitoneally for a period of 30 days. Another 24 control rats received 2 ml of sterile normal saline solution (0.85% NaCl)/kg body weight in an identical manner. A many-fold increase in concentration of lead was associated with a non-significant (p>0.05) decrease in the activities of superoxide dismutase (SOD) in the liver (27%) and kidneys (12%) and catalase in kidneys (22%). A significant (p<0.05) increase in lipid peroxide level was recorded in the liver (40%) compared with control values. There were significant (p<0.05) decreases in the total thiol and protein bound thiol contents in liver and an increase in non-protein bound thiol groups in the kidneys of lead exposed rats. During the 10 day observation period after withdrawal of lead administration, no significant change was observed with respect to any of the above parameters indicating that a 10 day withdrawal period was not enough for restoration of normality. It is concluded that the magnitude of response and the resultant changes in the lipid peroxide concentration, and the activities of SOD and catalase were not identical in the liver and kidneys of lead-exposed rats.

• Radiation Oncology Journal
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• 제35권2호
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• pp.172-179
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• 2017

Purpose: To evaluate the outcomes of stereotactic body radiation therapy (SBRT) for patients with liver oligo-recurrence and oligo-progression from various primary tumors. Materials and Methods: Between 2002 and 2013, 72 patients with liver oligo-recurrence (oligo-metastasis with a controlled primary tumor) and oligo-progression (contradictory progression of a few sites of disease despite an overall tumor burden response to therapy) underwent SBRT. Of these, 9 and 8 patients with uncontrollable distant metastases and patients immediate loss to follow-up, respectively, were excluded. The total planning target volume was used to select the SBRT dose (median, 48 Gy; range, 30 to 60 Gy, 3-4 fractions). Toxicity was evaluated using the Common Toxicity Criteria for Adverse Events v4.0. Results: We evaluated 55 patients (77 lesions) treated with SBRT for liver metastases. All patients had controlled primary lesions, and 28 patients had stable lesions at another site (oligo-progression). The most common primary site was the colon (36 patients), followed by the stomach (6 patients) and other sites (13 patients). The 2-year local control and progression-free survival rates were 68% and 22%, respectively. The 2- and 5-year overall survival rates were 56% and 20%, respectively. The most common adverse events were grade 1-2 fatigue, nausea, and vomiting; no grade ${\geq}3$ toxicities were observed. Univariate analysis revealed that oligo-progression associated with poor survival. Conclusion: SBRT for liver oligo-recurrence and oligo-progression appears safe, with similar local control rates. For liver oligo-progression, criteria are needed to select patients in whom improved overall survival can be expected through SBRT.

• Toxicological Research
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• 제24권4호
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• pp.281-287
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• 2008

Impairment of hepatic metabolism of sulfur-containing amino acids has been known to be linked with induction of liver injury. We determined the early changes in the transsulfuration reactions in liver of rats challenged with a toxic dose of $CCl_4$ (2 mmol/kg, ip). Both hepatic methionine concentration and methionine adenosyltransferase activity were increased, but S-adenosylmethionine level did not change. Hepatic cysteine was increased significantly from 4 h after $CCl_4$ treatment. Glutathione (GSH) concentration in liver was elevated in $4{\sim}8$ h and then returned to normal in accordance with the changes in glutamate cysteine ligase activity. Cysteine dioxygenase activity and hypotaurine concentration were also elevated from 4 h after the treatment. However, plasma GSH concentration was increased progressively, reaching a level at least several fold greater than normal in 24 h. ${\gamma}$-Glutamyltransferase activity in kidney or liver was not altered by $CCl_4$, suggesting that the increase in plasma GSH could not be attributed to a failure of GSH cycling. The results indicate that acute liver injury induced by $CCl_4$ is accompanied with extensive alterations in the metabolomics of sulfurcontaining amino acids and related substances. The major metabolites and products of the transsulfuration pathway, including methionine, cysteine, hypotaurine, and GSH, are all increased in liver and plasma. The physiological significance of the change in the metabolomics of sulfur-containing substances and its role in the induction of liver injury need to be explored in future studies.

• 대한수의학회지
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• 제50권2호
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• pp.145-149
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• 2010

This study was carried out to find whether phenidone (1-phenyl-3-pyrazolidinone), a cyclooxygenase as well as a lipoxygenase inhibitor, exhibits the preventive effect on carbon tetrachloride $(CCl_{4})-induced$ acute liver injury in rats. Rats were pretreated with phenidone at a dose of 50 or 200 mg/kg (p.o.) once daily for 3 consecutive days before $CCl_{4}$ administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Malondialdehyde (MDA) production was determined as an index of lipid peroxidation in the liver and serum. The histopathological changes in the liver were also examined in each group. The reduction in body weights was significantly inhibited in the phenidone-treated group than in the $CCl_{4}$ control group. Significant increase in the relative liver weights of the phenidone-treated groups was observed compared with either the vehicle or $CCl_{4}$ groups. Elevation of serum AST and ALT activities occurred after $CCl_{4}$ treatment was significantly attenuated by the pretreatment with phenidone. The elevation of MDA levels in liver and serum were completely inhibited in phenidone-treated groups. The protective effects on phenidone-treated groups were confirmed histopathologically. These results suggest that phenidone may be a useful protector through modulation of hepatic inflammation in $(CCl_{4})-induced$ acute liver injury.

• 대한한의학방제학회지
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• 제17권2호
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• pp.123-132
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• 2009

Acetaminophen (AP) is widely used as an over-the-counter analgesic and antipyretic drug. AP-induced hepatotoxicity is a common consequence of AP overdose and may lead to acute liver failure. In this study, we investigated the liver damage in mice using single dose (300 mg/kg) of AP and the possible protective effects of administration (50-200 mg/kg body weight) of Joo-Juk on acetaminophen-induced liver damage in mice. The alanine aminotransferase (ALT), and aspartate aminotransferase (AST) activities were determined in the plasma of mice. The effect of Joo-Juk on lipid peroxidation product thiobarbituric reacting substances (TBARS) and some antioxidant enzymes superoxide dismutase (SOD), catalase, d-aminolevulinate dehydratase ($\sigma$-ALA-D) activities, and gluthathione peroxidase (GPx), were also evaluated in the mouse liver homogenate. AP caused liver damage as evident by statistically significant increased in plasma activities of AST and ALT. There were statistically significant losses in the activities of SOD, catalase, $\sigma$-ALA-D, and GPx and an increase in TBARS in the liver of AP-treated group compared with the control group. However, Joo-Juk was able to counteract these effects. These results suggest that Joo-juk can act as hepato-protectant against AP toxicity and is a good candidate for further evaluation as an effective chemotherapeutic agent.