| Mitochondrial defects and cytotoxicity by antimycin A on cultured osteoblastic MC3T3-E1 cells. | |
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MedLine Citation:
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PMID: 21601611 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Antimycin A (AMA), which inhibits complex III of the electron transport system, has been used as a reactive oxygen species (ROS) generator in biological systems. We investigated the effects of AMA on various parameters related to mitochondrial function in osteoblastic MC3T3-E1 cells. Here, we show that AMA-induced cell death was accompanied by the loss of ATP, complex I and IV activities, and mitochondrial membrane potential. Moreover, AMA stimulated oxidative stress and induced cytochrome c release from mitochondria in osteoblasts. Our data support AMA-induced death in osteoblasts via a mitochondria-dependent pathway. These biochemical changes in mitochondria were effectively prevented upon pre-treatment with ROS scavengers, indicating that ROS plays a critical role as an upstream controller in the AMA-induced cell dysfunction. |
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Authors:
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Eun Mi Choi; Young Soon Lee |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-5-12 |
Journal Detail:
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Title: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association Volume: - ISSN: 1873-6351 ISO Abbreviation: - Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-5-23 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8207483 Medline TA: Food Chem Toxicol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Food and Nutrition, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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