Repair of 254nm Ultraviolet-Induced (6-4) Photoproducts: Monoclonal Antibody Recognition and Differential Defects in Xeroderma Pigmentosum Complementation Groups A, D, and Variant

Repair kinetics of ultraviolet (UV) light-induced (6–4) photoproducts in xeroderma pigmentosum complementation group A, D, and variant cells were studied by the enzyme-linked immunosorbent assay (ELISA) using a specific monoclonal antibody raised against (6–4) photoproducts, together with unscheduled DNA synthesis (UDS) and loss of T4 endonuclease V-susceptible sites (ESS). Group A XP35KO cells completely failed to repair both ESS (cyclobutane pyrimidine dimers) and antibody-recognizing (6–4) photoproducts until tested 24h after irradiation, and had 2% early-time UDS. Group D XP43KO cells showed about 10% removal of both (6–4) photoproducts and ESS in 24 h, despite showing a residually higher level of 40% early-time and cumulative UDS. Thus, the results substantiated the extreme UV hypersensitivity of XP group A and D cells. However, XP52KO variant cells exhibited the normal level of UDS and ESS loss, but a slightly reduced repair of antibody-recognizing (6–4) photo-products at 6 and 12h after irradiation, which may account for a small UV hypersensitivity of the XP variant cells