Photobiological information obtained from XPA gene-deficient mice.
The XPA gene-deficient mouse, an animal model of xeroderma pigmentosum (XP), develops enhanced photobiologic reactions including acute inflammation, immunosuppression and skin carcinogenesis, because of the defect in the excision repair of ultraviolet-induced DNA lesions. The results strongly suggest that nuclear DNA is an important chromophore to initiate acute and chronic skin damages. The model mouse is a useful experimental animal not only to investigate the mechanisms of photosensitivity in XP, but also to study physiological photobiology in humans, because photobiologic reactions are greatly intensified in this mouse.
Horio
Takeshi
T
Department of Dermatology, Kansai Medical University, Moriguchi, Osaka, Japan. horio@takii.kmu.ac.jp
Miyauchi-Hashimoto
Hiroko
H
Kuwamoto
Kazue
K
Yamazaki
Fumikazu
F
Okamoto
Hiroyuki
H
D000818:Animals; D004249:DNA Damage / Q000502:physiology / Q000528:radiation effects*; D006801:Humans; D007165:Immunosuppression Therapy / Q000662:veterinary; D007249:Inflammation / Q000473:pathology; D051379:Mice; D023421:Models, Animal; D018462:Photobiology; D010787:Photosensitivity Disorders / Q000235:genetics / Q000473:pathology; D012878:Skin Neoplasms / Q000473:pathology; D014466:Ultraviolet Rays / Q000009:adverse effects*; D014983:Xeroderma Pigmentosum / Q000235:genetics*; D051760:Xeroderma Pigmentosum Group A Protein / Q000235:genetics / Q000378:metabolism*
D051760:Xeroderma Pigmentosum Group A Protein; C497315:Xpa protein, mouse