Understanding the survival mechanisms of Deinococcus radiodurans against oxidative stress by targeting thioredoxin reduc
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ORIGINAL PAPER
Understanding the survival mechanisms of Deinococcus radiodurans against oxidative stress by targeting thioredoxin reductase redox system Illiyas Maqbool1 · Veeramani kandan Ponniresan1 · Kanimozhi Govindasamy1,2 · Nagarajan Rajendra Prasad1 Received: 20 March 2019 / Revised: 31 August 2019 / Accepted: 13 September 2019 © Springer-Verlag GmbH Germany, part of Springer Nature 2019
Abstract The principal objective of this study is to determine the resistance of Deinococcus radiodurans to hydrogen peroxide ( H2O2) induced oxidative stress by inhibiting its thioredoxin reductase (TrxR) antioxidant system. Treatment of D. radiodurans with different TrxR inhibitors such as ebselen, epigallocatechin gallate and auranofin displayed this organism sensitivity to H2O2 treatment in a concentration-dependent manner. We observed that D. radiodurans showed greater resistance to H 2O 2 treatment. Further, it has also been noticed that TrxR redox system was suppressed by TrxR inhibitors and that this response might be associated with the oxidative stress-mediated cell death in D. radiodurans. Thus, TrxR inhibitors affect the resistance of the D. radiodurans through suppression of its thioredoxin redox pathway via the inhibition of TrxR. Results from this study proved that TrxR plays an important role as an antioxidant enzyme by scavenging intracellular ROS, and thus contributing to the resistance of D. radiodurans towards oxidative stress. Keywords Deinococcus radiodurans · Thioredoxin reductase · Inhibitors · Resistance · EGCG · Antioxidants
Introduction The Deinococcus radiodurans R1 is a Gram-positive bacterium able to withstand exposures to extreme gamma radiation, ultraviolet radiation, oxidants and desiccation (Mattimore and Battista 1996; Cox and Battista 2005; Dennis et al. 2006). Its capability to resist exposure to extremely challenging conditions has been attributed to its multipartite and ploid genome, ring-like nucleoid organization, high manganese content, efficient DNA strand break repair and a higher ability to tolerate reactive oxygen species (ROS) (Eltsov and Dubochet 2006; Sharma et al. 2013; Krisko and Radman 2013). However, the mechanism responsible for its extremophilic nature is not understood well. The capability Communicated by Erko Stackebrandt. * Nagarajan Rajendra Prasad [email protected] 1
Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamil Nadu 608 002, India
Dharumapurm Gnanambikai Government Arts College, Dharumapuram Road, Nagapattinam, Mayiladuthurai, Tamil Nadu 609001, India
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of D. radiodurans to repair genomic damage could also be due to the protection of its proteome from oxidative damage i.e. its capability to preserve sufficient enzymatic activity for genome repair post-irradiation (Slade and Radman 2011). D. radiodurans has higher levels of antioxidant enzymatic systems and disturbance of superoxide dismutase (sod A) and catalase (kat A) genes resulted in amplified sensitivity of D. radiodurans to ionizing radiation e
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