Record number :
Title of article :
Mitochondrial defects and cytotoxicity by antimycin A on cultured osteoblastic MC3T3-E1 cells
Author/Authors :
Choi، نويسنده , , Eun Mi and Lee، نويسنده , , Young Soon، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2011
Pages :
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Abstract :
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.
Keywords :
Mitochondrial dysfunction , Osteoblastic MC3T3-E1 cells , Antimycin A
Journal title :
Food and Chemical Toxicology
Journal title :
Food and Chemical Toxicology
Serial Year :
Link To Document :