Ultraviolet (UV) light is a form of electromagnetic radiation with wavelengths shorter than visible light. This energy is a component of natural sunlight and is also emitted by artificial sources like tanning beds. DNA, or deoxyribonucleic acid, serves as the fundamental genetic material within nearly all living organisms, carrying the instructions essential for development, function, and reproduction.
Understanding UV Light and DNA Basics
UV radiation is categorized into three main types based on wavelength and energy: UVA, UVB, and UVC. UVA rays have the longest wavelengths (315-400 nm) and the lowest energy, penetrating deepest into the skin. UVB rays have medium wavelengths (280-315 nm) and higher energy than UVA, primarily affecting the outer layers of the skin and causing sunburns. UVC rays, with the shortest wavelengths (100-280 nm) and highest energy, are the most damaging but are fortunately absorbed by the Earth’s ozone layer before reaching the surface.
DNA is structured as a double helix. This structure is composed of repeating units called nucleotides, each containing a sugar, a phosphate group, and one of four nitrogenous bases: adenine (A), guanine (G), cytosine (C), and thymine (T). In the double helix, adenine always pairs with thymine, and guanine always pairs with cytosine.
How UV Light Damages DNA at a Molecular Level
When DNA absorbs UV photons, particularly from UVB radiation, it can directly alter the chemical structure of its building blocks. Pyrimidine bases, specifically thymine and cytosine, are particularly susceptible to this absorption.
The most common UV-induced lesions are cyclobutane pyrimidine dimers (CPDs). CPDs form when two adjacent pyrimidine bases, such as two thymines or a thymine and a cytosine, become covalently linked through a four-membered cyclobutane ring. These dimers introduce a kink or bulge in the DNA double helix, disrupting its normal structure.
Another type of photoproduct is the 6-4 photoproduct (6-4PP). These form through a different type of covalent bond between adjacent pyrimidines, creating a more significant distortion in the DNA helix compared to CPDs. Both CPDs and 6-4PPs interfere with the accurate reading and copying of the genetic code by cellular machinery, such as DNA polymerases and RNA polymerases, potentially halting replication and transcription.
Cellular Repair Mechanisms for UV Damage
Cells possess sophisticated mechanisms to detect and correct the DNA damage inflicted by UV light. The primary pathway responsible for repairing UV-induced lesions in humans is Nucleotide Excision Repair (NER). NER is a multi-step process that removes bulky DNA adducts like CPDs and 6-4 photoproducts.
The NER process begins with the recognition of the distorted DNA helix by specialized proteins. Following recognition, the DNA strands around the damaged site are unwound, making the lesion accessible. A segment of the damaged DNA strand is then excised by specific enzymes. After the removal of the damaged segment, DNA polymerase enzymes synthesize a new, correct DNA sequence using the undamaged complementary strand as a template. Finally, DNA ligase seals the newly synthesized segment into the existing DNA strand, restoring the DNA’s original integrity.
Consequences of Unrepaired UV DNA Damage
When UV-induced DNA damage remains unrepaired or is misrepaired, it can lead to permanent changes in the DNA sequence known as mutations. These mutations can specifically include C to T transitions, where a cytosine base is replaced by a thymine. This type of mutation is a common signature of UV exposure, particularly in skin cancers.
Such mutations can disrupt normal cellular processes. Unrepaired lesions can block DNA replication, preventing cells from dividing properly, or interfere with gene transcription, altering protein production. If the damage is extensive or affects critical genes, cells may activate a programmed self-destruction process called apoptosis to prevent the propagation of damaged genetic material.
Alternatively, unrepaired DNA damage can lead to uncontrolled cell proliferation. Mutations in genes that regulate cell growth, such as tumor suppressor genes or oncogenes, can contribute to the development of skin cancer. The accumulation of these mutations over time, particularly in genes like p53, is a factor in the initiation and progression of carcinogenesis.