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Data in this article depict patterns of methylation in lung tissues obtained from the offspring of B6129SF1/J dams and 129S1/SvImJ sires exposed in utero to benzo[a]pyrene (BaP) or dibenzo[def,p]chrysene (DBC) as compared to non-exposed offspring. Genome-wide methylation of lung tumors in adult offspring was determined using methylated DNA immunoprecipitation (MeDIP) with the NimbleGen mouse DNA methylation CpG island array. This data article refers to the research article “DNA methylation in lung tissues of mouse offspring exposed in utero to polycyclic aromatic hydrocarbons,” [1] in which comprehensive data interpretation and analysis are provided.

Photoactivation is a promising approach for modulating the biological activity of RuII compounds. In this work, RuII flavonolato compounds, [Ru(η6-p-cymene)(L)(3-Hfl)]OTf (8; 3-Hfl = monoanion of 3-hydroxyflavone; L = solvent) and [Ru(η6-p-cymene)Cl(3-Hfl-X)] (3a–3c; 3-Hfl-X = p-H, -Cl, or -F on the flavonolato phenyl substituent), have been evaluated for photoinduced reactivity within the flavonolato unit upon irradiation with UV (300 nm) or visible (419 nm) light under aerobic conditions. For each compound, irradiation in CH3CN was found to result in the loss of the p-cymene ligand and the formation of products resulting from oxidative ring opening of the flavonolato ligand in a dioxygenase-type reaction. This reaction also results in the release of carbon monoxide. The RuII products generated in these reactions are [RuII(solvent)(carboxylato)]+ and [Ru(CO)(solvent)(carboxylato)]+ (carboxylato = O-benzoylsalicylato or benzoato) species, as determined by ESI-MS. The amount of free CO generated depends on the wavelength of irradiation, with 300 nm light giving a higher amount of free CO. Evaluation of the photoinduced reactivity of 8 in DMSO/H2O (10:90) at 300 nm showed similar reactivity to that found in organic solvent, although the reaction occurs more slowly. The products of the photoreactions of 8 and 3a at 419 nm are nontoxic toward human T-lymphocyte (Jurkat) and non-small-cell lung carcinoma (A549) cells. This lack of toxicity versus the starting compounds is likely due to differences in interactions of the [RuII(solvent)(carboxylato)]+ and [RuII(CO)(solvent)(carboxylato)]+ species with biomolecules (e.g., serum proteins), thus resulting in reduced bioavailabilty. 1H NMR studies provide evidence that the photoreaction products coordinate to biologically relevant donors such as histidine and 5′-GMP in d 6-DMSO/D2O (10:90) and exhibit reactivity with these small molecules that is distinctly different from that exhibited by the starting compounds. Overall, the photoreactivity of 8 and 3a–3c may represent an approach toward altering the biological chemistry of these compounds.

Polycyclic aromatic hydrocarbons (PAHs) comprise an important class of environmental pollutants that are known to cause lung cancer in animals and are suspected lung carcinogens in humans. Moreover, evidence from cell-based studies points to PAHs as modulators of the epigenome. The objective of this work was to assess patterns of genome-wide DNA methylation in lung tissues of adult offspring initiated in utero with the transplacental PAH carcinogens dibenzo[def,p]chrysene (DBC) or benzo[a]pyrene (BaP). Genome-wide methylation patterns for normal (not exposed), normal adjacent and lung tumor tissues obtained from adult offspring were determined using methylated DNA immunoprecipitation (MeDIP) with the NimbleGen mouse DNA methylation CpG island array. Lung tumor incidence in 45-week old mice initiated with BaP was 32%, much lower than that of the DBC-exposed offspring at 96%. Also, male offspring appeared more susceptible to BaP as compared to females. Distinct patterns of DNA methylation were associated with non-exposed, normal adjacent and adenocarcinoma lung tissues, as determined by principal components, hierarchical clustering and gene ontology analyses. From these methylation profiles, a set of genes of interest was identified that includes potential important targets for epigenetic modification during the process of lung tumorigenesis in animals exposed to environmental PAHs.

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