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. For RNA lesions specifically, the most abundant types of endogenous damage include oxidation, alkylation, and chlorination. Phagocytic cells produce radical species that include hypochlorous acid (HOCl), nitric oxide (NO•), and peroxynitrite (ONOO−) to fight infections, and many cell types use nitric oxide as a signaling molecule. However, these radical species can also cause the pathways that form RNA lesions.