UV exposure doesn’t always lead directly to mutations in the DNA. In fact, UV-A radiation commonly damages DNA in an oxygen-dependent manner that involves photosensitization. This leads to the production of a free radical that then interacts with and oxidizes DNA bases.
Full Answer
UV radiation causes two classes of DNA lesions: cyclobutane pyrimidine dimers (CPDs, Figure 1) and 6-4 photoproducts (6-4 PPs, Figure 2). Both of these lesions distort DNA's structure, introducing bends or kinks and thereby impeding transcription and replication.
Induced mutations are those that result from an exposure to chemicals, UV rays, x-rays, or some other environmental agent. Spontaneous mutations occur without any exposure to any environmental agent; they are a result of natural reactions taking place within the body.
T-T dimers cause kinks in the DNA strand that prevent both replication and transcription of that part of the DNA. Because they block DNA replication (and therefore prevent cells from reproducing), T-T dimers and other forms of UV damage cannot be inherited, and thus do not constitute mutations.
Although it can damage various molecules in the cell, the most damage occurs when it hits DNA. When an excited oxygen hits DNA, it can cause a guanine to thymine transversion, which means that the purine guanine is replaced by the pyrimidine thymine.
Ultraviolet (UV) light induces specific mutations in the cellular and skin genome such as UV-signature and triplet mutations, the mechanism of which has been thought to involve translesion DNA synthesis (TLS) over UV-induced DNA base damage.
Which is the most efficient way to avoid DNA mutations from UV radiation? Avoid getting X-rays at the doctor's office.
DNA bases can be damaged by: (1) oxidative processes, (2) alkylation of bases, (3) base loss caused by the hydrolysis of bases, (4) bulky adduct formation, (5) DNA crosslinking, and (6) DNA strand breaks, including single and double stranded breaks. An overview of these types of damage are described below.
DNA repair Pyrimidine dimers introduce local conformational changes in the DNA structure, which allow recognition of the lesion by repair enzymes. In most organisms (excluding placental mammals such as humans) they can be repaired by photoreactivation.
UV radiation causes alkylation of guanine bases on the same DNA strand.
UV light damages the DNA of exposed cells by causing bonds to form between adjacent pyrimidine bases, usually thymines, in DNA chains. The thymine dimers inhibit correct replication of the DNA during reproduction of the cell.
UVA (and also UVB) radiation cause indirect damage to DNA via absorption of photons by non-DNA chromophores. This generates reactive oxygen species like singlet oxygen or hydrogen peroxide that oxidize the DNA bases causing mutations.
Ultraviolet (UV) light kills cells by damaging their DNA. The light initiates a reaction between two molecules of thymine, one of the bases that make up DNA.
DNA is our genetic code, the precious molecule containing all the information necessary to make up a living organism and it is therefore well protected inside a special structure, the nucleus, located deep inside each cell (Figure 1). DNA is composed of two complementary strands that are wound into a double helix (Figure 1). The hereditary message is chemically coded and made up of the four bases, the four ‘building blocks’: adenine (A), thymine (T), guanine (G) and cytosine (C ) (Figure 1).
Ultraviolet (UV) light is a type of electromagnetic radiation invisible to most humans and emitted mainly by the sun. However, UV can be released by artificial sources too such as electric arcs and specialized lights (e.g. tanning lamps). The wavelengths of UV rays range between 200 and 400 nm, which are shorter than the wavelengths of violet light (hence the name ultra-violet. Violet is at the higher end of the visible spectrum with a wavelength of around 380–450 nm).
When direct DNA damage fuses two base pairs together, the DNA ends up with a bulge in its normal double helix shape. Several enzymes travel around the DNA guarding it and looking for such abnormalities. When they find such a bulge, an abnormal notch, they activate repair proteins that cut out the damaged part of the DNA and put in the correct base pairs. This whole process is called nucleotide excision repair. The effect of indirect DNA damage is harder to detect because transversion does not result in a distorted helix. The mechanism that repairs this kind of damage is called base excision repair. Enzymes called DNA glycosylases remove a base pair misplaced by transversion; other enzymes then open up the DNA’s backbone so that DNA building enzymes can come through and fill the gap with the correct base pair.
This process happens when the double helix opens up to two single strands so that replication proteins can bind along the DNA backbone and start constructing a new strand according to the instructions they see on the original backbone. Every A base they come across ‘asks’ for a T base — as a pair — and vice versa, while every G they come across ‘screams’ for a C and vice versa. (This happens as A is chemically complementary to T, while G complements chemically C). Since the backbone is no longer ‘smooth’ due to the photoproduct of the pericyclic reaction, it is difficult for the replication proteins to determine what base pairs should be put across the fused, covalently-linked pyrimidines when the altered/ damaged DNA strand needs to be copied and a new DNA strand to be synthesized. This may result in a wrong base being put during the replication process (if the damage is not properly repaired on time). Exactly this base change resulting from the DNA lesion is called mutation.
There are different ways UV-excited DNA can react, but the fusion or dimerization of two adjacent bases (the building blocks of the DNA) is the most common. If two pyrimidine bases (thymine or cytosine; two out of the four bases that make up the DNA backbone. The other two are adenine and guanine) are next to each other, their two rings can fuse together forming a covalent link (Figure 2). This type of reaction, called a pericyclic reaction, is possible because of how close their rings are and how their symmetries align (Figure 2). Such a chemical change to the DNA is not a mutation but is rather DNA damage or a DNA lesion. The DNA at a damaged site is no longer truly DNA as it has a different chemical structure to the natural form of DNA and it is a chemical intermediate. This formation of a four-carbon ring between the pyrimidines (see red square on Figure 2) creates a ‘notch’ on the DNA backbone causing problems for essential procedures happening along the DNA backbone.
Figure 1 : DNA structure. Most DNA is found inside the nucleus of a cell, where it forms the chromosomes. Chromosomes have proteins called histones that bind to DNA and help it get compacted as the DNA molecule gets wound around them. DNA has two strands that twist into the shape of a spiral ladder called a helix. It is made up of four building blocks called nucleotides: adenine (A), thymine (T), guanine (G), and cytosine (C ). The nucleotides attach to each other (A with T, and G with C) to form chemical bonds called base pairs, which connect the two DNA strands. Genes are short pieces of DNA that carry specific genetic information. Image source: https://siteman.wustl.edu/glossary/cdr0000045671/
Part of what makes this type of DNA damage particularly dangerous is that it is caused by excited oxygen molecules, not the UV light itself. Excited oxygen has an unusually long lifespan for a reactive species, so the damage can occur in cells other than skin cells.
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Ultraviolet (UV) light induces specific mutations in the cellular and skin genome such as UV-signature and triplet mutations, the mechanism of which has been thought to involve translesion DNA synthesis (TLS) over UV-induced DNA base damage.
Daylight UV induces a characteristic UV-specific mutation, a UV-signature mutation occurring preferentially at methyl-CpG sites, which is also observed frequently after exposure to either UVB or UVA, but not to UVC.
Indeed, UVA produces oxidative DNA damage not only in cells but also in skin, which, however, does not seem sufficient to induce mutations in the normal skin genome. In contrast, it has been demonstrated that UVA exclusively induces the solar-UV signature mutations in vivo through CPD formation.