Effect of ultraviolet (UV) radiation and UVB-absorbing sunscreen ingredients on 7,12-dimethylbenz(a)anthracene-initiated skin tumorigenesis in hairless mice.
Reeve Ve, M. Bosnic, Christa Boehm‐Wilcox
Abstract
Reeve Ve, M. Bosnic, Christa Boehm‐Wilcox
Abstract
These experiments describe the enhancement of 7,12-dimethylbenz(a)anthracene (DMBA)-initiated skin tumorigenesis in hairless mice by subsequent chronic ultraviolet (UV) irradiation of the same skin site. Each carcinogen was administered at a level that separately resulted in threshold tumorigenesis. The cocarcinogenic response was evident as a marked increase in tumour incidence, tumour multiplicity and degree of tumour malignancy. Irradiation through the topically applied UVB (290-315 nm)-absorbing sunscreen ingredient, 2-ethylhexyl-p-methoxycinnamate, totally protected from the photoenhancement. However, irradiation through an alternative UVB absorber, octyl-N-dimethyl-p-aminobenzoate, failed to protect from photoenhancement. A possible immunologic role for the enhancement of DMBA tumorigenesis by UV radiation is proposed.
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These experiments describe the enhancement of 7,12-dimethylbenz(a)anthracene (DMBA)-initiated skin tumorigenesis in hairless mice by subsequent chronic ultraviolet (UV) irradiation of the same skin site. Each carcinogen was administered at a level that separately resulted in threshold tumorigenesis. The cocarcinogenic response was evident as a marked increase in tumour incidence, tumour multiplicity and degree of tumour malignancy. Irradiation through the topically applied UVB (290-315 nm)-absorbing sunscreen ingredient, 2-ethylhexyl-p-methoxycinnamate, totally protected from the photoenhancement. However, irradiation through an alternative UVB absorber, octyl-N-dimethyl-p-aminobenzoate, failed to protect from photoenhancement. A possible immunologic role for the enhancement of DMBA tumorigenesis by UV radiation is proposed.
Key concepts: Hairless, DMBA, Carcinogenesis, Carcinogen, Anthracene, Chemistry, Irradiation, Ultraviolet