Chromosome damage in PUVA-treated human lymphocytes is related to active oxygen species and clastogenic factors.

Besides the direct interaction of psoralens with DNA and other macromolecules, the role of reactive oxygen species in the PUVA-induced cellular injury has been stressed. The present study shows that treatment of human blood cultures with 5-methoxypsoralen or 8-methoxypsoralen, followed by UVA exposure, results in chromosome damage. The supernatant of these cultures contains secondarily formed chromosome damaging material, called clastogenic factor (CFs). Not only CF formation, but also CF action is inhibited by superoxide dismutase (SOD), suggesting that superoxide is formed on the pathway to chromosome aberration. CF is detectable in the cell culture supernatants after a minimal delay of 18 h, and reaches a plateau at 24 h of cultivation. SOD is no longer protective if added after 24 h, i.e., the enzyme can prevent, but not repair the oxyradical-induced damage.