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A more recent version of this article appeared on April 1, 2005

Papers In Press, published online ahead of print January 16, 2005
J. Lipid Res., doi:10.1194/jlr.M400392-JLR200
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Submitted on October 7, 2004
Revised on December 21, 2004
Accepted on January 10, 2005

The mitochondrial respiratory complex I is a target for 15 deoxy-delta-12,14-PGJ2 (15d-PGJ2) action

B. Martinez, A. Perez-Castillo, and A. Santos

Facultad de Medicina, Universidad Complutense, Madrid 28040

Corresponding Author: piedras3{at}med.ucm.es

The prostaglandin J2 derivate 15 deoxy-delta-12,14-PGJ2 (15d-PGJ2) is a very active compound with important effects on inflammation, apoptosis, and cell growth processes. To exert this broad range of effects, 15d-PGJ2 binds and alters the activity of diverse proteins, which consequently are postulated to be mediators of its action. Among them are the transcription factors PPARgamma and NF-kB, thought to play an essential role in the anti-tumorigenic and anti-inflammatory actions of 15d-PGJ2. Here, we show that 15d-PGJ2, at micromolar concentrations, efficiently blocks state 3 oxygen consumption in intact non-synaptic mitochondria isolated from rat cerebral cortex. This effect is due to the inhibition by this prostaglandin of the activity of the enzyme NADH-ubiquinone reductase (complex I) of the mitochondrial respiratory chain. In addition to this, 15d-PGJ2 dramatically increases the rate of ROS generation by complex I. The inhibition by 15d-PGJ2 of complex I activity was abolished by dithiothreitol, which rises the possibility that adduct formation with a critical component of complex I accounts for the inhibitory effect of this prostaglandin. These results clearly identify mitochondrial complex I as a new target for 15d-PGJ2 actions.


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