Abstract
Ultraviolet light (UV) is categorized according to their wavelength ranges into UVC (<280 nm), UVB (280-320 nm), and UVA (320-400 nm). UVA is subcategorized into UVA1 (340-400 nm) and UVA2 (320-340 nm). Although UV is generally known to induce C -> T mutation at dipyrimidine sites in DNA, wavelength differences could modify the situation, especially for mammals. Vertebrate genome is known to be methylated globally at some specific cytosine residues, and this methylation can enhance formation of one of the UV-specific DNA damage, cyclobutane pyrimidine dimers (CPD) induced, not by UVC, but by UVB or solar UV (>290 nm), which results in hotspot mutations at dipyrimidine sites with a methylated cytosine in mammalian genes, evidenced by mutations in the p53 gene found in human skin cancer.
We found previously, using lacZ-transgenic mice, that mutation induction in UVB-exposed skin epidermis was suppressed at a higher dose range and saturated to a leveled mutant frequency (Ikehata and Ono, Mutat. Res., 508:41-47, 2002). This epidermal phenomenon, called mutation induction suppression (MIS), has a wavelength dependence. The leveled mutant frequency in MIS varies by UV wavelength.
