Dose-dependent onset of regenerative program in neutron irradiated mouse skin.

Background: Tissue response to irradiation is not easily recapitulated by cell culture studies. The objective of this investigation was to characterize, the transcriptional response and the onset of regenerative processes in mouse skin irradiated with different doses of fast neutrons.

Methodology/principal Findings: To monitor general response to irradiation and individual animal to animal variation, we performed gene and protein expression analysis with both pooled and individual mouse samples.

Relationship between DNA lesions, DNA repair and chromosomal damage induced by acetaldehyde.

Acetaldehyde (AA) was tested along with two other crosslinking agents: formaldehyde (FA), an inducer of DNA-protein crosslinks (DPCs) and mitomycin C (MMC), an inducer of interstrand crosslinks (ICLs), to find out whether the mechanism of action of AA resembles more MMC or FA. Using a modification of the standard protocol for comet assay we demonstrate that AA induces crosslinks. Using a combination of alkaline comet version and proteinase-K, a clear abrogation of AA-induced reduction in DNA migration, like after FA treatment, was observed demonstrating that both agents induce DPCs, whereas MMC induces predominantly ICLs.

DNA repair deficiency and acetaldehyde-induced chromosomal alterations in CHO cells.

Induction of chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs) by acetaldehyde (AA) was evaluated in parental and different DNA repair-deficient Chinese hamster ovary (CHO) cell lines to elucidate the mechanisms involved in the protection against AA-induced chromosome damage. Cell lines employed included the parental (AA8), nucleotide excision repair (UV4, UV5, UV61), base excision repair (EM9), homologous recombination repair (HRR) (irs1SF, 51D1)-deficient and Fanconi-like (KO40) ones. The ranking of different cell lines for sensitivity to induction of CAs by AA was 51D1 > irs1SF > KO40 > UV4 > V33-EM9-AA8 > UV61-UV5 in a descending order.