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H2O2 induces translocation of APE/Ref-1 to mitochondria in the Raji B-cell line

✍ Scribed by Barbara Frossi; Gianluca Tell; Paola Spessotto; Alfonso Colombatti; Gaetano Vitale; Carlo Pucillo

Publisher
John Wiley and Sons
Year
2002
Tongue
English
Weight
243 KB
Volume
193
Category
Article
ISSN
0021-9541

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✦ Synopsis

Abstract

Reactive oxygen species (ROS) are generated as by‐products of respiration and are used as signal transducing intermediates in out–in signaling pathways. ROS are also generated during inflammatory responses and it has been shown that hydrogen peroxide may trigger activation of B‐lymphocytes, similar to cross‐linking of surface immunoglobulins. On the other hand, both exogenous and endogenous generated ROS are a major source of nuclear and mitochondrial DNA (mtDNA) damage. The base excision repair (BER) enzyme APE/Ref‐1 normally repairs small nuclear DNA lesion such as oxidized or alkylated bases. It is not clear though whether DNA repair mechanisms able to abolish oxidative damage from nuclear DNA are present into mitochondria too. Here we show by confocal microscopy and Western blot analysis that in the B‐lymphocyte Raji cell line a fraction of APE/Ref‐1 rapidly re‐localizes into mitochondria following H~2~O~2~ activation. Targeting of APE/Ref‐1 to mitochondria is not associated with cytochrome‐c loss or apoptosis induction. These findings indicate that the APE/Ref‐1 translocates to mitochondria in response to oxidative stress and thereby it might exert a protective function. © 2002 Wiley‐Liss, Inc.

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