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Involvement of Oxidative Stress and Poly(ADP-ribose) Polymerase Activation in 3-Nitropropionic Acid-induced Cytotoxicity in Human Neuroblastoma Cells
EunjooNam, YoungJaeLee, YoungAhOh, JinAhJung, HyeInIm, SeongEunKoh, SunghoMaeng, WanSeokJoo, YongSikKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.6 6 325-331 (7 pages)
3-Nitropropionic acid (3-NP) inhibits electron transport in mitochondria, leading to a metabolic failure. In order to elucidate the mechanism underlying this toxicity, we examined a few biochemical changes possibly involved in the process, such as metabolic inhibition, generation of reactive oxygen species (ROS), DNA strand breakage, and activation of Poly(ADP-ribose) polymerase (PARP). Exposure of SK-N-BE(2)C neuroblastoma cells to 3-NP for 48 h caused actual cell death, while inhibition of... -
PDTC Inhibits TNF-α-Induced Apoptosis in MC3T3E1 Cells
Han-JungChae, JeehyeonBae 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.4 2 199-205 (7 pages)
Osteoblasts are affected by TNF-α overproduction by immune cells during inflammation. It has been suggested that functional NF-κB sites are involved in TNF-α-induced bone resorption. Thus, we explored the effect of pyrrolidine dithiocarbamate (PDTC), which potently blocks the activation of nuclear factor (NF-κB), on the induction of TNF-α-induced activation of JNK/SAPK, AP-1, cytochrome c, caspase and apoptosis in MC3T3E1 osteoblasts. Pretreatment of the cells with PDTC blocked... -
Transduction of Tat-Superoxide Dismutase into Insulin-producing MIN6N Cells Reduces Streptozotocin-induced Cytotoxicity
InSoonChoung, WonSikEum, MingZhenLi, GyeSukSin, JungHoonKang, JinseuPark, SooYoungChoi, HyeokYilKwon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.3 7 163-168 (6 pages)
of Tat-SOD increased Bcl-2 and heat shock protein 70 (hsp70) expressions in cells exposed to STZ, which might be partly responsible for the effect of Tat-SOD. These results suggest that an increased of free radical scavenging activity by transduction of Tat-SOD enhanced the tolerance of the cell against oxidative stress in STZ-treated MIN6N cells. Therefore, this Tat-SOD transduction technique may provide a new strategy to protect the pancreatic β cell destruction in ROS-mediated diabetes. -
Involvement of NAD(P)H Oxidase in a Potential Link between Diabetes and Vascular Smooth Muscle Cell Proliferation
HyeYoungJeong, MiRanYun, ChiDaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.2 9 103-109 (7 pages)
a superoxide scavenger, but also by diphenyleneiodonium (DPI; 10μM), an NAD(P)H oxidase inhibitor. NAD(P)H oxidase activity in diabetic VSMC was significantly higher than that in control cell, accompanied with increased mRNA expression of p22phox, a membrane subunit of oxidase. Furthermore, inhibition of p22phox expression by transfection of antisense p22phox oligonucleotides into diabetic VSMC resulted in a decrease in superoxide production, which was accompanied by a significant inhibition of... -
The Protective Effect of Melatonin Administration against Adriamycin-induced Cardiotoxicity in Rats
JinHan, ChungheeKim, NariKim, JuheePark, YoungchurlYang, EuiyongKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.4 6 333-342 (10 pages)
stimulating the immune system, and acting as an antioxidant and radical scavenging effects. In the present study, we evaluated the effect of melatonin administration on adriamycin-induced cardiotoxicity in rat. Heart slices were prepared using a Stadie-Riggs microtome for the measurement of malondialdehyde (MDA) content used as an index of lipid peroxidation and lactate dehydrogenase (LDH) release as an indicator of lethal cell injury. Serious adriamycin-induced lethality was observed in rat by... -
Effect of Heme Oxygenase Induction by NO Donor on the Aortic Contractility
Chang-KyunKim, UyDongSohn, Seok-YongLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.1 12 87-92 (6 pages)
Carbon monoxide (CO) binds to soluble guanylate cyclase to lead its activation and elicits smooth muscle relaxation. The vascular tissues have a high capacity to produce CO, since heme oxygenase-2 (HO-2) is constitutively expressed in endothelial and smooth muscle cells, and HO-1 can be greatly up-regulated by oxidative stress. Moreover, the substrate of HO, heme, is readily available for catalysis in vascular tissue. Although the activation of heme oxygenase pathway under various stress... -
The Effect of Indomethacin on the Production of Eicosanoids and Edema during Ischemia-Reperfusion Injury in Skeletal Muscle
YoonJaeChung, ByungKyuSohn, KwangSoonHyun, SangHeeYoo, HyongKyunRyu, HyungGunKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.6 11 515-523 (9 pages)
During reperfusion of skeletal muscle after ischemia, lipid mediators, mainly eicosanoids, are released and may have a role in the pathogenesis of reperfusion injury. To validate the role of eicosanoids in the ischemia-reperfusion induced functional deficits in skeletal muscle, we compared muscle edema and the changes of eicosanoid concentration in the rat hind limb after ischemia-reperfusion injury by application of tourniquet. After 4 hours of ischemia, reperfusion was established for 4 hours... -
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)
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 apoptosis induced by each of the transition metal ions. Catalase or dimethylsulfoxide (DMSO) has less potent inhibitory effect on the apoptosis, compared with NAC, GSH or SOD. In line with the results, nitroblue tetrazolium (NBT) stain shows that each of the transition metals is a potent... -
Enhancement of Cyclosporine-Induced Oxidative Damage of Kidney Mitochondria by Iron
Yoon-YoungJang, Eun-SookHan, Chung-SooLee, Young-KiKim, Jin-HoSong, Yong-KyooShin 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.6 12 631-640 (10 pages)
The present study investigated the stimulatory effects of iron (or ascorbate) on cyclosporine-induced kidney mitochondrial damage. Damaging effect of 50 μM cyclosporine plus 20 μM Fe2 on mitochondrial lipids and proteins of rat kidney and hyaluronic acid was greater than the summation of oxidizing action of each compound alone, except sulfhydryl oxidation. Cyclosporine and 100 μM ascorbate showed an enhanced damaging effect on lipids but not on proteins. The peroxidative action of... -
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...


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