Abstract
Ethenoadducts have attracted considerable interest when they were detected in the reactions between DNA and occupational carcinogens such as vinyl chloride, urethane and acrylonitrile1. The deleterious effects of ethenobases were further attested by studies showing their high mutagenic potential2,3. Interestingly, background levels of 3,N 4-etheno2’-deoxycytidine (3,N 4-ɛdC) and 1,N 6-etheno-2’-deoxyadenosine (1,N 6-ɛdA) were detected in tissue DNA from untreated rodents and humans4. However, the origin of the adduct background is still open to debate. It is strongly suggested that increased oxidative stress and lipid peroxidation (LP) are implicated in this process1. In fact, most of LP final products are very efficient alkylating agents. Among these products, malonaldehyde and HNE, are the most extensively studied. However, only HNE was shown to form DNA ethenoadducts5. Due to the lack of information about other LP products, the bulk of the lesions have been attributed to HNE. Even though, other products are reported to be very cytotoxic and can also play an important role in the genotoxic effects associated with LP.
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Carvalho, V.M., Asahara, F., Di Mascio, P., de Campos, I.P.A., Cadet, J., Medeiros, M.H.G. (2001). 1,N 6-Etheno-2’-Deoxyadenosine Adducts from Trans, Trans-2,4-Decadienal and Trans-2-Octenal. In: Dansette, P.M., et al. Biological Reactive Intermediates VI. Advances in Experimental Medicine and Biology, vol 500. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0667-6_33
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DOI: https://doi.org/10.1007/978-1-4615-0667-6_33
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