School of Applied Science, Temasek Polytechnic, Singapore 529757, Singapore
Laboratory of Aquatic Animal Diseases, College of Veterinary Medicine, Gyeongsang National University, Jinju, Gyeongnam 660-701, Republic of Korea
Department of Biology, University of Crete, 71409 Heraklion, Crete, Greece
Aquaculture Genomics Research Unit, Faculty of Biosciences and Aquaculture, University of Nordland, 8049 Bodo, Norway
National Institute of Aquatic Resources, Technical University of Denmark, 9850 Hirtshals, Denmark
Embryos (morula stage) of Atlantic cod, Gadus morhua L., were collected and subjected to air exposure for 2 min. followed by recovery at ambient conditions in the rearing container. Total immunoreactive cortisol and transcription of selected stress- and apoptosis-related genes of the embryos were determined before the application of the stressor and at 0.5, 1 and 24 h post-exposure. There was no significant difference in the total cortisol levels of the fertilized eggs before and after handling stress. There was high expression level of hsp70 and sod before application of the stressor and significantly increased at 0.5 h post-exposure. The expression levels of cat and gpx were weak to moderate and were not affected by the stressor. The apoptotic genes, mcl1 and NR-13 were highly expressed and significantly increased after exposure to air. Bcl-X1 and Bcl-X2 were moderately expressed in the control samples, but only the expression level of Bcl-X1 significantly increased following exposure to air. Cluster analysis of the different gene expression levels indicated three categories: those genes that did not show any change in the expression levels post-air exposure; those that had low expression level in the control followed by a significant increase after air exposure; and those that had high expression levels in the control followed by a further increase in expression after air exposure. These results clearly demonstrate that there are potential molecular biomarkers of the response in cod embryos as a consequence of air exposure at a time when cortisol is not fully active.