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We investigated the effects of prostaglandin E 2  (PGE 2 ), an important inflammatory lipid mediator, on the cytotoxicity–genotoxicity induced by arsenite. With the use of a toxicity paradigm in which the metalloid uniquely induces mitochondrial superoxide (mitoO 2   −. ) formation, PGE 2  promoted conditions favoring the cytosolic accumulation of Bad and Bax and abolished mitochondrial permeability transition (MPT) and the ensuing lethal response through an E prostanoid receptor 2/adenylyl cyclase/protein kinase A (PKA) dependent signaling. It was, however, interesting to observe that, under the same conditions, PGE 2  also abolished the DNA-damaging effects of arsenite and that this response was associated with an unexpected suppression of mitoO 2   −.  formation. We conclude that PGE 2  promotes PKA-dependent inhibition of mitoO 2   −.  formation, thereby blunting the downstream responses mediated by these species, leading to DNA strand scission and MPT-dependent apoptosis. These findings are therefore consistent with the possibility that, in cells responding to arsenite with mitoO 2   −.  formation, PGE 2  fails to enhance—but rather decreases—the risk of neoplastic transformation associated with genotoxic events.

frontiers in pharmacology

Prostaglandin E2 Signals Through E Prostanoid Receptor 2 to Inhibit Mitochondrial Superoxide Formation and the Ensuing Downstream Cytotoxic and Genotoxic Effects Induced by Arsenite