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Am J Physiol Cell Physiol (August 22, 2002). doi:10.1152/ajpcell.00092.2002
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Articles in PresS, published online ahead of print August 22, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00092.2002
Submitted on February 28, 2002
Accepted on August 19, 2002

Endothelial cells maintain a reduced redox environment even as mitochondrial function declines

Ricarda Carlisle1, Carol A Rhoads1, Tak Yee Aw1, and Lynn Harrison1*

1 Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, LA, USA

* To whom correspondence should be addressed. E-mail: lclary{at}lsuhsc.edu.

Human umbilical vein endothelial cells (HUVECs) are an endothelial model of replicative senescence. Oxidative stress, possibly due to dysfunctional mitochondria, is believed to play a key role in replicative senescence and atherosclerosis, an age-related vascular disease. In this study, we determined the effect of cell division on genomic instability, mitochondrial function and redox status in HUVECs that were able to replicate for ~60 cumulative population doublings (CPD). After 20 CPD the nuclear genome deteriorated and the protein content of the cell population increased. This indicated an increase in cell size, which was accompanied by an increase in oxygen consumption, ATP production, mitochondrial genome copy number and ~10% increase in mitochondrial mass. The antioxidant capacity increased as seen by an increase in reduced glutathione, glutathione peroxidase, GSSG reductase and glucose-6-phosphate dehydrogenase. However, by CPD 52 the latter two enzymes decreased, as well as the ratio of mitochondrial to nuclear genome copies, the mitochondrial mass and the oxygen consumption/mg protein. Our results signify that HUVECs maintain a highly reducing (GSH) environment as they replicate despite genomic instability and loss of mitochondrial function.




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