DNA methylation by N-nitrosomethylbenzylamine in target and non-target tissues of NMRI mice

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Abstract
An enhanced reactivation of ultraviolet-damaged (u.v. at 254 nm) nuclear replicating double-stranded DNA viruses occurs when corresponding host cells are treated with radiation or carcinogens prior to infection. This phenomenon seems to be due to an induced DNA repair activity the nature of which is yet unknown. The u.v.-induced enhanced reactivation (ER) of u.v.-damaged herpes simplex virus (u.v.-HSV) was compared in dividing skin fibroblasts of 30 donors either normal or afflicted by genetic disorders, some of which confer a high risk for sunlight induced skin cancers. Cultures were exposed to a single dose of 0.1–25 J.m−2 from 0–60 h before infection with u.v.—HSV (at about 10−3 survival) and the rate of viral production was determined. ER was maximal for a 36 h time interval in all lines. The u.v. dose eliciting maximal ER was 15 J.m−2 in fibroblasts from normal donors, xeroderma pigmentosum (XP) heterozygotes, Mibelli's porokeratosis, diffused naevomatosis, Down's syndrome, xerodermoids, XP variants and epidermodysplasia verruciformis. However, in the latter 3 cases, ER was almost 10 times more pronounced than in the normal cases. The u.v. dose eliciting maximal ER was 0.1, 0.3 and 2 J.m−2 in excision deficient XP deficient XP fibroblasts from groups A, D and C, respectively, 2.5 J.m−2 in 11961 fibroblasts and 5 J.m−2 in fibroblast lines from Cockayne's syndrome.

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