Introduction

Unlike all other polymers in living cells, DNA cannot be completely broken down to monomers and rebuilt from scratch. Its synthesis always requires a pre-existing single strand of DNA as a template and a double-strand region at least several bp long, providing a 3'-OH group  from which the synthesis to start. The DNA of the cell is the single blueprint that contains all the information on how to make a new copy of any other polymer molecule in the cell. Therefore, it is sensible to make sure that the genetic information coded in DNA could always be recovered even from a single strand. The preservation of the genetic information in its original state is dependent not only on the accuracy of its copying during DNA replication, but also on the timely repair of any event which may compromise the integrity of the DNA molecule and/or may change its building blocks or their arrangement in any manner. Such events constitute DNA damage.

Causes

The most significant consequence of oxidative stress in the body is thought to be damage to DNA.  DNA may be modified in a variety of ways, which can ultimately lead to mutations and genomic instability. This could result in the development of a variety of cancers including colon, breast, and prostate. Here we discuss the various types of damage to DNA, including oxidative damage, hydrolytic damage, DNA strand breaks, and others.

Oxidative DNA damage refers to the oxidation of specific bases. 8-hydroxydeoxyguanosine (8-OHdG) is the most common marker for oxidative DNA damage and can be measured in virtually any species. It is formed and enhanced most often by chemical carcinogens. A similar oxidative damage can occur in RNA with the formation of 8-OHG (8-hydroxyguanosine), which has been implicated in various neurological disorders.

Hydrolytic DNA damage involves deamination or the total removal of individual bases. Loss of DNA bases, known as AP (apurinic/apyrimidinic) sites, can be particularly mutagenic and if left unrepaired they can inhibit transcription. Hydrolytic damage may result from the biochemical reactions of various metabolites as well as the overabundance of reactive oxygen species.

Ultraviolet and other types of radiation can damage DNA in the form of DNA strand breaks. This involves a cut in one or both DNA strands; double-strand breaks are especially dangerous and can be mutagenic, since they can potentially affect the expression of multiple genes. UV-induced damage can also result in the production of pyrimidine dimers, where covalent cross-links occur in cytosine and thymine residues. The most common pyrimidine dimers are cyclobutane pyrimidine dimers (CPD) and pyrimidine (6-4) pyrimidone photoproducts (6-4PP). CPD and 6-4PP are the most frequent DNA mutations found in the p53 protein in skin cancers. Pyrimidine dimers can disrupt polymerases and prevent proper replication of DNA.

Effects

DNA damage may also result from exposure to polycyclic aromatic hydrocarbons (PAHs). PAHs are potent, ubiquitous atmospheric pollutants commonly associated with oil, coal, cigarette smoke, and automobile exhaust fumes. A common marker for DNA damage due to PAHs is Benzo(a)pyrene diol epoxide (BPDE). BPDE is found to be very reactive, and known to bind covalently to proteins, lipids, and guanine residues of DNA to produce BPDE adducts. If left unrepaired, BPDE-DNA adducts may lead to permanent mutations resulting in cell transformation and ultimately tumor development.

Conclusion

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