Recent studies have shown the molecular mechanisms of UV-induced damage such as the production of cyclobutane pyrimidine dimers (CPDs),  increased apoptosis and DNA repair by photolyase. However, ultrastructural changes induced by UVB and subsequent mechanisms remain unsolved "in  vivo", due to the absence of suitable living animal models to investigate the photoreactivation following UV damage. In this study, we show that UVB- induced DNA damage and apoptosis arelimited in the integument of woodlice "Armadillidium vulgare in vivo" and that the DNA damage is repaired by a hotolyase excited by visible light. UVB (15.4 J/m2, 2.4 kJ/m2) radiation induces one type of DNA damage, CPD, in the integument of A. "vulgare", and the number of apoptotic cells increased 9 hr after UVB exposure. Treatment with visible light accelerated the reduction of CPD and suppressed the increase in apoptosis induced by UVB. This study also provides evidence showing that UVB is blocked by two kinds of pigment cells, black and yellow hromatophores, and that clusters of pigment granules, which are usually distributed within chromatophores, are excreted into the epidermal cell layer beneath the cuticle. These results suggest that the photoreactivation mechanism and the pigment cell layer are important to protection from UVB in living A. "vulgare"

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