What Mechanism Is Used To Find And Repair Dna Damage Caused By The Uv Light?

The Machinery of DNA Damage by UV Radiation

Solar ultraviolet radiation (UV) exposure triggers DNA damage, a preliminary stride in the process of carcinogenesis.

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The stability of Dna is extremely important for the proper functioning of all cellular processes. Exposure to UV radiation alters the structure of DNA, affecting the physiological processes of all living systems ranging from bacteria to humans.

Ultraviolet Radiation

Natural sunlight stimulates the production of vitamin D, an important food for the formation of healthy bones. However, sunlight is also a major source of UV radiation. Individuals who get excessive UV exposure are at a great risk of developing skin cancers. There are three types of UV rays: UVA, UVB and UVC.

UVC rays (100-280 nm) are the nigh energetic and damaging of the 3 rays. Fortunately, UVC is absorbed by the ozone layer before reaching the globe's surface.
UVA rays (315-400 nm) possess the lowest energy and is able to penetrate deep into the peel. Prolonged exposure has been linked to ageing and wrinkling of the skin. UVA is also the principal crusade of melanomas.
UVB rays (280-315 nm) possess higher energy than UVA rays and affect the outer layer of the skin leading to sunburns and tans. Basal jail cell carcinoma and squamous cell carcinoma are caused by UVB radiation.

Dna Damage past UV Radiations

DNA is composed of two complementary strands that are wound into a double helix. The hereditary message is chemically coded and fabricated up of the four nucleotides adenine (A), thymine (T), guanine (G) and cytosine (C).

UVB light interferes directly with the bonding betwixt the nucleotides in the Dna. The two main Deoxyribonucleic acid lesions formed past exposure to UVB are cyclobutane pyrimidine dimers (CPD) and vi-4 pyrimidine pyrimidone photoproducts (6-4PPs), and its Dewar isomers.

CPDs are formed when two side by side pyrimidine bases (thymine –TT or cytosine – CC) become covalently linked producing a cyclic ring structure. 6-4PPs upshot from a single covalent bond formed between the five' end of C6 and 3' end of C4 of side by side pyrimidines. This leads to the formation of an unstable oxetane or azetidine intermediate depending on whether the three' end base is a thymine or cytosine.

Subsequent spontaneous rearrangement of these intermediates gives rising to 6-4PP. The pyrimidine dimers cause a kink in the DNA backbone, halting transcription and protein synthesis. 6-4 pyrimidine pyrimidone adducts undergo isomerization to their Dewar form upon exposure to another photon of light from UVB or UVA radiations. The most common mutation induced by UVB is C to T transversion. Double base substitutions (CC to TT) too occur, albeit less frequently.

UVA (and also UVB) radiation cause indirect impairment to Dna via assimilation of photons by non-Deoxyribonucleic acid chromophores. This generates reactive oxygen species like singlet oxygen or hydrogen peroxide that oxidize the Dna bases causing mutations. The nigh common mutation is the G-T transversion wherein guanine gets oxidized into viii-oxo- 7,eight-dihydroguanine (viii-oxoG) hindering its pairing with cytosine. During the replication process, 8-oxoG pairs with adenine. When the second strand is synthesized, viii-oxoG is replaced with a thymine leading to a Chiliad-T transversion.

The importance of wearing sunscreen explained

Dna Repair

The genetic lesions produced by UV radiation are often repaired shortly after they are formed, through a process called nucleotide excision repair. A nuclease enzyme recognizes and removes a segment of DNA containing the lesion. Then, the polymerase inserts the correct bases and ligase seals the gap. However, if unrepaired lesions accrue or the repair mechanism is faulty, it tin can lead to cell expiry, mutagenesis and even cancer.

Sources:

Sinha RP, Häder DP "UV-induced Deoxyribonucleic acid harm and repair: A review." Photochem Photobiol Sci. 2002 Apr; 1(4):225-36. Review
Rastogi RP, Richa, Kumar A, Tyagi MB and Sinha RP "Molecular mechanisms of ultraviolet radiation-induced Dna damage and repair." J Nucleic Acids. 2010 Dec 16;2010:592980. doi: ten.4061/2010/592980
Ravanat JL, Douki T and Cadet J "Direct and indirect furnishings of UV radiation on Deoxyribonucleic acid and its components." J Photochem Photobiol B. 2001 October;63(i-3):88-102. Review

Citations

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APA

Subramanian, Supriya. (2019, Feb 26). The Machinery of DNA Impairment past UV Radiations. News-Medical. Retrieved on April 15, 2022 from https://www.news-medical.net/life-sciences/The-Mechanism-of-DNA-Impairment-by-UV-Radiations.aspx.
MLA

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Chicago

Subramanian, Supriya. "The Mechanism of Dna Damage by UV Radiation". News-Medical. https://www.news-medical.cyberspace/life-sciences/The-Mechanism-of-DNA-Harm-by-UV-Radiation.aspx. (accessed Apr 15, 2022).
Harvard

Subramanian, Supriya. 2022. The Mechanism of Deoxyribonucleic acid Harm by UV Radiation. News-Medical, viewed 15 Apr 2022, https://www.news-medical.net/life-sciences/The-Mechanism-of-Deoxyribonucleic acid-Damage-past-UV-Radiation.aspx.