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Research undertaken over the past few years has brought attention to the role of oxidative stress in the development of neoplasms by damaging nucleic acids, lipids, and proteins, thereby altering their normal function. In general, the levels of antioxidant enzymes are low in patients with neoplasms, and the biomarkers used to quantify oxidative stress have increased levels. Elevated levels of 8-hydroxy-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), as well as decreased levels of antioxidant enzymes, have been observed in patients diagnosed with colorectal cancer (CRC) at various stages of evolution, but further research is needed on the correlation between these biomarkers and disease progression. Inflammation enhances the production of reactive oxygen species and plays an important role in CRC development. Studies in the field of metabolomics have suggested that changes in serum metabolites might be indicators of the progression from adenoma to colorectal carcinoma, particularly those resulting from lipid metabolism. The role of lipidomics in the pathogenesis of CRC warrants further investigation, as these combinations of metabolites (metabolic fingerprints) may have the potential to become clinically useful markers. In this article, we review our current understanding of the interplay between oxidative stress, inflammatory markers and lipidomic products in the pathogenesis of CRC.
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Berechet et al. (2025) studied this question.
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