A variety of DNA damage can occur spontaneously or under the influence of external factors. Cells need a highly effective mechanism of reparation, since the integrity of the DNA is essential for cell survival and normal functioning, and the damage is occurring constantly. DNA contains about 3*109 basic pairs (in humans) and 2*1011 Covalent bonds, is a huge target for various damaging factors.
Use free sample research papers on DNA damage to learn that on the basis of known energy ties, you can calculate the typical DNA cells each day undergoing spontaneous about 10000 cases of depurinization (the loss of F or G base), 500 cases of depyrimidinization (the loss C or T base) and 160 cases of Cytidine deamination (C to T transformation). The main type of exogenous DNA damage is dimerization of pyrimidine bases. This occurs under the influence of UV light in the epidermis and leads to the formation of thymidine dimers (combined with cyclobutane ring) or thymidine-cytidine dimers.
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Such damage is repaired to the original state through photoreactivation with the help of the photolyase enzyme, using as a cofactor of reaction to visible light. In addition, such damage can be eliminated in the same way that 3D adducts. A number of exogenous factors leads to the formation of DNA adducts, which are divided into small and large.
Minor injuries include methylation and ethylating caused by, for example, nitrosamines (DEN) and (MNNG). Usually the site for such modification is the O6-guanine position and O4-thymine position. These oxygen atoms are typically found in the Keto-configuration for proper mating grounds. However, ethylating captures these atoms in the enol configuration, thus destabilizing the normal carbon bonding between the bases in opposite chains that often leads to point mutations. These adducts can be removed by the protein originally identified as methyltransferase. In the catalytic center of the enzyme there is a cysteine residue to which the alkyl group is bonded (methyl group more often than ethyl group) with O6-and O4-T. For the first time this enzyme was discovered in bacteria, where it participated in the methylation of DNA. The treatment of bacteria with small doses of MNNG can protect them in subsequent introductions of high doses, which may otherwise be lethal. This method of reparation is “expensive,” since the enzyme irreversibly inactivated by the migrating of alkyl group.
Thus, the cell must spend a lot of energy on the creation of a new protein when removing each adducts this way. Alkylating compounds can also form adducts with phosphate backbone. Because the resulting phosphtrioesters are unstable, hydrolyze can happens to one of three phospho-oxygen bonds. If the link to deoxyribose is broken, it breaks the sequence. If breaks in each chain are located nearby, this can lead to the rupture of chromosome.
The ways to reduce the destabilizing effect of alkylating compound chromosome include transposition, sharing sister chromatids, the destruction of or pulverizing of the chromosomes.
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