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Articles in PresS, published online ahead of print October 4, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00726.2001
Submitted on August 14, 2001
Accepted on October 3, 2001
1 Pathology and Laboratory Medicine, University of Texas Medical School, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: diane.l.bick{at}uth.tmc.edu.
The saturated fatty acid palmitate induces apoptosis in neonatal rat cardiomyocytes. This apoptosis is associated with early mitochondrial release of cytochrome c and a subsequent loss of mitochondrial membrane potential. Recent reports implicate a role for reactive oxygen species in palmitate-induced apoptosis. We studied the role of ROS in palmitate-induced apoptosis in the neonatal rat cardiomyocytes and report no evidence of ROS involvement. ROS production, NO production and NF
B activation were not increased above those observed using the non-apoptotic fatty acid, oleate. Indeed, the production of ROS was significantly higher in cells treated with oleate. Furthermore, the presence of antioxidants and ROS scavengers did not attenuate the induction of apoptosis by palmitate. Variations in the fatty acid to albumin ratio from 2:1 to 7:1 had no effect on the absence of ROS production or on the extent of apoptosis. No evidence was found for an increase in oxidative protein modification in palmitate-treated cells. Our results lead us to conclude that oxidative stress does not play a role in palmitate-induced apoptosis.
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