کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1939216 | 1050757 | 2006 | 7 صفحه PDF | دانلود رایگان |
We investigated the effect of parkin on mitochondrial function and apoptosis in SH-SY5Y, L6, RD, and COS-1 cells. Wild-type parkin attenuated reactive oxygen species (ROS) production in SH-SY5Y cells and mutant parkin enhanced ROS production in SH-SY5Y and L6 cells. Reactive oxygen intermediates, that were detected in mitochondria, were decreased in cells with overexpression of parkin. Parkin prevented apoptosis and enhanced mitochondrial membrane potentials in SH-SY5Y and L6 cells not in COS-1 cells. Expressions and enzymatic activities of mitochondrial respiratory chain complexes were not uniformly enhanced but those of complex 1 were selectively enhanced. The present results suggest the cell-selective function of parkin, i.e., parkin possesses anti-apoptotic and anti-oxidant function in neuronal or myogenic cells but not in kidney cells.
Journal: Biochemical and Biophysical Research Communications - Volume 348, Issue 3, 29 September 2006, Pages 787–793