Oral administration of dimethylarsinic acid, a main metabolite of inorganic arsenic, in mice promotes skin tumorigenesis initiated by dimethylbenz(a)anthracene with or without ultraviolet B as a promoter

Citation
K. Yamanaka et al., Oral administration of dimethylarsinic acid, a main metabolite of inorganic arsenic, in mice promotes skin tumorigenesis initiated by dimethylbenz(a)anthracene with or without ultraviolet B as a promoter, BIOL PHAR B, 24(5), 2001, pp. 510-514
Citations number
28
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BIOLOGICAL & PHARMACEUTICAL BULLETIN
ISSN journal
0918-6158 → ACNP
Volume
24
Issue
5
Year of publication
2001
Pages
510 - 514
Database
ISI
SICI code
0918-6158(200105)24:5<510:OAODAA>2.0.ZU;2-U
Abstract
Concerning arsenic-induced tumorigenesis, an animal model must be developed for understanding the mechanism of human carcinogenesis by arsenics. To de termine whether orally administered dimethylarsinic acid (DMA) promotes and causes the progression of skin tumorigenesis, an animal protocol by topica l application of dimethylbenz(a)anthracene (DMBA) with or without UVB, a tu mor promoter, in hairless mice was used. The administration of DMA by the o ral route promoted not only the formation of papillomas induced by DMBA alo ne but also the formation of malignant tumors induced by was of the formati on of atypical keratoses by treatment with DMBA and UVB, A phenomenon, the progression of keratoses --> atypical keratoses --> squamous cell carrinoma s (SCCs), observed in the present study may resemble the development of tum ors in arsenic-exposed humans. We also discussed the involvement of a react ive oxygen species (ROS), e,g,, the dimethylarsenic peroxy radical [(CH3)(2 )AsOO .], produced during the metabolic processing of DMA, in skin and in m ulti-organ tumorigenesis.