Abstract
The 8-oxodG content has been measured in chromosomal DNA of gilthead seabream ( Sparus aurata) by HPLC–EC. Susceptibility of different tissues to oxidative DNA damage was studied by exposing fish to model pollutants. Cu(II), paraquat (PQ) and malathion failed to promote DNA oxidation in liver, while dieldrin significantly increased the 8-oxodG content in this organ, but not in gills or blood. After PQ exposure, fish liver showed high levels of glucose-6-P dehydrogenase (G-6PDH) and GSSG reductase activities. The increased antioxidant status and the lack of a specific transport system could explain the lack of susceptibility of liver to DNA oxidative damage induced by PQ. Increased levels of 8-oxodG were detected in the gills of PQ-exposed fish after 8 and 24 h. In contrast, after 48 h exposed fish contained lower 8-oxodG levels than controls. The existence of a PQ transport system in this O 2-rich organ and the lack of a significant increase in antioxidant defenses would explain the sensitivity of gills to DNA damage promoted by PQ. Elimination of this soluble chemical and the putative induction of DNA-repair enzymes specific for oxidative damages could explain the drop of 8-oxodG levels at longer times. Fish exposed to moderate levels of urban and industrial pollution showed significantly high 8-oxodG content in hepatic DNA. We conclude that 8-oxodG determination in chromosomal DNA by HPLC–EC is a potentially useful biomarker of environmental pollution, although its response is still somewhat lower than that of other well-established biomarkers of oxidative stress.
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More From: Mutation Research/Genetic Toxicology and Environmental Mutagenesis
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