Question:
Ultraviolet (UV) radiation causes DNA damage primarily by which of the following mechanisms?
Ultraviolet (UV) radiation causes DNA damage primarily by which of the following mechanisms?
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Think of the lesion repaired by nucleotide excision repair and defective in xeroderma pigmentosum.
Updated On: Jun 25, 2026
- Formation of pyrimidine dimers
- Inhibition of p53
- Deamination of cytosine
- Increase in cyclins
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The Correct Option is A
Solution and Explanation
Step 1: Identify the lesion produced by UV light.
UV-B radiation (wavelength 280-320 nm) is directly absorbed by adjacent pyrimidine bases on the same DNA strand. This induces covalent linkage between two neighbouring pyrimidines (most commonly thymine), producing cyclobutane pyrimidine dimers (and 6-4 photoproducts).
Step 2: Effect of the dimer.
The dimer distorts the DNA double helix and blocks both replication and transcription. If unrepaired it leads to mutations, especially C to T transitions, which underlie UV-induced skin cancers.
Step 3: Repair pathway.
Pyrimidine dimers are removed by nucleotide excision repair (NER). A defect in NER causes xeroderma pigmentosum, characterised by extreme photosensitivity and early skin malignancy.
Step 4: Why the other options are wrong.
• Inhibition of p53 - p53 mutation can result from UV damage but is a downstream consequence, not the direct lesion.
• Deamination of cytosine - this is a spontaneous hydrolytic event (or caused by nitrous acid), giving uracil; it is not the UV mechanism.
• Increase in cyclins - unrelated to the primary DNA photolesion.
Key fact: UV light damages DNA by forming pyrimidine (thymine) dimers, repaired by nucleotide excision repair.
UV-B radiation (wavelength 280-320 nm) is directly absorbed by adjacent pyrimidine bases on the same DNA strand. This induces covalent linkage between two neighbouring pyrimidines (most commonly thymine), producing cyclobutane pyrimidine dimers (and 6-4 photoproducts).
Step 2: Effect of the dimer.
The dimer distorts the DNA double helix and blocks both replication and transcription. If unrepaired it leads to mutations, especially C to T transitions, which underlie UV-induced skin cancers.
Step 3: Repair pathway.
Pyrimidine dimers are removed by nucleotide excision repair (NER). A defect in NER causes xeroderma pigmentosum, characterised by extreme photosensitivity and early skin malignancy.
Step 4: Why the other options are wrong.
• Inhibition of p53 - p53 mutation can result from UV damage but is a downstream consequence, not the direct lesion.
• Deamination of cytosine - this is a spontaneous hydrolytic event (or caused by nitrous acid), giving uracil; it is not the UV mechanism.
• Increase in cyclins - unrelated to the primary DNA photolesion.
Key fact: UV light damages DNA by forming pyrimidine (thymine) dimers, repaired by nucleotide excision repair.
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