We evaluated the effects of two putative non-genotoxic hepatic carcinogens, hexabromocyclododecane (HBCD) and 17-beta oestradiol (E(2)) on global and CpG promoter DNA methylation in both primary human hepatocytes and hepatocellular carcinoma (HepG2) cells. The mRNA gene expression levels of genes involved particularly in cell cycle were also evaluated and potential correlation with DNA methylation status examined. HBCD at 0.
View Article and Find Full Text PDFAlteration of DNA methylation is a major epigenetic mechanism associated with the effects of nongenotoxic carcinogens. We evaluated the effects of two environmental pollutants, hexabromocyclododecane (HBCD), 17-beta oestradiol (E(2)) as well as 5-aza 2' deoxycytidine (5AdC) on global DNA methylation levels (5-methyl 2' deoxycytidine) in the liver and gonads of the three-spine stickleback (Gasterosteus aculeatus). HBCD at 30 and 300 ng/L of water did not produce statistically significant differences in global genomic methylation in liver of female stickleback.
View Article and Find Full Text PDFDNA strand breaks [as determined by the conventional and formamidopyrimidine glycosylase (FPG)-modified Comet assay] and antioxidant defense status [as indicated by superoxide dismutase (SOD) activity and reduced glutathione (GSH) concentration] were evaluated in healthy adult chub (Leuciscus cephalus) after exhaustive exercise [swimming to their critical swimming speed (U(crit)), twice in succession with a 40 min rest period between] vs. confined (unexercised) control fish. The conventional Comet assay revealed significantly higher DNA strand breaks in all the tissues (blood, liver, and gill), with the highest increase over background evident in the epithelial gill cells of swum fish compared to the controls.
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