LAUSR

Few published studies have examined whether the elevated concentrations of the nonessential toxic metal mercury (Hg) often observed in shark muscle also occur in the shark brain or whether Hg accumulation affects shark neurophysiology. Therefore, this study examined accumulation and distribution of Hg in the shark brain, as well as effects of Hg on oxidative stress in the shark central nervous system, with particular focus on the Atlantic sharpnose shark (Rhizoprionodon terraenovae). Sharks were collected along the southeastern U.S. coast throughout most of this species’ U.S. geographical range. Total Hg (THg) concentrations were measured in and compared between shark muscle and brain, whereas known biomarkers of Hg-induced neurological effects, including glutathione depletion, lipid peroxidation, and concentrations of a protein marker of glial cell damage (S100b), were measured in shark cerebrospinal fluid. Brain THg concentrations were correlated with muscle THg levels but were significantly lower and did not exceed most published thresholds for neurological effects, suggesting limited potential for detrimental responses. Biomarker concentrations supported this premise, because these data were not correlated with brain THg levels. Hg speciation also was examined. Unlike muscle, methylmercury (MeHg) did not comprise a high percentage of THg in the brain, suggesting that differential uptake or loss of organic and inorganic Hg and/or demethylation of MeHg may occur in this organ. Although Hg accumulation in the shark brain generally fell below toxicity thresholds, higher THg levels were measured in the shark forebrain compared with the midbrain and hindbrain. Therefore, there is potential for selective effects on certain aspects of shark neurophysiology if brain Hg accumulation is increased.