Role of mitochondrial permeability transition in human renal tubular epithelial cell death induced by aristolochic acid
文献类型：期刊论文
| 作者 | Qi, Xinming ; Cai, Yan; Likun, Gong; Liu, Linlin; Chen, Fangping; Xiao, Ying; Wu, Xiongfei; Li, Yan; Xue, Xiang; Ren, Jin
|
| 刊名 | TOXICOLOGY AND APPLIED PHARMACOLOGY
 |
| 出版日期 | 2007-07-01 |
| 卷号 | 222期号:1页码:105-110 |
| 关键词 | aristolochic acid (AA) mitochondrial permeability transition (MPT) adenine nucleotide translocator (ANT) |
| ISSN号 | 0041-008X |
| DOI | 10.1016/j.taap.2007.03.029 |
| 文献子类 | Article |
| 英文摘要 | Aristolochic acid (AA), a natural nephrotoxin and carcinogen, can induce a progressive tubulointerstitial nephropathy. However, the mechanism by which AA causes renal injury remains largely unknown. Here we reported that the mitochondrial permeability transition (MPT) plays all important role in the renal injury induced by aristolochic acid I (AA1). We found that in the presence of Ca2+, AAI caused mitochondrial swelling. leakage of Ca2+ membrane depolarization, and release of cytochrome c in isolated kidney initochondria. These alterations were suppressed by cyclosporin A (CsA), an agent known to inhibit NIPT. Culture of HK-2 cell, a human renal tubular epithelial cell line for 24 h with AAI caused a decrease ill Cellular ATP, initochondrial membrane depolarization, cytochrome c release, and increase of caspase 3 activity. These toxic effects of AA1 were attenuated by CsA and bongkrekic acid (BA), another specific MPT inhibitor. Furthermore, AAI,really inhibited the activity of initochondrial adenine nucleotide translocator (ANT) in isolated rnitochondria. We suggested that ANT may mediate, at least in part, the AAI-induced NIPT. Taken together, these results suggested that MPT plays a critical role in the pathogenesis of HK-2 cell injury induced by AAI and implied that MPT might contribute to human nephrotoxicity of aristolochic acid. (c) 2007 Elsevier Inc. All rights reserved. |
| WOS关键词 | ADP/ATP CARRIER ; CHINESE HERBS ; MEMBRANE-PERMEABILITY ; CYTOCHROME-C ; APOPTOSIS ; NEPHROPATHY ; NECROSIS ; PATHWAY ; CYTOTOXICITY ; INDUCTION |
| WOS研究方向 | Pharmacology & Pharmacy ; Toxicology |
| 语种 | 英语 |
| WOS记录号 | WOS:000247853900011 |
| 出版者 | ACADEMIC PRESS INC ELSEVIER SCIENCE |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/273220]  |
| 专题 | 药物安全性评价中心 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
| 通讯作者 | Ren, Jin |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China 2.Chinese Acad Sci, Grad Sch, Shanghai, Peoples R China |
| 推荐引用方式 GB/T 7714 | Qi, Xinming,Cai, Yan,Likun, Gong,et al. Role of mitochondrial permeability transition in human renal tubular epithelial cell death induced by aristolochic acid[J]. TOXICOLOGY AND APPLIED PHARMACOLOGY,2007,222(1):105-110. |
| APA | Qi, Xinming.,Cai, Yan.,Likun, Gong.,Liu, Linlin.,Chen, Fangping.,...&Ren, Jin.(2007).Role of mitochondrial permeability transition in human renal tubular epithelial cell death induced by aristolochic acid.TOXICOLOGY AND APPLIED PHARMACOLOGY,222(1),105-110. |
| MLA | Qi, Xinming,et al."Role of mitochondrial permeability transition in human renal tubular epithelial cell death induced by aristolochic acid".TOXICOLOGY AND APPLIED PHARMACOLOGY 222.1(2007):105-110. |
入库方式： OAI收割
来源：上海药物研究所
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