title: Mitochondrial defects and cytotoxicity by antimycin A on cultured osteoblastic MC3T3-E1 cells.
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.
authors: Department of Food and Nutrition, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea. cheunmi@hanmail.net
authors: Eun Mi
authors: EM
authors: Choi
authors: Young Soon
authors: YS
authors: Lee