Absence of selenium protection against methylmercury toxicity in harbour seal leucocytes in vitro

- Harbour seal lymphocytes were exposed in vitro to MeHg (0.75 μM) and Se.
- Molar ratio Hg:Se of 1:10 was chosen reflecting blood concentrations of wild seals.
- MeHg affected lymphocyte proliferation and mitochondrial membrane potential.
- Sodium selenite and seleno-L-methionine did not prevent MeHg toxicity in vitro.
- Preliminary data reflect the complexity of Hg-Se interactions.

Previous studies described high concentrations of mercury (Hg) and selenium (Se) in the blood of harbour seals, Phoca vitulina from the North Sea. In the present study, we evaluated the in vitro potential protective effects of sodium selenite (Na2SeO3) and selenomethionine (SeMet) on cell proliferation of harbour seal lymphocytes exposed to MeHgCl 0.75 μM. In vitro exposure of ConA-stimulated T lymphocytes resulted in severe inhibition of DNA synthesis, likely linked to severe loss of mitochondrial membrane potential at 0.75 μM. Neither selenite nor SeMet showed a protective effect against MeHg toxicity expressed at the T lymphocyte proliferation level for harbour seals. Selenite and SeMet did not show negative effects regarding lymphocyte proliferation and mitochondrial membrane potential.To conclude, our results clearly demonstrated that MeHg affected in vitro immune cells exposure with no protective effects of selenium at a molar ratio Hg:Se of 1:10 in harbour seals from the North Sea.