| Autor: |
Choi EM; a Department of Endocrinology & Metabolism , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Suh KS; a Department of Endocrinology & Metabolism , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Rhee SY; a Department of Endocrinology & Metabolism , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Oh S; a Department of Endocrinology & Metabolism , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Kim SW; a Department of Endocrinology & Metabolism , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Pak YK; b Department of Physiology , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Choe W; c Department of Biochemistry and Molecular Biology (BK21 project) , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Ha J; c Department of Biochemistry and Molecular Biology (BK21 project) , School of Medicine, Kyung Hee University , Seoul , Republic of Korea., Chon S; a Department of Endocrinology & Metabolism , School of Medicine, Kyung Hee University , Seoul , Republic of Korea. |
| Abstrakt: |
This study was undertaken to investigate the possible involvement of oxidative stress in tetrabromobisphenol A (TBBPA)-induced toxicity in osteoblastic MC3T3-E1 cells. To examine the potential effect of TBBPA on cultured osteoblastic cells, we measured cell viability, apoptosis, reactive oxygen species (ROS), mitochondrial superoxide, and mitochondrial parameters including adenosine triphosphate (ATP) level, cardiolipin content, cytochrome c release, cyclophilin levels, and differentiation markers in osteoblastic MC3T3-E1 cells. TBBPA exposure for 48 h caused the apoptosis and cytotoxicity of MC3T3-E1 cells. TBBPA also induced ROS and mitochondrial superoxide production in a concentration-dependent manner. These results suggest that TBBPA induces osteoblast apoptosis and ROS production, resulting in bone diseases. Moreover, TBBPA induced cardiolipin peroxidation, cytochrome c release, and decreased ATP levels which induced apoptosis or necrosis. TBBPA decreased the differentiation markers, collagen synthesis, alkaline phosphatase activity, and calcium deposition in cells. Additionally, TBBPA decreased cyclophilin A and B releases. Taken together, these data support the notion that TBBPA inhibits osteoblast function and has detrimental effects on osteoblasts through a mechanism involving oxidative stress and mitochondrial dysfunction. |
