Mitochondrial defects and cytotoxicity by antimycin A on cultured osteoblastic MC3T3-E1 cells

作者：Choi Eun Mi^*; Lee Young Soon

来源：Food and Chemical Toxicology, 2011, 49(9): 2459-2463.

DOI：10.1016/j.fct.2011.04.037

• Mitochondrial dysfunction
• Osteoblastic MC3T3-E1 cells
• Antimycin A

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 land 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.

• 出版日期2011-9