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学科主题: Pharmacology & Pharmacy; Toxicology
题名: The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat
作者: Qiu, Tong1; Xie, Ping1; Liu, Ying1; Li, Guangyu1; Xiong, Qian1; Hao, Le1; Li, Huiying1
通讯作者: Xie, P, Chinese Acad Sci, Donghu Expt Stn Lake Ecosyst, State Key Lab Freshwater Ecol & Biotechnol China, Inst Hydrobiol, Wuhan 430072, Peoples R China
关键词: Heart ; Microcystin ; Mitochondria ; Oxidative stress ; Physiological and pathological changes ; Real-time PCR
刊名: TOXICOLOGY
发表日期: 2009-03-04
DOI: 10.1016/j.tox.2008.12.012
卷: 257, 期:1-2, 页:86-94
收录类别: SCI
文章类型: Article
部门归属: [Qiu, Tong; Xie, Ping; Liu, Ying; Li, Guangyu; Xiong, Qian; Hao, Le; Li, Huiying] Chinese Acad Sci, Donghu Expt Stn Lake Ecosyst, State Key Lab Freshwater Ecol & Biotechnol China, Inst Hydrobiol, Wuhan 430072, Peoples R China
WOS标题词: Science & Technology ; Life Sciences & Biomedicine
资助者: National Basic Research Program of China (973 Program) [2008CB418101]
类目[WOS]: Pharmacology & Pharmacy ; Toxicology
研究领域[WOS]: Pharmacology & Pharmacy ; Toxicology
摘要: Deaths from microcystin toxication have widely been attributed to hypovolemic shock due to hepatic interstitial hemorrhage, while some recent studies suggest that cardiogenic complication is also involved. So far, information on cardiotoxic effects of MC has been rare and the underlying mechanism is still puzzling. The present study examined toxic effects of microcystins on heart muscle of rats intravenously injected with extracted MC at two doses, 0.16LD(50) (14 mu g MC-LReq kg(-1) body weight) and 1LD(50) (87 mu g MC-LReq kg(-1) body weight). In the dead rats, both TTC staining and maximum elevations of troponin I levels confirmed myocardial infarction after MC exposure, besides a serious interstitial hemorrhage in liver. In the 1LD(50) dose group, the coincident falls in heart rate and blood pressure were related to mitochondria dysfunction in heart, while increases in creatine kinase and troponin I levels indicated cardiac cell injury. The corresponding pathological alterations were mainly characterized as loss of adherence between cardiac myocytes and swollen or ruptured mitochondria at the ultrastructural level. MC administration at a dose of 1LD(50) not only enhanced activities and up-regulated mRNA transcription levels of antioxidant enzymes, but also increased GSH content. At both doses, level of lipid peroxides increased obviously, suggesting serious oxidative stress in mitochondria. Simultaneously. complex I and III were significantly inhibited, indicating blocks in electron flow along the mitochondrial respiratory chain in heart. In conclusion, the findings of this study implicate a role for MC-induced cardiotoxicity as a potential factor that should be considered when evaluating the mechanisms of death associated with microcystin intoxication in Brazil. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
英文摘要: Deaths from microcystin toxication have widely been attributed to hypovolemic shock due to hepatic interstitial hemorrhage, while some recent studies suggest that cardiogenic complication is also involved. So far, information on cardiotoxic effects of MC has been rare and the underlying mechanism is still puzzling. The present study examined toxic effects of microcystins on heart muscle of rats intravenously injected with extracted MC at two doses, 0.16LD(50) (14 mu g MC-LReq kg(-1) body weight) and 1LD(50) (87 mu g MC-LReq kg(-1) body weight). In the dead rats, both TTC staining and maximum elevations of troponin I levels confirmed myocardial infarction after MC exposure, besides a serious interstitial hemorrhage in liver. In the 1LD(50) dose group, the coincident falls in heart rate and blood pressure were related to mitochondria dysfunction in heart, while increases in creatine kinase and troponin I levels indicated cardiac cell injury. The corresponding pathological alterations were mainly characterized as loss of adherence between cardiac myocytes and swollen or ruptured mitochondria at the ultrastructural level. MC administration at a dose of 1LD(50) not only enhanced activities and up-regulated mRNA transcription levels of antioxidant enzymes, but also increased GSH content. At both doses, level of lipid peroxides increased obviously, suggesting serious oxidative stress in mitochondria. Simultaneously. complex I and III were significantly inhibited, indicating blocks in electron flow along the mitochondrial respiratory chain in heart. In conclusion, the findings of this study implicate a role for MC-induced cardiotoxicity as a potential factor that should be considered when evaluating the mechanisms of death associated with microcystin intoxication in Brazil. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
关键词[WOS]: OXIDATIVE STRESS ; LIPID-PEROXIDATION ; IN-VIVO ; CARASSIUS-AURATUS ; COMPLEX-I ; LR ; OXYGEN ; HEART ; LIVER ; MEMBRANE
语种: 英语
WOS记录号: WOS:000263654700012
ISSN号: 0300-483X
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.ihb.ac.cn/handle/152342/7848
Appears in Collections:中科院水生所知识产出(2009年前)_期刊论文

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作者单位: 1.Chinese Acad Sci, Donghu Expt Stn Lake Ecosyst, State Key Lab Freshwater Ecol & Biotechnol China, Inst Hydrobiol, Wuhan 430072, Peoples R China

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Qiu, Tong; Xie, Ping; Liu, Ying; Li, Guangyu; Xiong, Qian; Hao, Le; Li, Huiying.The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat,TOXICOLOGY,2009,257(1-2):86-94
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