Reactive oxygen species and the implication in Biomedicine
Abstract
Reactive oxygen species (ROS) act as intracellular regulator when they are generated under control in specific cell spots. They modify proteins function by cysteine reversible oxidation. There are protein kinases and phosphatases, transcription factors and ionic channels that are regulated by ROS. Oxidative stress and cell damage arise when the protection antioxidant mechanisms are unable to keep low the intracellular ROS level. Under these conditions, ROS induce cell viability loss in heart and brain degenerative pathologies and promote unlimited cell proliferation in tumor processes. Alteration of the mitochondrial function is a key player in the oxidative stress generation and therefore it is preferential therapeutic target for prevention or attenuation of the ROS-induced oxidative damage.
Downloads
References
BEDARD K, KRAUSE KH. 2007. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol. Rev. 87: 245-313.
BUETLER TM, KRAUSKOPF A, RUEGG UT. 2004. Role of superoxide as a signaling molecule. News Physiol. Sci. 19: 120-123.
CADENAS S. 2018. ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection. Free Radic. Biol. Med. 117: 76-89.
DEBERARDINIS JR, CHANDEL NS. 2016. Fundamentals of cancer metabolism. Sci. Adv. 2: e1600200.
DRÖGE W. 2002. Free radicals in the physiological control of cell function. Physiol. Rev. 82: 47-95.
DWORAKOWSKI R, ANILKUMAR N, ZHANG M, SHAH AM. 2006. Redox signalling involving NADPH oxidase-derived reactive oxygen species. Biochem. Soc. Trans. 34: 960-964.
FINKEL T. 2011. Signal transduction by reactive oxygen species. J. Cell Biol. 194: 7-15.
HELD P. 2015. An introduction to reactive oxygen species. Measurement of ROS in cells.https://www.biotek.com/assets/tech_resources/ROS%20White%20Paper_2015.pdf
KALOGERIS T, BAO Y, KORTHUIS RJ. 2014. Mitochondrial reactive oxygen species: A double edged sword in ischemia/reperfusion vs preconditioning. Redox Biol. 2: 702-714.
KIM GH, KIM JE, RHIE SJ, YOON S. 2015. The role of oxidative stress in neurodegenerative diseases. Exp. Neurobiol. 24: 325-340.
KUMARI S, BADANA AK, G MM, G S, MALLA R. 2018. Reactive oxygen species: A key constituent in cancer survival. Biomark. Insights 13: 1-9.
LENNICKE C, RAHN J, LICHTENFELS R, WESSJOHANN LA, SELIGER B. 2015. Hydrogen peroxide - production, fate and role in redox signaling of tumor cells. Cell Commun. Signal. 13-39.
LIN MT, BEAL F. 2006. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 443: 787-795.
LIU Z, ZHOU T, ZIEGLER AC, DIMITRION P, ZUO L. 2017. Oxidative stress in neurodegenerative diseases: from molecular mechanisms to clinical applications. Oxid. Med. Cell. Longev. 2017: 2525967.
LUSHCHAK VI. 2014. Free radicals, reactive oxygen species, oxidative stress and its classification. Chem. Biol. Interact. 224: 164-175.
MAEJIMA Y, KURODA J, MATSUSHIMA S, AGO T, SADOSHIMA J. 2011. Regulation of myocardial growth and death by NADPH oxidase. J. Mol. Cell. Cardiol. 50: 408-416.
RHEE SG. 2006. A necessary evil for cell signaling. Science 312: 1882-1883.
SAG CM, SANTOS CX, SHAH AJ. 2014. Redox regulation of cardiac hypertrophy. J. Mol. Cell. Cardiol. 73: 103-109.
SCHIEBER M, CHANDEL NS. 2014. ROS function in redox signaling and oxidative stress. Curr. Biol. 24: R453-R462.
WINTERBOURN CC, HAMPTON MB. 2008. Thiol chemistry and specificity in redox signaling. Free Radic. Biol. Med. 45: 549-561.
YANG W, ZOU L, HUANG C, LEI Y. 2014. Redox regulation of cancer metastasis: molecular signaling and therapeutic opportunities. Drug Dev. Res. 75: 331-341.
Copyright (c) 2020 Anales de Veterinaria de Murcia
This work is licensed under a Creative Commons Attribution 4.0 International License.
Creative Commons Attribution 4.0
The works published in this journal are subject to the following terms:
1. The Publications Service of the University of Murcia (the publisher) retains the property rights (copyright) of published works, and encourages and enables the reuse of the same under the license specified in paragraph 2.
© Servicio de Publicaciones, Universidad de Murcia, 2019
2. The works are published in the online edition of the journal under a Creative Commons Attribution-NonCommercial 4.0 (legal text). You can copy, use, distribute, transmit and publicly display, provided that: i) you cite the author and the original source of publication (journal, editorial and URL of the work), ii) are not used for commercial purposes, iii ) mentions the existence and specifications of this license.
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
3. Conditions of self-archiving. Is allowed and encouraged the authors to disseminate electronically pre-print versions (version before being evaluated and sent to the journal) and / or post-print (version reviewed and accepted for publication) of their works before publication, as it encourages its earliest circulation and diffusion and thus a possible increase in its citation and scope between the academic community. RoMEO Color: Green.