Concept

Molecular lesion

Résumé
A molecular lesion or point lesion is damage to the structure of a biological molecule such as DNA, RNA, or protein. This damage may result in the reduction or absence of normal function, and in rare cases the gain of a new function. Lesions in DNA may consist of breaks or other changes in chemical structure of the helix, ultimately preventing transcription. Meanwhile, lesions in proteins consist of both broken bonds and improper folding of the amino acid chain. While many nucleic acid lesions are general across DNA and RNA, some are specific to one, such as thymine dimers being found exclusively in DNA. Several cellular repair mechanisms exist, ranging from global to specific, in order to prevent lasting damage resulting from lesions. There are two broad causes of nucleic acid lesions, endogenous and exogenous factors. Endogenous factors, or endogeny, refer to the resulting conditions that develop within an organism. This is in contrast with exogenous factors which originate from outside the organism. DNA and RNA lesions caused by endogenous factors generally occur more frequently than damage caused by exogenous ones. Endogenous sources of specific DNA damage include pathways like hydrolysis, oxidation, alkylation, mismatch of DNA bases, depurination, depyrimidination, double-strand breaks (DSS), and cytosine deamination. DNA lesions can also naturally occur from the release of specific compounds such as reactive oxygen species (ROS), reactive nitrogen species (RNS), reactive carbonyl species (RCS), lipid peroxidation products, adducts, and alkylating agents through metabolic processes. ROS is one of the major endogenous sources of DNA damage and the most studied oxidative DNA adduct is 8-oxo-dG. Other adducts known to form are etheno-, propano-, and malondialdehyde-derived DNA adducts. The aldehydes formed from lipid peroxidation also pose another threat to DNA. Proteins such as “damage-up” proteins (DDPs) can promote endogenous DNA lesions by either increasing the amount of reactive oxygen by transmembrane transporters, losing chromosomes by replisome binding, and stalling replication by transcription factors.
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