ABSTRACT
Among the most prominent DNA-damaging agents, the ultraviolet (UV) spectrum of sunlight induces lesions in DNA that may alter the genetic information and lead to genomic instability and carcinogenesis. To eliminate DNA damage, an extremely accurate system of complementary DNA-repair mechanisms has evolved (1). A defect in any of these repair pathways reveals their biological importance in counteracting DNA damage. The consequences of defective repair of UVinduced DNA damage are depicted in three rare autosomal recessive photosensitive syndromes: xeroderma pigmentosum (XP), Cockayne syndrome (CS), and the photosensitive form of the brittle hair disease trichothiodystrophy (TTD) (2).
