The protective potency of marine animal meat against the neurotoxicity of methylmercury: Its relationship with the organ distribution of mercury and selenium in the rat

Ohi, Gen; Nishigaki, Susumu; Seki, Humitake; Tamura, Y.; Maki, Toshio; Minowa, Keiko; Shimamura, Yasuhiro; Mizoguchi, Isao; Inaba, Yutaka; Takizawa, Yukio; Kawanishi, Yuji

doi:10.1016/0015-6264(80)90067-x

Cited by 35 publications

(16 citation statements)

References 22 publications

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“…The tuna supplied approximately 0.3 μg/g more dietary Se [1,4,6,14], and we observed a protective effect of tuna that provided about 0.5 μg/g more Se compared to a corn-soy diet [2] in Japanese quail fed high levels of added MeHg (20 μg/g Hg). It seems likely that the higher content of Se in tuna compared to freshwater pike and other dietary protein sources was a factor involved in our studies and those of others [4,14] that demonstrated protective effects of fish or fish products against MeHg toxicity. Little is known about the chemical forms of Se in the marine world, in contrast to other trace elements such as arsenic.…”

Section: Discussionmentioning

confidence: 77%

Factors in Fish Modifying Methylmercury Toxicity and Metabolism

Ganther

Sunde

2007

Biol Trace Elem Res

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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.

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Section: Discussionmentioning

confidence: 77%

Factors in Fish Modifying Methylmercury Toxicity and Metabolism

Ganther

Sunde

2007

Biol Trace Elem Res

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“…Based on the abundance of Se and its favorable molar excess over Hg, ocean fish appear more likely to protect against Hg toxicity than to contribute to causing it. Several studies have demonstrated that Se from yellowfin tuna [7,17], menhaden [18], swordfish [19], and rockfish [20] counteract the adverse impacts of Hg exposure, further supporting the likelihood that Se from fish provides significant natural protection. However, risks associated with consumption of certain seafoods that contain high and disproportionate amounts of Hg in molar excess of Se are expected to be directly related to their Hg to Se ratios.…”

Section: Discussionmentioning

confidence: 95%

“…However, the molecular mechanisms responsible for these toxic effects remain incompletely defined, making it difficult to evaluate risks associated with low-level MeHg exposures from seafood consumption [1][2][3][4]. Selenium (Se)-dependent protection against Hg toxicity has been recognized for 50 years [5] and has since been demonstrated in all species evaluated [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22], but the molecular mechanism responsible for Se-dependent protective effects remains as incompletely defined as those of Hg toxicity. However, because of the high binding affinity (10 45 M) between Hg and Se [23], direct Hg sequestration by Se has often been assumed responsible for the mechanism of Se's protective effect [1,24,25].…”

mentioning

confidence: 99%

Importance of Molar Ratios in Selenium-Dependent Protection Against Methylmercury Toxicity

Ralston

Blackwell

Raymond

2007

Biol Trace Elem Res

163

155

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The influence of dietary selenium (Se) on mercury (Hg) toxicity was studied in weanling male Long Evans rats. Rats were fed AIN-93G-based low-Se torula yeast diets or diets augmented with sodium selenite to attain adequate- or rich-Se levels (0.1, 1.0 or 15 micromol/kg, respectively) These diets were prepared with no added methylmercury (MeHg) or with moderate- or high-MeHg (0.2, 10 or 60 micromol/kg, respectively). Health and weights were monitored weekly. By the end of the 9-week study, MeHg toxicity had impaired growth of rats fed high-MeHg, low-Se diets by approximately 24% (p < 0.05) compared to the controls. Growth of rats fed high-MeHg, adequate-Se diets was impaired by approximately 8% (p < 0.05) relative to their control group, but rats fed high-MeHg, rich-Se diets did not show any growth impairment. Low-MeHg exposure did not affect rat growth at any dietary Se level. Concentrations of Hg in hair and blood reflected dietary MeHg exposure, but Hg toxicity was more directly related to the Hg to Se ratios. Results support the hypothesis that Hg-dependent sequestration of Se is a primary mechanism of Hg toxicity. Therefore, Hg to Se molar ratios provide a more reliable and comprehensive criteria for evaluating risks associated with MeHg exposure.

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“…Studies demonstrating Se-dependent amelioration of MeHg toxicity have included Se from yellowfin tuna (Ohi et al, 1976;Ganther et al, 1972), menhaden (Stillings et al, 1974), swordfish (Freidman et al, 1978), and rockfish (Ohi et al, 1980). Therefore, the organic forms of Se present in ocean fish are bioavailable and effective in counteracting MeHg toxicity.…”

Section: Mercury Interactions With Seleniummentioning

confidence: 98%

Selenium Health Benefit Values as Seafood Safety Criteria

Ralston

2008

EcoHealth

140

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Selenium (Se) is absolutely required for activity of 25-30 genetically unique enzymes (selenoenzymes). All forms of life that have nervous systems possess selenoenzymes to protect their brains from oxidative damage. Homeostatic mechanisms normally maintain optimal selenoenzyme activities in brain tissues, but high methylmercury (MeHg) exposures sequester Se and irreversibly inhibit selenoenzyme activities. However, nutritionally relevant amounts of Se can replace the Se sequestered by MeHg and maintain normal selenoenzyme activities, thus preventing oxidative brain damage and other adverse consequences of MeHg toxicity. Findings of studies that seem contradictory from MeHg exposure perspectives are entirely consistent from MeHg:Se molar ratio perspectives. Studies that have reported dose-dependent consequences of maternal MeHg exposures on child development uniformly involved seafoods that contained much more Hg than Se. Meanwhile more typical varieties of ocean fish contain much more Se than Hg. This may explain why maternal MeHg exposure from eating ocean fish is associated with major IQ benefits in children instead of harm. Therefore, instead of being avoided, ocean fish consumption should be encouraged during pregnancy. However, the safety of freshwater fish consumption is less certain. In freshwater fish, MeHg bioaccumulation and toxicity are both inversely related to Se bioavailability. Their Se can be far lower than their MeHg contents, potentially making them more dangerous than pilot whale meats. Therefore, to provide accurate and appropriate regulatory advice regarding maternal consumption of seafoods and freshwater fish, Hg:Se molar ratios need to be incorporated in food safety criteria.

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The protective potency of marine animal meat against the neurotoxicity of methylmercury: Its relationship with the organ distribution of mercury and selenium in the rat

Cited by 35 publications

References 22 publications

Factors in Fish Modifying Methylmercury Toxicity and Metabolism

Factors in Fish Modifying Methylmercury Toxicity and Metabolism

Importance of Molar Ratios in Selenium-Dependent Protection Against Methylmercury Toxicity

Selenium Health Benefit Values as Seafood Safety Criteria

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