DNA that binds to a chemical carcinogen. Some adducts that cause lesions to DNA included oxidatively modified bases, propano-, etheno-, and MDA-induced adducts. 5‐Hydroxymethyluracil is an example of an oxidatively modified base where oxidation of the methyl group of thymine occurs. This adduct interferes with the binding of transcription factors to DNA which can trigger apoptosis or result in deletion mutations. Propano adducts are derived by species generated by lipid peroxidation. For example, HNE is a major toxic product of the process. It regulates the expression of genes that are involved in cell cycle regulation and apoptosis. Some of the aldehydes from lipid peroxidation can be converted to epoxy aldehydes by oxidation reactions. These epoxy aldehydes can damage DNA by producing etheno adducts. An increase in this type of DNA lesion exhibits conditions resulting in oxidative stress which is known to be associated with an increased risk of cancer. Malondialdehyde (MDA) is another highly toxic product from lipid peroxidation and also in the synthesis of prostaglandin. MDA reacts with DNA to form the M1dG adduct which causes DNA lesions. Disease Effects 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 Alzheimer’s, Huntington’s, and Parkinson’s 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, Friedrich’s 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