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Ceramide is involved in MPP+-induced Cytotoxicity in Human Neuroblastoma Cells
Eun-JooNam, Hye-SookLee, YoungJaeLee, Wan-SeokJoo, SunghoMaeng, Hye-InIm, Chan-WoongPark, YongSikKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2002, Vol.6 No.6 1 281-286 (6 pages)
To understand the cytotoxic mechanism of MPP, we examined the involvement of ceramide in MPP- induced cytotoxicity to human neuroblastoma SH-SY5Y cells. When SH-SY5Y cells were exposed to MPP, MPP induced dose-dependent cytotoxicity accompanied by 2-fold elevation of intracellular ceramide levels in SH-SY5Y cells. Three methods were used to test the hypothesis that the elevated intracellular ceramide is related to MPP-induced cytotoxicity: C2-ceramide was... -
Role of Calmodulin in the Generation of Reactive Oxygen Species and Apoptosis Induced by Tamoxifen in HepG2 Human Hepatoma Cells
YongSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2002, Vol.6 No.4 3 187-192 (6 pages)
Tamoxifen, an antiestrogen, has previously been shown to induce apoptosis in HepG2 human hepatoblastoma cells through activation of the pathways independent of estrogen receptors, i.e., intracellular Ca2 increase and generation of reactive oxygen species (ROS). However, the mechanism of tamoxifen to link increased intracellular Ca2 to ROS generation is currently unknown. Thus, in this study we investigated the possible involvement of calmodulin, a Ca2 activated protein, and... -
The Role of Lipid Peroxidation and Glutathione on the Glycochenodeoxycholic Acid-Induced Cell Death in Primary Cultured Rat Hepatocytes
SangHuiChu, WolMiPark, KyungEunLee, YoungSookPae 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.2 6 121-127 (7 pages)
Intracellular accumulation of bile acids in the hepatocytes during cholestasis is thought to be pathogenic in cholestatic liver diseases. The objective of this study was to determine the role of lipid peroxidation and glutathione on the bile acid-induced hepatic cell death mechanism in primary cultured rat hepatocytes. To induce hepatic cell death, we incubated primary cultured rat hepatocytes with glycochenodeoxycholic acid (GCDC; 0∼400μM) for 3 hours. In electron microscopic examination and... -
Transition Metal Induces Apoptosis in MC3T3E1 Osteoblast Evidence of Free Radical Release
Han-JungChae, , Soo-WanChae, Jang-SookKang, Dong-HyeonYun, Byung-GwanBang, Mi-RaKang, Hyung-MinKim, Hyung-RyongKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.1 7 47-54 (8 pages)
radical scavengers-N-acetyl cysteine (NAC), reduced glutathione (GSH), or superoxide dismutase (SOD). First, we have observed that selenium (10μM), cadmium (100μM), mercury (100μM) or manganese (1 mM) treatment induced apoptotic phenomena like DNA fragmentation, chromatin condensation and caspase-3-like cysteine protease activation in MC3T3E1 osteoblasts. Concomitant treatment of antioxidant; N-acetyl-L-cysteine (NAC), reduced-form glutathione (GSH), or superoxide dismutase (SOD), prevented... -
Glycochenodeoxycholic Acid Induces Cell Death in Primary Cultured Rat Hepatocyte Apoptosis and Necrosis
SangHuiChu, WolMiPark, KyungEunLee, YoungSookPae 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.6 4 565-570 (6 pages)
Intracellular accumulation of bile acids in the hepatocytes during cholestasis is thought to be pathogenic in cholestatic liver injury. Due to the detergent-like effect of the hydrophobic bile acids, hepatocellular injury has been attributed to direct membrane damage. However histological findings of cholestatic liver diseases suggest apoptosis can be a mechanism of cell death during cholestatic liver diseases instead of necrosis. To determine the pattern of hepatocellular toxicity induced by... -
Effect of the Inhibition of Phospholipase A2 in Generation of Free Radicals in Intestinal Ischemia/Reperfusion Induced Acute Lung Injury
YoungManLee, Yoon-yubPark, TeoanKim, HyunG.Cho, YoonJeongLee, JohnE.Repine 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 11 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.3 4 263-273 (11 pages)
The role of phospholipase A2 (PLA2) in acute lung leak induced by intestinal ischemia was investigated in association with neutrophilic respiratory burst. To induce lung leak, we generated intestinal ischemia for 60 min prior to the 120 min reperfusion by clamping superior mesenteric artery in Sprague-Dawley rats. Acute lung leak was confirmed by the increased lung leak index and protein content in bronchoalveolar fluid. These changes were inhibited by mepacrine, the non-specific PLA2... -
Acute Pulmonary Responses in Vivo to Silica Complexed with H+, Zn2+, or Fe3+
JiheeLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.2 8 183-189 (7 pages)
This investigation is to determine whether the surface complexation of iron influence acute pulmonary responses induced by silica. For this study, three varieties of cation complexed silica were used: silica-H, -Zn2, and -Fe3, since the first two are not active in the transport of electrons and generate little free radicals relative to the dust with the surface iron. Rats (270 to 280 g) were intratracheally (IT) instilled with saline, silica-H, -Zn2, or... -
Activation of SAPK and Increase in Bak Levels during Ceramide and Indomethacin-Induced Apoptosis in HT29 Cells
JuHoKim, SaeOckOh, SungSookJun, JinSupJung, JaeSukWoo, YongKeunKim, SangHoLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.1 10 75-82 (8 pages)
It has been reported that activation of sphingomyelin pathway and nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the promotion of colon carcinoma. Ceramide, a metabolite of sphingomyelin, and indomethacin were shown to induce apoptosis in colon carcinoma cells. However, the mechanisms of ceramide- and indomethacin-induced apoptosis in the colon carcinoma cells are not clearly elucidated. Recent studys showed that indomethacin-induced apoptosis in colon cancer cells through the... -
The Mechanism of t-Butylhydroperoxide-Induced Apoptosis in IMR- 32 Human Neuroblastoma Cells
Jung-AeKim, YongSooLee, KeunHuh 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.1 3 19-28 (10 pages)
butylhydroperoxide (TBHP), which was confirmed by significantly reduced glutathione content and glutathione reductase activity, and increased glutathione peroxidase activity. TBHP induced decrease in cell viability and increase in DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. TBHP also induced a sustained increase in intracellular Ca2 concentration, which was completely prevented either by EGTA, an extracellular Ca2 chelator or by flufenamic acid (FA), a... -
Effect of Cisplatin on Sodium-Dependent Hexose Transport in LLC-PK1 Renal Epithelial Cells
SukKyuLee, JeeYeunKim, TaiHyunYu, KyoungRyongKim, KwangHyukKim, YangSaengPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1997, Vol.1 No.1 5 35-43 (9 pages)
Cis-dichlorodiammine platinum II (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC-PK1 cell line was selected as a cell model and the sugar transport activity was evaluated during a course of cisplatin treatment. Cells grown to confluence were treated with cisplatin for 60 min, washed, and then incubated for up to 5 days. At appropriate...


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