Types of DNA Damage

This assignment delves into the various types of DNA damage that can occur in living organisms. It explores both spontaneous damage mechanisms, such as deamination and depurination, as well as non-spontaneous damage caused by factors like UV light, alkylation, oxidation, and carcinogenic agents. The text provides detailed explanations of each type of damage and its potential consequences for cellular function.

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Types of DNA Damage
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Types of DNA Damage
DNA is the hereditary material present in living organisms and transfers information
contained in the genes from one generation to the next. However, damages to the DNA interfere
with the appropriate production of proteins and proper execution of cell activities. Mutations
caused by DNA damage may adversely affect the health of the organisms, sometimes, even
leading to cancer and death (Helleday, 2014). Damage to the DNA can be spontaneous or non-
spontaneous.
Spontaneous DNA damage can be categorized into 2 forms:
1. Deamination of bases like cytosine, guanine, and adenine. The most important and
frequent type of hydrolytic damage occurs on the base cytosine. The deamination of
cytosine, adenine, and guanine generates uracil, hypoxanthine, and xanthine,
respectively. Uracil has a tendency to pair with adenine, and hypoxanthine and xanthine
pair with cytosine, thereby, introducing wrong bases in the corresponding regions of
opposite strand post-replication (Kow, 2002).
2. Depurination: This is the spontaneous hydrolysis of N-glycosyl linkage producing an
abasic site (deoxyribose lacking a base). Depurination can occur in all the 4 bases, i.e.,
adenine, guanine, cytosine and thymine (An et al., 2014).
The nonspontaneous DNA damage can be categorized into the following forms:
1. UV light-induced DNA damage: UV light is responsible for inducing pyrimidine dimer
formation (2 adjacent pyrimidines like thymine join by a cyclobutane ring structure).
2. Alkylation and oxidation: Alkylation includes the transfer of methyl or methyl groups to
the reactive site present on the bases and to phosphates in the backbone of DNA. E.g.
nitrosamines. The most vulnerable site of alkylation is keto group and C6 of guanine
producing O6-methyl guanine, which pairs with thymine.
3. Oxidation: DNA undergoes attack from reactive oxygen species like O2-, H2O2 and
OH, free radicals, e.g., guanine oxidation produces 7,8-dihydro-8-oxoguanine/oxoG,
which can base pair with both adenine and cytosine.

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4. Carcinogenic/intercalating agents: Base analogs are structurally similar to proper bases
and thus, can be incorporated into DNA during replication e.g. 5-bromouracil (analog of
thymine).
5. Intercalating agents are flat molecules having many polycyclic rings, which bind to
DNA bases, e.g., ethidium bromide.

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Bibliography
An, R., Jia, Y., Wan, B., Zhang, Y., Dong, P., Li, J., & Liang, X. (2014). ‘Non-enzymatic
depurination of nucleic acids: Factors and mechanisms.’ PLoS ONE, vol. 9, pp. e115950.
Helleday, T. (2014). ‘Mechanisms underlying mutational signatures in human cancers.’ Nature
Reviews Genetics, vol. 15, pp. 585–598.
Kow, Y. (2002). ‘Repair of deaminated bases in DNA.’ Free radical biology & medicine., vol.
33, pp. 886–893.