Factors in Fish Modifying Methylmercury Toxicity and Metabolism

Abstract

We report here some results of a long-term (19 month) study with cats fed methylmercury (MeHg) in nutritionally balanced diets based on fish. By using either freshwater pike (low in Se) or canned tuna (high in Se) as the major protein source, basal diets with low levels of MeHg were prepared having different Se content, all Se being of natural origin. The basal diets produced no signs of toxicity or pathological changes over the l9-month period. In cats fed basal diets spiked with medium or high levels of MeHg, evidence for delayed onset of toxic effects from the added MeHg was observed with the tuna diets compared to pike diets. In brain, muscle, and blood, the activity of GSH peroxidase, a selenoenzyme, was decreased by Hg. In liver, substantial accumulation of Hg with Se occured (molar Hg/Se ratio approximately 1.4 to 1.8) but GSH peroxidase activity was unaffected. We suggest that the coaccumulation of Hg and Se in liver measures the extent to which MeHg has been metabolically transformed by metabolism to Hg++, and inactivated by deposition as a Hg/Se complex of low bioavailability. The accumulation of Hg and Se in liver was much greater in cats fed tuna compared to pike, out of proportion to the relatively small differences in Hg and Se content of the tuna and pike basal diets. Some mechanisms are described by which selenium, vitamin E, and other factors might facilitate MeHg breakdown to inorganic Hg during long term low level exposure to MeHg.

Liver and kidney concentrations of strontium, barium, cadmium, copper, zinc, manganese, chromium, antimony, selenium and lead in cats

“…When Na 2 SeO 3 or organic Se was added to the control diet, the hepatic Se concentrations (4.24 ± 0.59 μg/g DM and 4.79 ± 0.37 μg/g DM), but especially the renal Se excretion increased. Another study [31] found marked higher Se concentrations in the liver (mean: 0.69-21.4 μg/g, fresh basis) and kidneys (mean: 1.54-4.15 μg/g, fresh basis) of cats fed different experimental diets when the data are compared with the results of the present study.…”

Theoretical study of molecular and electronic structure of 2‐Se‐(2‐methyl‐2‐propenyl)‐1‐benzoic acid

“…Several of these compounds have been examined in different organs, with a chemopreventive effect found in animal models 11–14. Some potential mechanisms of cancer prevention with selenium have recently been reviewed 15.…”

No evidence of selenosis from a selenium-rich diet in the Brazilian Amazon

“…Indeed, animal studies have suggested that specific selenoproteins such as selenoprotein P may protect against Hg toxicity by binding to Hg and reducing its availability for target proteins and organs (Yoneda and Suzuki, 1997). Conversely, some authors have suggested that selenoproteins may be key targets of Hg toxicity; the very high affinity of Hg for selenol groups in the active site of selenoproteins could result in Hg binding and compromise selenoproteins enzymatic functions (Carvalho et al, 2008;Ganther and Sunde, 2007;Ralston and Raymond, 2010;Seppänen et al, 2004). Therefore, in a situation with elevated Hg and Se, there may be less 'excess' of Se and consequently little or no Se toxicity (Khan and Wang, 2009).…”