ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells
Reactive oxygen species (ROS) are by-products of normal cell activity. They are produced in many cellular compartments and play a major role in signaling pathways. Overproduction of ROS is associated with the development of various human diseases (including cancer, cardiovascular, neurodegenerative,...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-17 |
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| creator | Dmitriev, Alexey A. Melnikova, Nataliya V. Savvateeva, Maria V. Kardymon, Olga L. Kudryavtseva, Anna V. Snezhkina, Anastasiya V. Krasnov, George S. |
| description | Reactive oxygen species (ROS) are by-products of normal cell activity. They are produced in many cellular compartments and play a major role in signaling pathways. Overproduction of ROS is associated with the development of various human diseases (including cancer, cardiovascular, neurodegenerative, and metabolic disorders), inflammation, and aging. Tumors continuously generate ROS at increased levels that have a dual role in their development. Oxidative stress can promote tumor initiation, progression, and resistance to therapy through DNA damage, leading to the accumulation of mutations and genome instability, as well as reprogramming cell metabolism and signaling. On the contrary, elevated ROS levels can induce tumor cell death. This review covers the current data on the mechanisms of ROS generation and existing antioxidant systems balancing the redox state in mammalian cells that can also be related to tumors. |
| doi_str_mv | 10.1155/2019/6175804 |
| format | Article |
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They are produced in many cellular compartments and play a major role in signaling pathways. Overproduction of ROS is associated with the development of various human diseases (including cancer, cardiovascular, neurodegenerative, and metabolic disorders), inflammation, and aging. Tumors continuously generate ROS at increased levels that have a dual role in their development. Oxidative stress can promote tumor initiation, progression, and resistance to therapy through DNA damage, leading to the accumulation of mutations and genome instability, as well as reprogramming cell metabolism and signaling. On the contrary, elevated ROS levels can induce tumor cell death. This review covers the current data on the mechanisms of ROS generation and existing antioxidant systems balancing the redox state in mammalian cells that can also be related to tumors.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2019/6175804</identifier><identifier>PMID: 31467634</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antioxidants ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Cancer therapies ; Cell Count ; Cell death ; Cell Transformation, Neoplastic - metabolism ; Cells ; Cytochrome ; Defense industry ; Dehydrogenases ; Deoxyribonucleic acid ; DNA ; Enzymes ; Genetic aspects ; Genomes ; Glycerol ; Humans ; Hydrogen peroxide ; Metabolism ; Mitochondria ; Mitochondrial DNA ; Oxidation ; Oxidative stress ; Physiological aspects ; Polyamines ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Review</subject><ispartof>Oxidative medicine and cellular longevity, 2019, Vol.2019 (2019), p.1-17</ispartof><rights>Copyright © 2019 Anastasiya V. Snezhkina et al.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>Copyright © 2019 Anastasiya V. Snezhkina et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Anastasiya V. Snezhkina et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-4e3ed5d6bf16bd8474dc3222897d28f18b1946fb94dc786e5af0e0737995f4d03</citedby><cites>FETCH-LOGICAL-c499t-4e3ed5d6bf16bd8474dc3222897d28f18b1946fb94dc786e5af0e0737995f4d03</cites><orcidid>0000-0002-3722-8207 ; 0000-0001-8083-3018 ; 0000-0002-6827-9584 ; 0000-0002-5593-7867 ; 0000-0002-6493-8378 ; 0000-0002-4421-4364</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6701375/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6701375/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31467634$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Isaguliants, Maria</contributor><creatorcontrib>Dmitriev, Alexey A.</creatorcontrib><creatorcontrib>Melnikova, Nataliya V.</creatorcontrib><creatorcontrib>Savvateeva, Maria V.</creatorcontrib><creatorcontrib>Kardymon, Olga L.</creatorcontrib><creatorcontrib>Kudryavtseva, Anna V.</creatorcontrib><creatorcontrib>Snezhkina, Anastasiya V.</creatorcontrib><creatorcontrib>Krasnov, George S.</creatorcontrib><title>ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Reactive oxygen species (ROS) are by-products of normal cell activity. They are produced in many cellular compartments and play a major role in signaling pathways. Overproduction of ROS is associated with the development of various human diseases (including cancer, cardiovascular, neurodegenerative, and metabolic disorders), inflammation, and aging. Tumors continuously generate ROS at increased levels that have a dual role in their development. Oxidative stress can promote tumor initiation, progression, and resistance to therapy through DNA damage, leading to the accumulation of mutations and genome instability, as well as reprogramming cell metabolism and signaling. On the contrary, elevated ROS levels can induce tumor cell death. This review covers the current data on the mechanisms of ROS generation and existing antioxidant systems balancing the redox state in mammalian cells that can also be related to tumors.</description><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Cancer therapies</subject><subject>Cell Count</subject><subject>Cell death</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cells</subject><subject>Cytochrome</subject><subject>Defense industry</subject><subject>Dehydrogenases</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Enzymes</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Glycerol</subject><subject>Humans</subject><subject>Hydrogen peroxide</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Physiological aspects</subject><subject>Polyamines</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Review</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0U1vEzEQBmALgWgp3Dijlbgg0VB_f1yQokALUqAShbPlXY9TV7veYm-A_vs6TUiBEyeP7EevZzQIPSf4DSFCnFBMzIkkSmjMH6BDYjidYWP4w32N8QF6UsoVxpJRTh6jA0a4VJLxQ7T8cn7RnEGC7KY4psYl38xTLX9F79LUvIMAqUBzcVMmGEoTU_N5zIPr7-Qn18dV2rgF9H15ih4F1xd4tjuP0LfT918XH2bL87OPi_ly1nFjphkHBl542QYiW6-54r5jlFJtlKc6EN3WxmVoTb1XWoJwAQNWTBkjAveYHaG329zrdTuA7yBN2fX2OsfB5Rs7umj_fknx0q7GH1YqTJgSNeDVLiCP39dQJjvE0tURXIJxXWzthRGsOVWVvvyHXo3rnOp4VSmBpajyXq1cDzamMNZ_u02onUtMMNWa8aqOt6rLYykZwr5lgu1mmXazTLtbZuUv_hxzj39vr4LXW3AZk3c_43_GQTUQ3L2mmHPN2C0DY65_</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Dmitriev, Alexey A.</creator><creator>Melnikova, Nataliya V.</creator><creator>Savvateeva, Maria V.</creator><creator>Kardymon, Olga L.</creator><creator>Kudryavtseva, Anna V.</creator><creator>Snezhkina, Anastasiya V.</creator><creator>Krasnov, George S.</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3722-8207</orcidid><orcidid>https://orcid.org/0000-0001-8083-3018</orcidid><orcidid>https://orcid.org/0000-0002-6827-9584</orcidid><orcidid>https://orcid.org/0000-0002-5593-7867</orcidid><orcidid>https://orcid.org/0000-0002-6493-8378</orcidid><orcidid>https://orcid.org/0000-0002-4421-4364</orcidid></search><sort><creationdate>2019</creationdate><title>ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells</title><author>Dmitriev, Alexey A. ; 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| subjects | Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Cancer therapies Cell Count Cell death Cell Transformation, Neoplastic - metabolism Cells Cytochrome Defense industry Dehydrogenases Deoxyribonucleic acid DNA Enzymes Genetic aspects Genomes Glycerol Humans Hydrogen peroxide Metabolism Mitochondria Mitochondrial DNA Oxidation Oxidative stress Physiological aspects Polyamines Reactive oxygen species Reactive Oxygen Species - metabolism Review |
| title | ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells |
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