Review Question - QID 106252

In the case of an apurinic/apyrimidinic site secondary to cleavage of the bond between the nucleotide and the ribose sugar, the cell uses base excision repair to repair this site.

Radiation can cause a wide variety of DNA damage such as phosphodiester cleavage, double-stranded DNA breaks, and cleavage of the bond between the nucleotide and the ribose sugar leaving an apurinic/apyrimidinic site. Base excision repair (BER) is utilized by the cell to correct damage done to DNA when a nucleotide is missing from the sugar-phophate backbone or when spontaneous deamination converts a cytosine residue to a uracil residue. The BER pathway starts off with a DNA glycosylase recognizing and removing the damaged base. An apurinic/apyrimidinic endonuclease cleaves the backbone, removing the remaining sugar fragment. The gap is then filled with the cell's DNA replication machinery - DNA polymerase and ligase.

Kim and Wilson review in greater depth the mechanisms of BER and the roles that BER plays in the cellular response to chemotherapeutic agents such as alkylators, nucleoside analogs, and radiation.

Berkey discusses management of the side effects of radiation treatment. Radiation dermatitis often complicates treatment of breast, prostate, perineal, and head and neck malignancies. There is no agreement on treatments, however, topical steroids and emollient creams are often used.

Video V shows the mechanism of BER.

Incorrect Answers:
Answer 1: Nucleotide excision repair is involved in repairing DNA helix-distorting damage.
Answer 3: Mismatch repair is involved in repairing insertions and deletions of bases during DNA replication.
Answers 4 & 5: Nonhomologous end joining and homologous recombination are involved in repairing double stranded breaks.