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Updated: Aug 17, 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
[DNA damage induced by products of lipid peroxidation]
Waldemar M Przybyszewski1, Janusz Kasperczyk, Katarzyna Stokłosa
1Zakład Radiobiologii Doświadczalnej i Klinicznej, Centrum Onkologii, Instytut im.M.Skłodowskiej-Curie, Oddział w Gliwicach, 44-101 Gliwice. wmp@io.gliwice.pl
Abstract:
The adduction of the aldehydic end-products of lipid peroxidation to DNA induces bulky adducts, leading to genome instability. The bulky-DNA adducts are miscoding and thus play a fundamental role in mutagenesis and cancerogenesis. Special attention is given to the etheno- and propanoadducts, recognized as DNA modifiers. Such DNA lesions are repaired by different DNA repair mechanisms, mainly base excision repair (BER) and nucleotide excision repair (NER), as well as nucleotide incision repair (NIR) and transcription-coupled repair (TCR).
Insights
Lipid peroxidation products form bulky DNA adducts, causing genome instability and promoting cancer. DNA repair pathways like base excision repair (BER) and nucleotide excision repair (NER) help fix these harmful lesions.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Context:
- Lipid peroxidation generates reactive aldehydes.
- These aldehydes adduct to DNA, forming bulky lesions.
- Bulky DNA adducts are implicated in mutagenesis and cancer.
Purpose:
- To highlight the role of bulky DNA adducts in genome instability.
- To discuss specific adducts like etheno- and propanoadducts.
- To review DNA repair mechanisms involved in lesion removal.
Summary:
- Adduction of aldehydic end-products of lipid peroxidation to DNA creates bulky adducts, leading to genome instability.
- These bulky-DNA adducts are miscoding and contribute to mutagenesis and cancerogenesis.
- Etheno- and propanoadducts are key DNA modifiers repaired by base excision repair (BER), nucleotide excision repair (NER), nucleotide incision repair (NIR), and transcription-coupled repair (TCR).
Impact:
- Understanding these adducts and repair pathways is crucial for cancer prevention and treatment.
- This knowledge can inform strategies to mitigate DNA damage from oxidative stress.
- Identifying specific repair mechanisms provides targets for therapeutic intervention.
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