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The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat
Qiu, Tong; Xie, Ping; Liu, Ying; Li, Guangyu; Xiong, Qian; Hao, Le; Li, Huiying; Xie, P, Chinese Acad Sci, Donghu Expt Stn Lake Ecosyst, State Key Lab Freshwater Ecol & Biotechnol China, Inst Hydrobiol, Wuhan 430072, Peoples R China
2009-03-04
Source PublicationTOXICOLOGY
ISSN0300-483X
Volume257Issue:1-2Pages:86-94
AbstractDeaths 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.; 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.
SubtypeArticle
KeywordHeart Microcystin Mitochondria Oxidative Stress Physiological And Pathological Changes Real-time Pcr
Department[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
Subject AreaPharmacology & Pharmacy ; Toxicology
DOI10.1016/j.tox.2008.12.012
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Funding OrganizationNational Basic Research Program of China (973 Program) [2008CB418101] ; National Basic Research Program of China (973 Program) [2008CB418101] ; National Basic Research Program of China (973 Program) [2008CB418101] ; National Basic Research Program of China (973 Program) [2008CB418101]
Indexed BySCI
Language英语
WOS Research AreaPharmacology & Pharmacy ; Toxicology
WOS SubjectPharmacology & Pharmacy ; Toxicology
WOS IDWOS:000263654700012
WOS KeywordOXIDATIVE STRESS ; LIPID-PEROXIDATION ; IN-VIVO ; CARASSIUS-AURATUS ; COMPLEX-I ; LR ; OXYGEN ; HEART ; LIVER ; MEMBRANE
Funding OrganizationNational Basic Research Program of China (973 Program) [2008CB418101] ; National Basic Research Program of China (973 Program) [2008CB418101] ; National Basic Research Program of China (973 Program) [2008CB418101] ; National Basic Research Program of China (973 Program) [2008CB418101]
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Cited Times:45[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/152342/7848
Collection期刊论文
Corresponding AuthorXie, P, Chinese Acad Sci, Donghu Expt Stn Lake Ecosyst, State Key Lab Freshwater Ecol & Biotechnol China, Inst Hydrobiol, Wuhan 430072, Peoples R China
AffiliationChinese Acad Sci, Donghu Expt Stn Lake Ecosyst, State Key Lab Freshwater Ecol & Biotechnol China, Inst Hydrobiol, Wuhan 430072, Peoples R China
Recommended Citation
GB/T 7714
Qiu, Tong,Xie, Ping,Liu, Ying,et al. The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat[J]. TOXICOLOGY,2009,257(1-2):86-94.
APA Qiu, Tong.,Xie, Ping.,Liu, Ying.,Li, Guangyu.,Xiong, Qian.,...&Xie, P, Chinese Acad Sci, Donghu Expt Stn Lake Ecosyst, State Key Lab Freshwater Ecol & Biotechnol China, Inst Hydrobiol, Wuhan 430072, Peoples R China.(2009).The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat.TOXICOLOGY,257(1-2),86-94.
MLA Qiu, Tong,et al."The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat".TOXICOLOGY 257.1-2(2009):86-94.
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