Final answer:
Prolonged UV exposure causes thymine dimerization in DNA, damaging the helix structure and potentially leading to skin cancer. Conditions like xeroderma pigmentosa highlight the criticality of DNA repair mechanisms, as affected individuals can't repair UV-induced damage, increasing cancer risk.
Step-by-step explanation:
Effect of UV Light on DNA and Skin Health:
Individuals who spend long periods over many years developing a tan can acquire thick and wrinkled skin as a result of prolonged exposure to ultraviolet (UV) light. The primary molecular damage occurs when UV-B radiation excites DNA molecules, distorting the DNA helix. This leads to the formation of pyrimidine dimers, particularly between thymine bases, creating thymine dimers. These dimers are often repaired by nucleotide excision repair mechanisms in normal skin cells; however, in conditions like xeroderma pigmentosum, this repair process is defective, resulting in the accumulation of DNA damage.
Continuous exposure to UV light can also damage collagen fibers, accelerating the aging process of the skin and leading to the formation of wrinkles. Moreover, repeated sun exposure can cause skin cancer, with some studies suggesting a link between overexposure to sunlight at a young age and the development of melanoma later in life.
A well-documented example of when this repair process is defective is seen in individuals with xeroderma pigmentosa. They are unable to correct the damage due to a defect in the nucleotide excision repair enzymes. Consequently, people with this condition have a heightened risk of developing skin cancer. The tanning response itself is a defense mechanism where the body produces pigments to shield the living cells from future UV exposures.