English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Treatment of monkey kidney cells with low doses of carcinogen enhances the survival of UV-irradiated simian virus 40 (SV40). This is true for compounds with UV-like effects (metabolites of aflatoxin B1, N-acetoxyacetylaminofluorene) and compounds with x-ray-like effects (methyl methanesulfonate, ethyl methanesulfonate). This phenomenon resembles the UV-reactivation of viruses in eukaryotic cells. The carcinogen-induced enhancement of the survival of UV-irradiated SV40 is correlated with the inhibition of host-cell DNA synthesis, suggesting that the inhibition is an inducing agent. An enhancement of UV-irradiated SV40 survival is also obtained in cells treated with hydroxyurea or cycloheximide for long enough that there is still inhibition of host DNA synthesis during the early stage of SV40 infection. We hypothesize that treatment of host cells with carcinogens induces a new recovery pathway that facilitates the replication of damaged DNA, bypassing the lesions and resulting in the enhanced survival of UV-irradiated SV40. This inducible process might represent the expression of "SOS repair" functions in eukaryotic cells analogous to the previously demonstrated induction of SOS repair in bacteria after UV or carcinogen treatment.

Carcinogens enhance survival of UV-irradiated simian virus 40 in treated monkey kidney cells: induction of a recovery pathway?