Mercury in the brain of polar bears (Ursus maritimus ) and ringed seals (Pusa hispida).

The exposure of marine mammals to mercury (Hg) is a concern to animal health yet concentrations in the brains of Arctic marine mammals and the neurotoxic effects have been insufficiently studied. Total Hg (THg), inorganic Hg (iHg) and methyl Hg (MeHg) were analyzed in different brain regions of ringed seals (Pusa hispida) and polar bears (Ursus maritimus). The concentration of THg was <2.5 μg/g dry weight (dw) in brain tissue of ringed seals (median MeHg >90%) and <1 μg/g dw in polar bears (100% MeHg). Mercury concentrations which have been linked to neurotoxicity in laboratory studies and wildlife observations have been identified. Total Hg concentrations in polar bear brains were below levels that elicit neurobehavioural effects while THg concentrations in ringed seals were within the range that induces neurobehavioural effects and few individuals exceeded the threshold for neurochemical changes. Concentration-response experiments demonstrated that iHg was a more potent inhibitor of choline esterase (ChE) and monoamine oxidase (MAO) activity and muscarinic acetylcholine receptor (mAChR) binding than MeHg in polar bear brain isolates in vitro but in environmentally-exposed samples higher THg concentrations were only linked to lower MAO activity. Higher THg and iHg concentrations were associated with lower MAO activity in ringed seal brain. Furthermore, in ringed seals, MeHg and iHg concentrations were related to N-methyl-d-aspartate receptor (NMDA-R) binding. These findings support the hypothesis that NMDA-R binding is an indicator of early effects of Hg exposure and show that MAO activity is sensitive to Hg exposure in ringed seal and polar bear brain. There was a significant relationship of Hg concentration in blood and brain tissue of ringed seals, thus blood could be a useful indicator of brain concentration. Both the comparison of Hg concentrations linked to neurotoxic endpoints and the characterization of neurochemical disruption in relation to toxicant exposure in wildlife populations repre