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Updated: May 25, 2026

Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
Published on: May 29, 2019
Damage of DNA and proteins by major lipid peroxidation products in genome stability
Alicja Winczura1, Daria Zdżalik, Barbara Tudek
1Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawińskiego 02-106 Warsaw, Poland.
Abstract:
Oxidative 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.
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