DNA damage in Atlantic cod (Gadus Morhua) tissues

• Main Author: Njah, Relindis Ghai
• Other Authors: Ketil Hylland,Tor Fredrik Holth and Gunnar Brunborg
• Format: Master Thesis
• Language: English
• Published: 2012
• Subjects: VDP::489; atlantic cod; Gadus morhua
• Online Access: http://hdl.handle.net/10852/33994; http://urn.nb.no/URN:NBN:no-32632

Aquatic organisms are exposed to more or less continuous inputs of a wide range of potentially hazardous substances. The sources of the substances could be natural and/ or anthropogenic. This exposure may have deleterious effects on the health of organisms. The intensity of such effects may vary between different tissues. The main aim of this study was therefore to clarify if cells from different tissues differed in their sensitivity to DNA damage and to quantify DNA repair following oxidative stress. This was done using different tissues from the Atlantic cod (Gadus morhua). Cells from blood, gills, liver and intestinal mucosa were exposed to two concentrations of peroxide (5 μM and 300 μM). Exposure was followed by the enzyme amended comet assay, using lesion-specific enzymes (fpg and ogg1). The results indicated high background damage in all tissues, with intestinal mucosa being the most sensitive and liver the least. Causes for the high baseline damage were not clear although it may be speculated that the sampling method for the cells was too aggressive. However, some significant increases were observed in gill and liver cells that were exposed to 5 μM H2O2 when compared to the unexposed cells while those exposed to 300 μM H2O2 did not cause any significant difference from unexposed cells. This could have been due to high variability, which may have masked effects at high doses. Digestion with enzymes indicated significant increases in oxidative stress for most cells. All these increases were mostly observed at 300 μM H2O2, except for liver cells that indicated differences at 0 μM H2O2. Earlier studies have also indicated increases in oxidative stress with the use of fpg and ogg1. The enzyme amendment of the comet assay did not produce clear results in this study, possibly because the high baseline DNA damage masked the effects of repair endonucleases.