Vol 63, No 4 (2004)
Original article
Published online: 2004-09-16
Fast perinuclear clustering of mitochondria in oxidatively stressed human choriocarcinoma cells
Folia Morphol 2004;63(4):407-412.
Abstract
Mitochondrial dysfunction plays a crucial role in cell types that exhibit necrosislike
death after activation of their death program. Tumour necrosis factor (TNF)
induces abnormal, perinuclear clustering of mitochondria from an evenly spread
distribution throughout the cytoplasm. The mitochondria withdraw from the
cell periphery and aggregate in a unipolar perinuclear cluster. TNF-induced mitochondrial
clustering is caused by impaired kinesin-mediated transportation of
mitochondria. In this report, we describe a novel activity of menadione (MEN),
namely the induction of an altered spatial distribution of mitochondria in the
choriocarcinoma JAR cells. Strikingly, 2 hours of cell exposition to menadione
did not disrupt the integrity of the plasma membrane, while the intracellular
ATP level significantly decreased. Control (untreated) cells displayed a typically
scattered distribution of filamentary mitochondria inside the cell. After 2 hours
of MEN treatment the spatial distribution of the mitochondria was markedly
altered to an asymmetric perinuclear clustered distribution. Menadione-stressed
cells displayed a highly asymmetrical perinuclear clustered distribution of the
mitochondria. The exposure of cells to MEN also results in a change in shape of
the mitochondria into a population of enlarged granular structures. The results
of our study demonstrate that in JAR cells menadione causes mitochondria to
translocate from the cell periphery into the perinuclear region several hours
before disruption of cell membrane integrity and cell death.
Keywords: JAR cellsmenadioneTNFoxidative stressmitochondrial translocation