Associations between vitamins A and E and legacy POP levels in highly contaminated Greenland sharks (Somniosus microcephalus)

The Greenland shark (Somniosus microcephalus) is a top predator in Arctic marine ecosystems, and the species bioaccumulates high levels of biomagnifying persistent organic pollutants (POP). In teleost fish, as well as in marine mammals and seabirds, legacy POP have been shown to interfere with the vitamin A and vitamin E homeostasis. Thus, there is the potential for negative health effects from these legacy compounds in Greenland sharks. In the present study we examined associations among plasma levels of legacy POP and plasma vitamin A (refinol [RET], retinyl palmitate [RPA]) and vitamin E (alpha-tocopherol [alpha-TOC]) in Greenland sharks from Svalbard, Norway. Plasma levels of POP were on average higher than the hepatic levels previously reported in Greenland sharks from Iceland and Davis Strait, Canada. Levels were also higher than the plasma levels reported in Arctic marine mammals. DDTs (mean 8069 ng/g l.w., range: 900-59,707 ng/g l.w.), PCBs (mean 5766 ng/g l.w., range 1344-16,106 ng/g l.w.) and chlordanes (mean 1551 ng/g l.w., range: 323-5756 ng/g l.w.) had the highest concentrations among the POP groups studied. There were significant inverse relationships between RET concentrations and the concentrations of the dioxin-like compounds PCB-118 and PCB-156/171, and the non-dioxin-like compounds PCB-99 and PCB-128. There were also significant inverse relationships between RPA and 18 of the 38 POP compounds measured. Furthermore, there were significant positive associations between a-TOC and 13 of the 27 PCB congeners. The study suggests that these vitamin systems can be affected by the relatively high POP concentrations exhibited by Greenland sharks at Svalbard. However, the present study is correlative and thus the potential interplay between POP and vitamin dynamics of Greenland sharks must be interpreted cautiously, pending further research on this issue among elasmobranchs. (C) 2012 Elsevier B.V. All rights reserved.