Parental exposure to natural mixtures of persistent organic pollutants (POP) induced changes in transcription of apoptosis-related genes in offspring zebrafish embryos

ABSTRACT

Apoptosis is an integral element of development that may also be initiated by environmental contaminants. The aim of the present study was to assess potential changes in the regulation of apoptotic genes in zebrafish embryos following parental exposure to two natural mixtures of persistent organic pollutants (POP). The mixture from Lake Mjøsa contained exceptionally high concentrations of polybrominated diphenyl ethers (PBDE), as well as relatively high levels of polychlorinated biphenyls (PCB) and dichlorodiphenyltrichloroethane (DDT). The mixture from Lake Losna contained background concentrations of POP. Genes involved in the apoptotic machinery were screened for their expression profile at four time points during embryonic development. Thirteen and 15 genes involved in apoptosis were found to be significantly upregulated in the high-exposure and background exposure groups, respectively, compared with controls. Modulation of apoptotic genes was restricted only to the first time point, which corresponds with the blastula stage. Although there were substantial differences in POP concentrations between mixtures, genes underlying the apoptosis process showed almost similar responses to the two mixtures. In both exposure groups the main executors of apoptosis p53, casp 2, casp 6, cassp 8, and BAX displayed upregulation compared to controls, suggesting that these POP induce apoptosis via a p53-dependent mechanism. Upregulation of genes that play a critical role in apoptosis suggests that disturbance of normal apoptotic signaling during gametogenesis and embryogenesis may be one of the central mechanisms involved in adverse reproductive effects produced by POP in zebrafish.

Funding

We thank Vidar Berg, Janneche U. Skaare, Anja B. Kristoffersen, for their scientific and technical support. This work was funded by grant 172017/V10 from the Norwegian Research Council and by FRISC (Norwegian Financial Mechanism and EEA Financial Mechanism funds) project number PL0419: Factors of Population Extinction Risk FRISC (2009–2011).

Additional information

Funding

We thank Vidar Berg, Janneche U. Skaare, Anja B. Kristoffersen, for their scientific and technical support. This work was funded by grant 172017/V10 from the Norwegian Research Council and by FRISC (Norwegian Financial Mechanism and EEA Financial Mechanism funds) project number PL0419: Factors of Population Extinction Risk FRISC (2009–2011).