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Doxorubicin유발 심장독성에 미치는 L-Carnitine의 효과
김형춘,송계용,전구석,허인회,Kim, Hyoung-Chun,Song, Ke-Yong,Jeon, Ku-Seok,Huh, In-Hoi 대한약학회 1988 약학회지 Vol.32 No.4
This study was undertaken to elucidate the role of L-carnitine on cardiotoxicity induced by doxorubicin in mice. We designed to investigate both lipoperoxidation and histopathology in experimental group. The results obtained from prior with concurrent treatment of L-carnitine showed as follows; 1) Combination of L-carnitine showed significant inhibition of lipoperoxide in liver than heart. 2) By means of electron microscopy, we obtained histological evidence that doxorubicin-induced cardiomyopathy, is prevented by L-carnitine.
Mercuric chloride 유발 신부전에서 산소유리기에 미치는 Sodium selenite의 영향
김형춘,주왕기,허인회,Kim, Hyoung-Chun,Jhoo, Wang-Kee,Huh, In-Hoi 대한약학회 1988 약학회지 Vol.32 No.4
Oxygen free radical have recently been found to mediate cell injury after ischemia in the kidney. The purpose of our study was to determine whether selenium had an effect on damge mediated by oxygen free radical in inorganic mercury induced renal failure, toxic model of renal failure. Toxic renal failure model was produced by subcutaneous injection of mercuric chloride (4mg/kg) once a day for 7 consecutive days. In additionally, coadministration of sodium selenite (1mg/kg) was performed by the same condition. As a consequence of this study, we were able to detect partially unequivocal role of selenium as below dipicted. The combination of sodium selenite showed that markedly inhibited production of superoxide radical in mercuric chloride alone. On the other hand, combined sodium selenite was unable to enhance against significantly lowered superoxide dismutase activity after mercuric chloride insult. However, simultaneous administration of sodium selenite was inclined to induce mitochondrial superoxide dismutase and catalase.
김형춘(Hyoung Chun Kim),전완주(Wan Jhoo Chun),이현우(Hyun Woo Lee),권명상(Myung Sang Kwon),송계용(Kye Yong Song),주왕기(Wang Kee Jhoo) 대한약학회 1992 약학회지 Vol.36 No.2
This study investigated the hypothesis that carcinogen-induced elevation of oxyradical during the hepatocarcinogenesis in rat. The hepatic preneoplastic lesions in the Spraque-Dawley rats were induced by the carcinogen treatment such as diethylnitrosamine(DEN) and acetylaminofluorene(AAF) in combination with partial hepatectomy(PH). The liver sample was taken at 2,6,10 and 16 months after carcinogen treatments followed by PH. Carcinogen treatments initially increased the indices of oxidative damage(activities of xanthine oxidase and production rates of superoxide anion, microsomal hydrogen peroxide, hydroxyl radical ) in the liver compared to PH groups. However, cytosolic hydrogen peroxide did not change significantly throughout the full time period. Of hydrogen peroxide scavenger, the catalase was remained lower than PH groups, whereas the peroxidase was increased after carcinogen treatments. Morphologically, the immunohistochemical analysis with glutathione-S-transferase of a placenta form(GSTP) antibody was used to detect the induction of preneoplastic nodules. During the hepatocarcinogenesis, both production rate of hydroxyl radical and activity of glutathione-S-transferase(GST) markedly increased with the appearance of the preneoplastic nodule. These results indicated that the hydroxyl radical of reactive oxygen species seemed to have a major influence on the hepatocarcinogenesis and the effect of time after removal of the carcinogen also appeared to be highly critical in the hepatocarcinogenesis.
사염화탄소-유발지방간에 대한 L-글루탐산 일나트륨의 보호작용
김형춘(Hyoung Chun Kim),이왕섭(Wang Seop Lee),전완주(Wan Jhoo Chun),최용순(Yong Soon Choi),김수희(Soo Hee Kim),이현우(Hyun Woo Lee),주왕기(Wang Kee Jhoo) 대한약학회 1992 약학회지 Vol.36 No.1
To achieve better understanding of the effects of monosodium-L-glutamate(MSG) against CCl4 fatty liver in Wister male rats, 5% MSG solution was given as drinking water and CCl4 0.1ml/kg was injected subcutaneously twice a week for four weeks. It was showed that increased hepatic phospholipid and hepatic triacylglycerol levels by CCl4 challenge were significantly decreased by additional MSG, respectively. However, MSG had no apparent effect on the elevated hepatic cholesterol level in the presence of CCl4. Histrionically, additional MSG markedly inhibited fatty degeneration, spotty necrosis, inflammation and periportal vascular proliferation manifested by CCl4. respectively. Theses results indicated that effects of MSG against CCl4 induced-fatty liver appeared to be involved with partial restoration of altered hepatic lipid composition.
사염화탄소와 Monosodium-L-Glutamate 병용투여에 의한 간조직의 환원형글루타치온 함량 및 그의 관련효소활성의 변화
김형춘(Hyoung Chun Kim),이왕섭(Wang Seop Lee),전완주(Wan Jhoo Chun),김수희(Soo Hee Kim),주왕기(Wang Kee Jhoo) 大韓藥學會 1991 약학회지 Vol.35 No.5
To explore the effect of monosodium-L-glutamate(MSG) on CCl4-damaged liver in Wister male rat, 5% MSG solution as drink water were administered after S.C. injection of 0.1 mg/kg CCl4 twice a week for 4 weeks. After last administration of MSG, heptic glutathione(GSH) dependent system was assayed. It showed that MSG increased significantly hepatic glutathione(GSH) and glutathione peroxidase(GSHpx), but decreased glutathione-S-transferase(GST) activity in normal rats. MSG increased significantly the GSHpx. and GST activities in rats with CCl4-induced liver damage. These results indicate that decrease of GSH dependent systems in CCl4 liver injury might be partially elevated by coadministration of MSG.
사염화탄소 및 에탄올에 의해 유도된 만성간 손상에 미치는 말로틸레이트의 항산화 작용
김형춘(Hyoung Chun Kim),허인회(In Hoi Hur) 대한약학회 1990 약학회지 Vol.34 No.4
To achieve a better understanding of antioxidant action manifested by malotilate, the dithiol malonates, we monitored the oxy radical-scavenging system against the chronic hepatic damage induced by CCl4 alone or in combination with ethanol. Malotilate was given orally at a dose of 100mg/kg/day and CCl4 1.5ml/kg was injected subcutaneously twice a week for 4 weeks. In each group receiving ethanol, drinking water was replaced by 20% aqueous solution or glucose, isocaloric amounts of ethanol, as a control of ethanol was diluted in its drinking water. Each rat was killed as a starved state at 18 hours after the period of the experiment, four weeks. The results were summarized as follows: 1)Malotilate inhibited the rate of generation of superoxide radicals, the accumulation of lipoperoxides, and promoted the synthesis of glutathione in the liver. 2)Malotilate stimulated the enhancement of activity of superoxide dismutase in hepatic mitochondria. 3)Malotilate had no effects on the hepatic H202 contents. 4)Malotilate showed the increase of catalase activity in the liver poisoned with CCl4, and also gave a tendency to increase it in the liver intoxicated with ethanol. Thus, our data suggested that the activation of hepatic antioxidant system in the presence of malotilate would play a role in protecting liver against the toxic effects of oxy radical and/or lipid peroxides under the hepatotoxic conditions induced by CCl4 with or without ethanol. However, the effects of malotilate against the ethanol-induced hepatotoxicity appear to be insignificant.
사염화탄소 및 에탄올 중독간에서 Malotilate(Diisopropyl 1.3-dithiol 2-ylidene malonate)의 보호효과에 관한 전자현미경적 관찰
김동헌,김형춘,송계용 중앙대학교 의과대학 의과학연구소 1987 中央醫大誌 Vol.12 No.3
To observe the protective effects of malotilate(diisopropyl 2-ylidene malonate, MLT) on the hepatic injury induced by carbon tetrachloride(CCl_4)or ethanol,an electron microscopic study was carried out. The 42 rats were used and weighed between 140∼200g divided into acute and chronic expreimental group. Acute groups consist of control, adminstered with malotilate(MLT), CCl_4, CCl_4 with MLT,ethanol, ethanol with MLT, CCl_4 with ethanol, and CCl_4 with MLT with ethanol. Chronic groups were divided into 4 weeks and 8weeks group. Chronic groups(4 weeks) consisted of rats administered for 4 weeks with MLT,CCl_4, CCl_4 with MLT,ethanol, ethanol with MLT, CCl_4 with ethanol, and CCl_4 with MLT with ethanol. Chronic groups(8 weeks) consisted of rats administered for 8 weeks with MLT(4 w), followed by ethanol(4 w),CCl_4(4 w) followed by ethanol(4 w), CCl_4 with MLT(4 w) followed by ethanol with MLT(4 w), and ethanol with MLT(4 w followed by CCl_4 with MLT(4 w). Electron microscopic processes with liver tissue were carried out in each experimental group. The results were as follows: 1 Acute groups A. Moderate to maked vascuolar changes in the hepatocytes in CCl_4 and CCl_4 with ethanol intoxication were improved with decrease of number and size of vacuolar changes by malotilate administration but slightly improved in ethanol with malotilate administration. B. Moderate vascuolar changes were seen in the hepatocytes with the ethanol intoxication and slightly improved with additional malotilate administration. 2. Chronic groups(4 weeks) Moderate to maked vascuolar changes in the hepatocytes in CCl_4 and CCl_4 followed by malotilate with ethanol intoxication for 4 weeks were improved with additional malotilate administration by decrease in number and size of vacuolar change but slightly improved in ethanol intoxication . 3. Chronic groups(8 weeks) A. Mild to moderate increase of collagen fibers and mild vacuolar changes in the liver and hepatocytes in CCl_4 or ethanol administration were improved by decrease of vacuolar changes and collagen fibers followed by additional malotilate administration. B. More increase of vacuolar changes were seen in the hepatocytes with ethanol with MLT followed by CCl_4 with additional MLT than CCl_4 with MLT followed by ethanol with MLT administration. Therefore, malotilate showed remarkable protective effects on carbon tertrachloride intoxication in liver but slight effects on ethanol intoxication. Significantly decreased or even worse effects of malotilate were observed when ethanol was administered for four weeks before CCl_4 intoxication.