Final answer:
Individuals with xeroderma pigmentosum cannot repair DNA damage caused by ultraviolet (UV) irradiation, specifically thymine dimers, due to defective nucleotide excision repair enzymes, leading to an increased risk of skin cancer.
Step-by-step explanation:
The type of DNA damage that is not recognized by the cells of individuals with the inherited disease xeroderma pigmentosum is ultraviolet (UV) irradiation damage. In this condition, when individuals are exposed to UV light, thymine dimers are formed in the DNA, which distorts the DNA's double helix structure. Unfortunately, due to a deficiency in the nucleotide excision repair enzymes, individuals with xeroderma pigmentosum are unable to repair these thymine dimers, leading to an increased risk of developing skin cancer.
Individuals with the inherited disease xeroderma pigmentosum are not able to recognize and repair UV irradiation damage caused by exposure to UV rays from the sun.
When people with xeroderma pigmentosum are exposed to UV light, thymine dimers are formed in the DNA, which distort the structure of the DNA double helix.
Due to a defect in the nucleotide excision repair enzymes, individuals with xeroderma pigmentosum cannot repair the thymine dimers and are therefore at a higher risk of contracting skin cancer compared to those without the condition.