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전체 선택해제
총 95건 검색
본문검색 결과만 보기
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Alterations in antioxidant function and cell apoptosis in duck spleen exposed to molybdenum and/or cadmium
Mengmeng Zhang, Junrong Luo, Caiying Zhang, Huabin Cao, Bing Xia, Guoliang Hu 대한수의학회 Journal of Veterinary Science 8 Pages
대한수의학회 Journal of Veterinary Science 2017, 제 18권 제 2호 9 193-200 (8 pages)
To investigate the effects of molybdenum (Mo) and/or cadmium (Cd) on antioxidant function and the apoptosis-related genes in duck spleens. Sixty healthy 11-day-old ducks were randomly divided into six groups of 10 ducks (control, low Mo group, high Mo, Cd, low Mo + Cd, and high Mo + Cd groups). All were fed a basal diet containing low or high dietary doses of Mo and/or Cd. Relative spleen weight, antioxidant indices, apoptosis-related gene mRNA expression levels, and ultrastructural changes were... -
Cadmium induces apoptosis in primary rat osteoblasts through caspase and mitogen-activated protein kinase pathways
Hongyan Zhao, Wei Liu, Yi Wang, Nannan Dai, Jianhong Gu, Yan Yuan, Xuezhong Liu, Jianchun Bian, Zong-Ping Liu 대한수의학회 Journal of Veterinary Science 10 Pages
대한수의학회 Journal of Veterinary Science 2015, 제 16권 제 3호 7 297-306 (10 pages)
Exposure to cadmium (Cd) induces apoptosis in osteoblasts (OBs); however, little information is available regarding the specific mechanisms of Cd-induced primary rat OB apoptosis. In this study, Cd reduced cell viability, damaged cell membranes and induced apoptosis in OBs. We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increased concentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment.... -
The Critical Roles of Zinc: Beyond Impact on Myocardial Signaling
SungRyulLee, SuJinNoh, JuliusRyanPronto, YuJeongJeong, HyoungKyuKim, InSungSong, ZhelongXu, HyogYoungKwon, SeChanKang, Eun-HwaSohn, KyungS 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 12 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.5 1 389-400 (12 pages)
in cellular processes. Whole body and cellular Zn2+ levels are largely regulated by metallothioneins (MTs), Zn2+ importers (ZIPs), and Zn2+ transporters (ZnTs). Numerous proteins involved in signaling pathways, mitochondrial metabolism, and ion channels that play a pivotal role in controlling cardiac contractility are common targets of Zn2+. However, these regulatory actions of Zn2+ are not limited to the function of the heart, but also extend to numerous other organ systems, such as the central... -
Bis is Induced by Oxidative Stress via Activation of HSF1
HyungJaeYoo, Chang-NimIm, Dong-YeYoun, HyeHyeonYun, Jeong-HwaLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2014, Vol.18 No.5 8 403-409 (7 pages)
The Bis protein is known to be involved in a variety of cellular processes including apoptosis, migration, autophagy as well as protein quality control. Bis expression is induced in response to a number of types of stress, such as heat shock or a proteasome inhibitor via the activation of heat shock factor (HSF)1. We report herein that Bis expression is increased at the transcriptional level in HK-2 kidney tubular cells and A172 glioma cells by exposure to oxidative stress such as H2O2 treatment... -
Neuroprotective Effects of Lithium on NMDA-induced Excitotoxicity in Mouse Cerebrum
Gee-younKwon, Soo-kyungKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 12 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.3 1 111-122 (12 pages)
Neuroprotective properties of lithium were evaluated by using in vivo NMDA excitotoxicity model. Systemic injection of NMDA to young mice induced neuronal apoptosis mediated by both TNFR-1 and Fas ligand, and long-term lithium treatment showed noticeable neuroprotection against NMDA-induced excitotoxicity: NMDA-damaged neurons expressed several apoptosis-related gene products such as TNFR-1, Fas ligand, and caspase-3, and these gene expressions were not found in the brain of mice chronically... -
Lysophosphatidylcholine Attenuates Endothelium-dependent Relaxation Responses through Inhibition of ACh-induced Endothelial [Ca2+]i Increase
Seong-ChunKwon, Yong-HoLee, TaicksangNam, Duck-SunAhn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.1 5 25-30 (6 pages)
Lysophosphatidylcholine (LPC), which accumulates in atherosclerotic arteries, has been reported to inhibit endothelium-dependent relaxation (EDR) in many different species. However, the underlying mechanism of LPC-induced inhibition of EDR is still uncertain. In the present study, we measured simultaneously both isometric tension and cytosolic free Ca2 ([Ca2]i) in rabbit carotid strips, and examined the effect of LPC on tension and [Ca2]i. In carotid strips with... -
Mechanism of Acetylcholine-induced Endothelium-dependent Relaxation in the Rabbit Carotid Artery by M3-receptor Activation
Yong-JinSong, Seong-ChunKwon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.6 4 313-318 (6 pages)
The present study were designed to characterize the action mechanisms of acetylcholine (ACh)- induced endothelium-dependent relaxation in arteries precontracted with high K (70 mM). For this, we simultaneously measured both muscle tension and cytosolic free Ca2 concentration ([Ca2]i), using fura-2, in endothelium-intact, rabbit carotid arterial strips. In the artery with endothelium, high K increased both [Ca2]i and muscle tension whereas ACh (10μM)... -
Renal Handling of Sodium and Potassium in Cadmium Exposed Rats
YungKyuKimYangSaengPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1998, Vol.2 No.4 12 503-510 (8 pages)
load was decreased by reduction in GFR, but the renal Na excretion returned to the control level due to impaired Na transport in the proximal tubule. Urinary excretion of K did not change during the early phase, but it rose markedly during the late phase of cadmium treatment. These results indicate that a light cadmium intoxication induces a Na retention, and a heavy intoxication results in a K loss. Possible mechanisms for these changes are discussed.
