Many systems are in place to repair DNA and RNA lesions but it is possible for lesions to escape these measures. This may lead to mutations or large genome abnormalities, which can threaten the cell or organism's ability to live. Several cancers are a result of DNA lesions. Even repair mechanisms to heal the damage may end up causing more damage. Mismatch repair defects, for example, cause instability that predisposes to colorectal and endometrial carcinomas.
DNA lesions in neurons may lead to neurodegenerative disorders such as Alzheimers, Huntingtons, and Parkinsons diseases. These come as a result of neurons generally being associated with high mitochondrial respiration and redox species production, which can damage nuclear DNA. Since these cells often cannot be replaced after being damaged, the damage done to them leads to dire consequences. Other disorders stemming from DNA lesions and their association with neurons include but are not limited to Fragile X syndrome, Friedreichs ataxia, and Spinocerebellar ataxias.
During replication, usually DNA polymerases are unable to go past the lesioned area, however, some cells are equipped with special polymerases which allow for translesion synthesis (TLS). TLS polymerases allow for the replication of DNA past lesions and risk generating mutations at a high frequency. Common mutations that occur after undergoing this process are point mutations and frameshift mutations. Several diseases come as a result of this process including several cancers and Xeroderma pigmentosum.
The effect of oxidatively damaged RNA has resulted in a number of human diseases and is especially associated with chronic degeneration. This type of damage has been observed in many neurodegenerative diseases such as Amyotrophic lateral sclerosis, Alzheimers, Parkinsons, dementia with Lewy bodies, and several prion diseases. It is important to note that this list is rapidly growing and data suggests that RNA oxidation occurs early in the development of these diseases, rather than as an effect of cellular decay. RNA and DNA lesions are both associated with the development of diabetes mellitus type 2.