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Damage of DNA and proteins by major lipid peroxidation products in genome stability

Damage of DNA and proteins by major lipid peroxidation products in genome stability AbstractOxidative stress and lipid peroxidation (LPO) accompanying infections and chronic inflammation may induce several human cancers. LPO products are characterized by carbohydrate chains of different length, reactive aldehyde groups and double bonds, which make these molecules reactive to nucleic acids, proteins and cellular thiols. LPO-derived adducts to DNA bases form etheno-type and propano-type exocyclic rings, which have profound mutagenic potential, and are elevated in several cancer-prone diseases. Adducts of long chain LPO products to DNA bases inhibit transcription. Elimination from DNA of LPO-induced lesions is executed by several repair systems: base excision repair (BER), direct reversal by AlkB family proteins, nucleotide excision repair (NER) and recombination. Modifications of proteins with LPO products may regulate cellular processes like apoptosis, cell signalling and senescence. This review summarizes consequences of LPO products’ presence in cell, particularly 4-hydroxy-2-nonenal, in terms of genomic stability. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Free Radical Research Taylor & Francis

Damage of DNA and proteins by major lipid peroxidation products in genome stability

18 pages

 
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References (164)

Publisher
Taylor & Francis
Copyright
© 2012 Informa UK, Ltd.
ISSN
1029-2470
eISSN
1071-5762
DOI
10.3109/10715762.2012.658516
pmid
22257221
Publisher site
See Article on Publisher Site

Abstract

AbstractOxidative stress and lipid peroxidation (LPO) accompanying infections and chronic inflammation may induce several human cancers. LPO products are characterized by carbohydrate chains of different length, reactive aldehyde groups and double bonds, which make these molecules reactive to nucleic acids, proteins and cellular thiols. LPO-derived adducts to DNA bases form etheno-type and propano-type exocyclic rings, which have profound mutagenic potential, and are elevated in several cancer-prone diseases. Adducts of long chain LPO products to DNA bases inhibit transcription. Elimination from DNA of LPO-induced lesions is executed by several repair systems: base excision repair (BER), direct reversal by AlkB family proteins, nucleotide excision repair (NER) and recombination. Modifications of proteins with LPO products may regulate cellular processes like apoptosis, cell signalling and senescence. This review summarizes consequences of LPO products’ presence in cell, particularly 4-hydroxy-2-nonenal, in terms of genomic stability.

Journal

Free Radical ResearchTaylor & Francis

Published: Apr 1, 2012

Keywords: HNE; DNA repair; lipid peroxidation; DNA-adducts

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