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Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology
Volume 148, Issue 3, September 2008, Pages 204-210
 
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doi:10.1016/j.cbpc.2008.05.008    How to Cite or Link Using DOI (Opens New Window)
Copyright © 2008 Elsevier Inc. All rights reserved.

In vivo studies on the toxic effects of microcystins on mitochondrial electron transport chain and ion regulation in liver and heart of rabbit

Yanyan Zhaoa, Ping Xieb, a, Corresponding Author Contact Information, E-mail The Corresponding Author, Rong Tanga, b, Xuezhen Zhanga, Li Lia and Dapeng Lia, b

aFisheries College of Huazhong Agricultural University; Key Lab of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Wuhan 430070, People's Republic of China bDonghu Experimental Station of Lake Ecosystems, State Key Laboratory of Freshwater Ecology and Biotechnology of China, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, People's Republic of China

Received 29 March 2008; 
revised 19 May 2008; 
accepted 20 May 2008. 
Available online 27 May 2008.

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Abstract

This study examined the toxic effects of microcystins on mitochondria of liver and heart of rabbit in vivo. Rabbits were injected i.p. with extracted microcystins (mainly MC-RR and -LR) at two doses, 12.5 and 50 MC-LReq. µg/kg bw, and the changes in mitochondria of liver and heart were studied at 1, 3, 12, 24 and 48 h after injection. MCs induced damage of mitochondrial morphology and lipid peroxidation in both liver and heart. MCs influenced respiratory activity through inhibiting NADH dehydrogenase and enhancing succinate dehydrogenase (SDH). MCs altered Na+–K+-ATPase and Ca2+–Mg2+-ATPase activities of mitochondria and consequently disrupted ionic homeostasis, which might be partly responsible for the loss of mitochondrial membrane potential (MMP). MCs were highly toxic to mitochondria with more serious damage in liver than in heart. Damage of mitochondria showed reduction at 48 h in the low dose group, suggesting that the low dose of MCs might have stimulated a compensatory response in the rabbits.

Keywords: Ion regulation; Microcystins; Mitochondria; Oxidative stress; Respiratory chain enzymes; Ultrastructural changes

Article Outline

1. Introduction
2. Materials and methods
2 1. Toxin
2 2. Animals
2 3. Exposure and sampling
2 4. Isolation of mitochondria
2 5. Transmission electron microscopic observation
2 6. Analysis of lipid peroxidation (LPO)
2 7. Measurement of superoxide dismutase activity
2 8. Assays of respiratory chain enzymes
2 9. Measurement of ATPase activity
2 10. Statistical analysis
3. Results
3 1. Animal deaths
3 2. Ultrastructural change of mitochondria
3 3. MDA assays
3 4. SOD activity
3 5. Respiratory chain enzymes
3 6. ATPase activity
4. Discussion
Acknowledgements
References







 
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