| Summary: | Oceans are global sinks for persistent organic pollutants (POPs). Those lipophilic compounds biomagnify in the marine trophic chain. As a result, top predators such as marine mammals accumulate important levels of POPs and are thus more vulnerable to POP-related health effects. The aim of this thesis was to evaluate the lactational transfer of PCBs, PBDEs, OCPs and their metabolites in grey seal (Halichoerus grypus). Their dynamics were compared with those of vitamin A, a non-specific biomarker of effect for POP contamination. Interactions of those pollutants with the vitamin A status of the mothers and their pups were also examined. Mother-pup pairs were captured 2 to 3 times during the lactation period in order to collect maternal blubber, maternal serum, milk and pup serum. We observed that POPs and vitamin A accumulated in maternal inner blubber during lactation and that POPs appeared to be selectively mobilised from maternal inner blubber into maternal serum. Additionally, only low amounts of HO-PCBs were transferred via the milk. Besides, negative relationships between PCBs in milk and pup serum and circulating vitamin A in pups were revealed. By contrast, in mothers, PCBs and PBDEs were positively correlated to vitamin A in both inner blubber and serum, suggesting an enhanced mobilisation of hepatic vitamin A stores and redistribution in the inner blubber. Since vitamin A is essential for the immune system homeostasis, we attempted to assess the effects of this nutrient as well as environmentally relevant PCB and PBDE concentrations on the apoptosis, proliferation and cell cycle of mouse splenocytes and a harbour seal lymphoma B cell line. No modulation of the investigated parameters could be observed after PCB or PDBE treatment in the 2 models. Finally, we confirmed that vitamin A modulated the cell cycle machinery in LPS-induced mouse splenocytes but not in the harbour seal cell line. (BIOL 3) -- UCL, 2012
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