Oxidative stress protection and the repair response to hydrogen peroxide in the hyperthermophilic archaeon Pyrococcus fu
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ORIGINAL PAPER
Oxidative stress protection and the repair response to hydrogen peroxide in the hyperthermophilic archaeon Pyrococcus furiosus and in related species Kari R. Strand · Chengjun Sun · Ting Li · Francis E. Jenney Jr. · Gerrit J. Schut · Michael W. W. Adams
Received: 28 September 2009 / Revised: 23 March 2010 / Accepted: 25 March 2010 / Published online: 9 April 2010 © Springer-Verlag 2010
Abstract Pyrococcus furiosus is a shallow marine, anaerobic archaeon that grows optimally at 100°C. Addition of H2O2 (0.5 mM) to a growing culture resulted in the cessation of growth with a 2-h lag before normal growth resumed. Whole genome transcriptional proWling revealed that the main response occurs within 30 min of peroxide addition, with the up-regulation of 62 open reading frames (ORFs), 36 of which are part of 10 potential operons. More than half of the up-regulated ORFs are of unknown function, while some others encode proteins that are involved potentially in sequestering iron and sulWde, in DNA repair and in generating NADPH. This response is thought to involve primarily damage repair rather than protection, since cultures exposed to sub-toxic levels of H2O2 were not
more resistant to the subsequent addition of H2O2 (0.5– 5.0 mM). Consequently, there is little if any induced protective response to peroxide. The organism maintains a constitutive protective mechanism involving high levels of oxidoreductase-type enzymes such as superoxide reductase, rubrerythrin, and alkyl hydroperoxide reductase. Related hyperthermophiles contain homologs of the proteins involved in the constitutive protective mechanism but these organisms were more sensitive to peroxide than P. furiosus and lack several of its peroxide-responsive ORFs. Keywords Hyperthermophile · Anaerobic · Oxidative stress · Peroxide response
Introduction Communicated by Harald Huber. Electronic supplementary material The online version of this article (doi:10.1007/s00203-010-0570-z) contains supplementary material, which is available to authorized users. K. R. Strand · C. Sun · T. Li · F. E. Jenney Jr. · G. J. Schut · M. W. W. Adams (&) Department of Biochemistry and Molecular Biology, University of Georgia, Life Sciences Bldg., Athens, GA 30602-7229, USA e-mail: [email protected] Present Address: K. R. Strand Department of Molecular Biosciences, University of Oslo, Oslo, Norway Present Address: F. E. Jenney Jr. Department of Basic Sciences, Georgia Campus Philadelphia College of Osteopathic Medicine, Suwanee, GA 30024, USA
Oxidative stress is a universal phenomenon experienced by both aerobic and anaerobic organisms from all three domains of life (Imlay 2003, 2008a, b; Jenney et al. 1999). There is evidence that oxidative damage is related to mutagenesis, aging, and a variety of human diseases, including cancer. Oxidative stress is caused by reactive oxygen species (ROS) that are formed by the incomplete reduction of oxygen, such as the superoxide radical (O2¡), hydrogen peroxide (H2O2), and the hydroxyl radical (OH•) (Fridovich 1978). ROS are also ge
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