Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1977417 | Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology | 2011 | 16 Pages |
Abstract
Reactive oxygen species (ROS) are continuously produced and eliminated by living organisms normally maintaining ROS at certain steady-state levels. Under some circumstances, the balance between ROS generation and elimination is disturbed leading to enhanced ROS level called “oxidative stress”. The primary goal of this review is to characterize two principal mechanisms of protection against oxidative stress - regulation of membrane permeability and antioxidant potential. The ancillary goals of this work are to describe up to date knowledge on the regulation of the previously mentioned mechanisms and to identify areas of prospective research and emerging directions in investigation of adaptation to oxidative stress. The ubiquity for challenges leading to oxidative stress development calls for identification of common mechanisms. They are cysteine residues and [Fe,S]-clusters of specific regulatory proteins. The latter mechanism is realized via SoxR bacterial protein, whereas the former mechanism is involved in operation of bacterial OxyR regulon, yeast H2O2-stimulon, plant NPR1/TGA and Rap2.4a systems, and animal Keap1/Nrf2, NF-κB and AP-1, and others. Although hundreds of studies have been carried out in the field with different taxa, the comparative analysis of adaptive response is quite incomplete and therefore, this work aims to cover a plethora of phylogenetic groups to delineate common mechanisms. In addition, this article raises some questions to be elucidated and points out future directions of this research. The comparative approach is used to shed light on fundamental principles and mechanisms of regulation of antioxidant systems. The idea is to provide starting points from which we can develop novel tools and hypothesis to facilitate meaningful investigations in the physiology and biochemistry of organismic response to oxidative stress.
Keywords
NPR1CRDMPTAP-1HIF-1αPKCIKKVCAM-1IKBCUL3DPHG6PDHinhibitory protein of NF-κBGSH1NF-κBIkB kinaseTMA-DPHOxyRTRX2MAP-kinasesSoxRSTrimethylammonium diphenylhexatrieneGSH2soxRalkylhydroperoxide reductaseγ-glutamylcysteine synthaseouter membrane protein FSARPPARMDRRNSAHRNOSnESbZIPNrf2ERKGSHEpRENO-synthaseOmpFPKR-like endoplasmic reticulum kinaseROSjasmonic acidSalicylic acidmitochondrial permeability transition poreThioredoxin reductase 1Oxidative stresscysteine rich domainDiphenylhexatrieneSODsuperoxide dismutasessystemic acquired resistanceNF-E2-related factor 2antioxidant response elementelectrophile response elementnuclear factor-κBMultidrug resistanceVascular cell adhesion molecule 1AREKelch-like ECH-associated protein 1Protein kinase CPERKPathogenesis-related geneCullin 3extracellular signal-regulated kinasesmitogen-activated protein kinasesGlutathioneglutathione synthaseGlutathione peroxidasesglucose-6-phosphate dehydrogenasereactive nitrogen speciesReactive speciesReactive oxygen speciesaryl hydrocarbon receptorperoxisome proliferator-activated receptor
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Authors
Volodymyr I. Lushchak,