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Toxicol In Vitro. 2011 Aug;25(5):1085-8. doi: 10.1016/j.tiv.2011.03.022. Epub 2011 Apr 3.

Involvement of PI3K/Akt/CREB and redox changes in mitochondrial defect of osteoblastic MC3T3-E1 cells.

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Department of Food and Nutrition, Kyung Hee University, 1, Hoegi-Dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea.


Antimycin A (AMA) is an inhibitor of mitochondrial electron transport via its binding to complex III. In the present study, the mechanisms involved in AMA-induced cell damage were investigated. Treatment of osteoblastic MC3T3-E1 cells with AMA decreased adenosine 3',5'-cyclic monophosphate (cAMP) level, activities of phosphoinositide 3-kinase (PI3K) and Akt (protein kinase B), and phosphorylated CREB (cAMP-response element-binding protein). To examine whether AMA-induced cell damage involves altered metabolism of pyridine nucleotides, the levels of NAD(+), NADH, NADP(+), and NADPH were measured. Treatment with AMA significantly decreased the levels of NAD(+) and NADPH. Moreover, the activities of aconitase and thioredoxin reductase were decreased by AMA treatment. These results suggest that PI3K/Akt/CREB pathway and pyridine nucleotide (NAD(+) and NADPH) are related to mitochondria function of osteoblasts.

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