Maternal seafood consumption is associated with improved selenium status: Implications for child health.

Selenium (Se) is required for synthesis of selenocysteine (Sec), an amino acid expressed in the active sites of Se-dependent enzymes (selenoenzymes), including forms with essential functions in fetal development, brain activities, thyroid hormone metabolism, calcium regulation, and to prevent or reverse oxidative damage. Homeostatic mechanisms normally ensure the brain is preferentially supplied with Se to maintain selenoenzymes, but high methylmercury (CH3Hg) exposures irreversibly inhibit their activities and impair Sec synthesis. Due to Hg's high affinity for sulfur, CH3Hg initially binds with the cysteine (Cys) moieties of thiomolecules which are selenoenzyme substrates. These CH3Hg-Cys adducts enter selenoenzyme active sites and transfer CH3Hg to Sec, thus irreversibly inhibiting their activities. High CH3Hg exposures are uniquely able to induce a conditioned Se-deficiency that impairs synthesis of brain selenoenzymes. Since the fetal brain lacks Se reserves, it is far more vulnerable to CH3Hg exposures than adult brains. This prompted concerns that maternal exposures to CH3Hg present in seafood might impair child neurodevelopment. However, typical varieties of ocean fish contain far more Se than CH3Hg. Therefore, eating them should augment Se-status and thus prevent Hg-dependent loss of fetal selenoenzyme activities. To assess this hypothesis, umbilical cord blood and placental tissue samples were collected following delivery of a cohort of 100 babies born on Oahu, Hawaii. Dietary food frequency surveys of the mother's last month of pregnancy identified groups with no (0 g/wk), low (0-12 g/wk), or high (12 + g/wk) levels of ocean fish consumption. Maternal seafood consumption increased Hg contents in fetal tissues and resulted in ∼34% of cord blood samples exceeding the EPA Hg reference level of 5.8 ppb (0.029 µM). However, Se concentrations in these tissues were orders of magnitude higher and ocean fish consumption caused cord blood Se to increase ∼9.4 times faster than Hg. Therefore, this study supports the hypothesis that maternal consumption of typical varieties of ocean fish provides substantial amounts of Se that protect against Hg-dependent losses in Se bioavailability. Recognizing the pivotal nature of the Hg:Se relationship provides a consilient perspective of seafood benefits vs. risks and clarifies the reasons for the contrasting findings of certain early studies.

Net effects explains the benefits to children from maternal fish consumption despite methylmercury in fish.

In 2001 the U.S. Food and Drug Administration (FDA) issued precautionary advice to pregnant women to limit fish consumption over concern that the methylmercury content might harm their children's neurodevelopment. This concern was based largely on results from an epidemiological study of mothers primarily exposed to methylmercury from consuming pilot whale. Subsequently, FDA and the World Health Organization/Food and Agriculture Organization (WHO/FAO) undertook independent assessments of fish consumption that considered net effects from both fish nutrients, primarily omega-3 fatty acids, as beneficial and methylmercury as harmful. Both assessments estimated that when mothers regularly consume fish during pregnancy, their children are likely to have improved neurodevelopment compared to children of non-fish eaters despite their exposure to methylmercury. These estimated improvements included gains of two to over five full scale IQ points from levels of maternal consumption that are achievable in most of the world. Consistent with those estimates, human research on fish consumption and child neurodevelopment from more than 200,000 mother-child pairs now collectively reports 51 beneficial associations with neurodevelopmental outcomes and three adverse associations, the latter with no discernable pattern. These associations include full scale IQ gains similar to, or somewhat higher than, those estimated by FDA and FAO/WHO. Also consistent with the FDA and FAO/WHO estimates, research has reported beneficial associations with fish consumption when pregnant women are exposed to methylmercury from fish in excess of the U.S. Environmental Protection Agency's (EPA) Reference Dose (RfD). Our analysis evaluates how the net effects approach as utilized by FDA and FAO/WHO provides a holistic explanation for these results with implications for public health policy. This concordance of net effects modeling and empirical scientific evidence supports a clarification of current public health recommendations to focus on greater fish consumption by pregnant women for their children's neurodevelopment.

Concomitant selenoenzyme inhibitor exposures as etiologic contributors to disease: Implications for preventative medicine.

The physiological activities of selenium (Se) occur through enzymes that incorporate selenocysteine (Sec), a rare but important amino acid. The human genome includes 25 genes coding for Sec that employ it to catalyze challenging reactions. Selenoenzymes control thyroid hormones, calcium activities, immune responses, and perform other vital roles, but most are devoted to preventing and reversing oxidative damage. As the most potent intracellular nucleophile (pKa 5.2), Sec is vulnerable to binding by metallic and organic soft electrophiles (E*). These electron poor reactants initially form covalent bonds with nucleophiles such as cysteine (Cys) whose thiol (pKa 8.3) forms adducts which function as suicide substrates for selenoenzymes. These adducts orient E* to interact with Sec and since Se has a higher affinity for E* than sulfur, the E* transfers to Sec and irreversibly inhibits the enzyme's activity. Organic electrophiles have lower Se-binding affinities than metallic E*, but exposure sources are more abundant. Individuals with poor Se status are more vulnerable to the toxic effects of high E* exposures. The relative E*:Se stoichiometries remain undefined, but the aggregate effects of multiple E* exposures are predicted to be additive and possibly synergistic under certain conditions. The potential for the combined Se-binding effects of common pharmaceutical, dietary, or environmental E* require study, but even temporary loss of selenoenzyme activities would accentuate oxidative damage to tissues. As various degenerative diseases are associated with accumulating DNA damage, defining the effects of complementary E* exposures on selenoenzyme activities may enhance the ability of preventative medicine to support healthy aging.

Seafood and health: What you need to know?

Seafood, including fish and shellfish, provides an ideal package of nutrients and is an important part of a healthy diet. Strong evidence has shown that eating fish and other seafoods improve brain, eye, and heart health. The new 2020-2025 Dietary Guidelines for Americans (DGA) recommend that Americans of all ages should eat more seafood-at least twice a week-particularly pregnant women and young children. However, less than one in five Americans heed that advice. About one-third of Americans eat seafood once a week, while nearly half eat fish only occasionally or not at all. This calls for a drastic shift in the American diet to vary protein sources and include more seafood products in order to receive the most health benefits. This chapter covers (1) seafood nutrition and health benefits, (2) seafood's protective effects against mercury toxicity, (3) selenium health benefit values (HBVs), and (4) challenges and opportunities for seafood production, demand and sustainability. This chapter aims to convey recent advances in science-based information to increase public awareness of seafood safety, nutrition and health benefits of seafood as part of a healthy diet, and to advocate healthy eating with smart food choices by promoting two servings of seafood per week. This will support the healthy eating patterns and promotes a minimum two to three servings of seafood recommended by the current DGA.

Mercury: selenium interactions and health implications.

Measuring the amount of mercury present in the environment or food sources may provide an inadequate reflection of the potential for health risks if the protective effects of selenium are not also considered. Selenium's involvement is apparent throughout the mercury cycle, influencing its transport, biogeochemical exposure, bioavailability, toxicological consequences, and remediation. Likewise, numerous studies indicate that selenium, present in many foods (including fish), protects against mercury exposure. Studies have also shown mercury exposure reduces the activity of selenium dependent enzymes. While seemingly distinct, these concepts may actually be complementary perspectives of the mercury-selenium binding interaction. Owing to the extremely high affinity between mercury and selenium, selenium sequesters mercury and reduces its biological availability. It is obvious that the converse is also true; as a result of the high affinity complexes formed, mercury sequesters selenium. This is important because selenium is required for normal activity of numerous selenium dependent enzymes. Through diversion of selenium into formation of insoluble mercury-selenides, mercury may inhibit the formation of selenium dependent enzymes while supplemental selenium supports their continued synthesis. Further research into mercury-selenium interactions will help us understand the consequences of mercury exposure and identify populations which may be protected or at greater risk to mercury's toxic effects.

Selenium health benefit values provide a reliable index of seafood benefits vs. risks.

BACKGROUND: Methylmercury (CH3Hg) toxicity causes irreversible inhibition of selenium (Se)-dependent enzymes, including those that are required to prevent and reverse oxidative damage in the brain. Fish consumption provides numerous essential nutrients required for optimal health, but is also associated with CH3Hg exposure risks, especially during fetal development. Therefore, it is necessary to assess the amounts of both elements in seafood to evaluate relative risks or benefits. Consumption of ocean fish containing Se in molar excess of CH3Hg will prevent interruption of selenoenzyme activities, thereby alleviating Hg-exposure risks. Because dietary Se is a pivotal determinant of CH3Hg's effects, the Selenium Health Benefit Value (HBV) criterion was developed to predict risks or benefits as a result of seafood consumption. A negative HBV indicates Hg is present in molar excess of Se and may impair Se availability while a positive HBV indicates consumption will improve the Se status of the consumer, thus negating risks of Hg toxicity. OBJECTIVE: This study examined the Hg and Se contents of varieties of seafood to establish those with positive HBV's offering benefits and those having negative HBVs indicating potential consumption risks. METHODS: The Hg and Se molar concentrations in samples of meat from pilot whale, mako shark, thresher shark, swordfish, bigeye tuna, and skipjack tuna were used to determine their HBV's in relation to body weight. RESULTS: The HBVs of pilot whale, mako shark, and swordfish were typically negative and inversely related to body weight, indicating their consumption may impair Se availability. However, the HBV's of thresher shark, bigeye tuna, and skipjack tuna were uniformly positive regardless of body weights, indicating their consumption counteracts Hg-dependent risks of selenoenzyme impairment. CONCLUSIONS: The HBV criterion provides a reliable basis for differentiating seafoods whose intake should be limited during pregnancy from those that should be consumed to obtain health benefits.

Trace minerals in tilapia fillets: Status in the United States marketplace and selenium supplementation strategy for improving consumer's health.

This goal of this study was to highlight the importance of minerals in the diet of fish for meeting micronutrient requirements in the human diet. First arsenic, calcium, cadmium, copper, iron, molybdenum, magnesium, manganese, sodium, phosphorus, potassium, selenium, and zinc concentrations of twelve commercially available tilapia samples were measured. The nutritional value of fillets in regard to their mineral content were assessed to establish potential health benefits or risks for consumers. The health benefit value of selenium was also calculated. Positive health benefit values indicate that tilapia fillets in the United States marketplace of this study do not pose health risks associated with mercury exposures. Selenium was the trace mineral of interest. After the market study, a seven-week fish feeding trial was conducted to study the influence of organic versus inorganic dietary selenium on Nile tilapia (Oreochromis niloticus). Fish were fed two different diets enriched with the same concentration (0.01g kg-1) of selenium in form of inorganic (sodium selenite) or organic (seleno-L-methionine) selenium in triplicate groups. There were no significant differences between growth and biometrics of fish fed different diets (p>0.05). At the end of trial twelve fish from each treatment were collected. Fillets of fish fed organic selenium had selenium concentrations of 0.55 ± 0.01 µg g-1 which were significantly (p<0.05) higher than fish fed inorganic selenium at levels of 0.22 ± 0.008 µg g-1 or fish samples from the marketplace with a selenium level of 0.2 ± 0.03 µg g-1. Fish fed organic selenium also had significantly higher (p<0.05) plasma and kidney selenium in comparison to fish fed inorganic selenium. No significant differences (p>0.05) were observed in glutathione peroxidase activities in either the plasma or liver of Nile tilapia in the different treatment groups. This study shows that organic selenium is a better option for production of Nile tilapia fillets rich in selenium.

Mercury's neurotoxicity is characterized by its disruption of selenium biochemistry.

BACKGROUND: Methylmercury (CH3Hg+) toxicity is characterized by challenging conundrums: 1) "selenium (Se)-protective" effects, 2) undefined biochemical mechanism/s of toxicity, 3) brain-specific oxidative damage, 4) fetal vulnerability, and 5) its latency effect. The "protective effects of Se" against CH3Hg+ toxicity were first recognized >50 years ago, but awareness of Se's vital functions in the brain has transformed understanding of CH3Hg+ biochemical mechanisms. Mercury's affinity for Se is ~1 million times greater than its affinity for sulfur, revealing it as the primary target of CH3Hg+ toxicity. SCOPE OF REVIEW: This focused review examined research literature regarding distinctive characteristics of CH3Hg+ toxicity to identify Se-dependent aspects of its biochemical mechanisms and effects. CONCLUSIONS: Research indicates that CH3Hg+ irreversibly inhibits the selenoenzymes that normally prevent/reverse oxidative damage in the brain. Unless supplemental Se is provided, consequences increase as CH3Hg+ approaches/exceeds equimolar stoichiometries with Se, thus forming HgSe and inducing a conditioned Se deficiency. As the biochemical target of CH3Hg+ toxicity, Se-physiology provides perspectives on the brain specificity of its oxidative damage, accentuated fetal vulnerability, and latency. This review reconsiders the concept that Se is a "tonic" that protects against CH3Hg+ toxicity and recognizes Se's role as Hg's molecular "target". As the most potent intracellular nucleophile, the selenoenzyme inhibition paradigm has broad implications in toxicology, including resolution of conundrums of CH3Hg+ toxicity. GENERAL SIGNIFICANCE: Mercury-dependent sequestration of selenium and the irreversible inhibition of selenoenzymes, especially those required to prevent and reverse oxidative damage in the brain, are primarily responsible for the characteristic effects of mercury toxicity.

Selenium Health Benefit Values: Updated Criteria for Mercury Risk Assessments.

Selenium (Se)-dependent enzymes (selenoenzymes) protect brain tissues against oxidative damage and perform other vital functions, but their synthesis requires a steady supply of Se. High methylmercury (CH3Hg) exposures can severely diminish Se transport across the placenta and irreversibly inhibit fetal brain selenoenzymes. However, supplemental dietary Se preserves their activities and thus prevents pathological consequences. The modified Se health benefit value (HBVSe) is a risk assessment criterion based on the molar concentrations of CH3Hg and Se present in a fish or seafood. It was developed to reflect the contrasting effects of maternal CH3Hg and Se intakes on fetal brain selenoenzyme activities. However, the original equation was prone to divide-by-zero-type errors whereby the calculated values increased exponentially in samples with low CH3Hg contents. The equation was refined to provide an improved index to better reflect the risks of CH3Hg exposures and the benefits provided by dietary Se. The HBVSe provides a biochemically based perspective that confirms and supports the FDA/EPA advice for pregnant and breast-feeding women regarding seafoods that should be avoided vs. those that are beneficial to consume. Since Se can be highly variable between watersheds, further evaluation of freshwater fish is needed to identify locations where fish with negative HBVSe may arise and be consumed by vulnerable subpopulation groups.

Umbilical cord blood and placental mercury, selenium and selenoprotein expression in relation to maternal fish consumption.

Seafood is an important source of nutrients for fetal neurodevelopment. Most individuals are exposed to the toxic element mercury through seafood. Due to the neurotoxic effects of mercury, United States government agencies recommend no more than 340g (12oz) per week of seafood consumption during pregnancy. However, recent studies have shown that selenium, also abundant in seafood, can have protective effects against mercury toxicity. In this study, we analyzed mercury and selenium levels and selenoprotein mRNA, protein, and activity in placenta of a cohort of women in Hawaii in relation to maternal seafood consumption assessed with dietary surveys. Fish consumption resulted in differences in mercury levels in placenta and cord blood. When taken as a group, those who consumed no fish exhibited the lowest mercury levels in placenta and cord blood. However, there were numerous individuals who either had higher mercury with no fish consumption or lower mercury with high fish consumption, indicating a lack of correlation. Placental expression of selenoprotein mRNAs, proteins and enzyme activity was not statistically different in any region among the different dietary groups. While the absence of seafood consumption correlates with lower average placental and cord blood mercury levels, no strong correlations were seen between seafood consumption or its absence and the levels of either selenoproteins or selenoenzyme activity.

Potential Role of Selenoenzymes and Antioxidant Metabolism in relation to Autism Etiology and Pathology.

Autism and autism spectrum disorders (ASDs) are behaviorally defined, but the biochemical pathogenesis of the underlying disease process remains uncharacterized. Studies indicate that antioxidant status is diminished in autistic subjects, suggesting its pathology is associated with augmented production of oxidative species and/or compromised antioxidant metabolism. This suggests ASD may result from defects in the metabolism of cellular antioxidants which maintain intracellular redox status by quenching reactive oxygen species (ROS). Selenium-dependent enzymes (selenoenzymes) are important in maintaining intercellular reducing conditions, particularly in the brain. Selenoenzymes are a family of ~25 genetically unique proteins, several of which have roles in preventing and reversing oxidative damage in brain and endocrine tissues. Since the brain's high rate of oxygen consumption is accompanied by high ROS production, selenoenzyme activities are particularly important in this tissue. Because selenoenzymes can be irreversibly inhibited by many electrophiles, exposure to these organic and inorganic agents can diminish selenoenzyme-dependent antioxidant functions. This can impair brain development, particularly via the adverse influence of oxidative stress on epigenetic regulation. Here we review the physiological roles of selenoproteins in relation to potential biochemical mechanisms of ASD etiology and pathology.

The nail as a noninvasive indicator of methylmercury exposures and mercury/selenium molar ratios in brain, kidney, and livers of Long-Evans rats.

Animal studies indicate that the toxic effects of methylmercury (MeHg) exposures increase when selenium (Se) status is low. Toxicity is directly proportional to Hg/Se molar ratios in critical tissues such as brain and increase dramatically as molar ratios exceed 1:1. In this study, we examined the nail as a biomonitor of Hg/Se molar ratios in kidney, liver, and brain tissues of weanling male Long-Evans rats fed controlled diets containing varying amounts of Se and MeHg. Linear regression analyses indicate that the natural log transform of the Hg/Se ratio in the nails is strongly related to the Hg/Se molar ratio in kidney, liver, and brain (p < 0.01 in all cases). The nail appears to be a reliably accurate noninvasive biomonitor of the Hg/Se molar ratio in tissues and should, therefore, be considered for use in human studies.

Dietary selenium's protective effects against methylmercury toxicity.

Dietary selenium (Se) status is inversely related to vulnerability to methylmercury (MeHg) toxicity. Mercury exposures that are uniformly neurotoxic and lethal among animals fed low dietary Se are far less serious among those with normal Se intakes and are without observable consequences in those fed Se-enriched diets. Although these effects have been known since 1967, they have only lately become well understood. Recent studies have shown that Se-enriched diets not only prevent MeHg toxicity, but can also rapidly reverse some of its most severe symptoms. It is now understood that MeHg is a highly specific, irreversible inhibitor of Se-dependent enzymes (selenoenzymes). Selenoenzymes are required to prevent and reverse oxidative damage throughout the body, particularly in the brain and neuroendocrine tissues. Inhibition of selenoenzyme activities in these vulnerable tissues appears to be the proximal cause of the pathological effects known to accompany MeHg toxicity. Because Hg's binding affinities for Se are up to a million times higher than for sulfur, its second-best binding partner, MeHg inexorably sequesters Se, directly impairing selenoenzyme activities and their synthesis. This may explain why studies of maternal populations exposed to foods that contain Hg in molar excess of Se, such as shark or pilot whale meats, have found adverse child outcomes, but studies of populations exposed to MeHg by eating Se-rich ocean fish observe improved child IQs instead of harm. However, since the Se contents of freshwater fish are dependent on local soil Se status, fish with high MeHg from regions with poor Se availability may be cause for concern. Further studies of these relationships are needed to assist regulatory agencies in protecting and improving child health.

How might selenium moderate the toxic effects of mercury in stream fish of the western U.S.?

The ability of selenium (Se) to moderate mercury (Hg) toxicity is well established in the literature. Mercury exposures that might otherwise produce toxic effects are counteracted by Se, particularly when Se:Hg molar ratios approach or exceed 1. We analyzed whole body Se and Hg concentrations in 468 fish representing 40 species from 137 sites across 12 western U.S. states. The fish samples were evaluated relative to a published wildlife protective Hg threshold (0.1 sg Hg x g(-1) wet wt.), the currenttissue based methylmercury (MeHg) water quality criterion (WQC) for the protection of humans (0.3 microg Hg x g(-1) wet wt) and to presumed protections against Hg toxicity when Se:Hg molar ratios are >1. A large proportion (56%) of our total fish sample exceeded the wildlife Hg threshold, whereas a smaller, but significant proportion (12%), exceeded the MeHg WQC. However, 97.5% of the total fish sample contained more Se than Hg (molar ratio >1) leaving only 2.5% with Se: Hg ratios <1. All but one of the fish with Se:Hg <1, were of the genus Ptychochelius (pikeminnow). Scientific literature on Se counteracting Hg toxicity and our finding that 97.5% of the freshwater fish in our survey have sufficient Se to potentially protect them and their consumers against Hg toxicity suggests that Se in fish tissue (Se:Hg molar ratio) must be considered when assessing the potential toxic effects of Hg.

Dietary and tissue selenium in relation to methylmercury toxicity.

Selenium (Se) supplementation in the nutritionally relevant range counteracts methylmercury (MeHg) toxicity. Since Se tends to be abundant in fish, MeHg exposures alone may not provide an accurate index of risk from fish consumption. Molar ratios of MeHg:Se in the diets and Hg:Se in tissues of exposed individuals may provide a more accurate index. This experiment compared MeHg toxicity in relation to MeHg exposure vs. Hg:Se molar ratios in diets and tissues. Diets were prepared using low-Se torula yeast basal diets supplemented with Na(2)SeO(4) to contain 0.1, 1.0, or 10.0 micromol Se/kg ( approximately 0.01, 0.08, or 0.8 ppm Se), reflecting low-, adequate-, or rich-Se intakes, respectively. Diets contained either low or high (0.5 micromol or 50 micromol MeHg/kg) ( approximately 0.10 or 10 ppm Hg). Sixty weanling male Long Evans rats were distributed into six weight-matched groups (three Se levels x two MeHg levels) that were supplied with water and their respective diets ab libitum for 18 weeks. No Se-dependent differences in growth were noted among rats fed low-MeHg diets, but growth impairments among rats fed high-MeHg were inversely related to dietary Se. After 3 weeks on the diet, growth impairments were evident among rats fed high-MeHg with low- or adequate-Se and after 10 weeks, rats fed low-Se, high-MeHg diets started to lose weight and displayed hind limb crossing. No weight loss or hind limb crossing was noted among animals fed high-MeHg, rich-Se diets. Methylmercury toxicity was not predictable by tissue Hg, but was inversely related to tissue Se (P<0.001) and directly related to Hg:Se ratios (P<0.001). Methylmercury-selenocysteine complexes (proposed name; pseudomethionine) appear likely to impair Se bioavailability, interrupting synthesis of selenium-dependent enzymes (selenoenzymes) that provide antioxidant protection in brain. Therefore, selenoenzymes may be the molecular target of methylmercury toxicity.

Selenium health benefit values as seafood safety criteria.

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.

Mercury toxicity and the mitigating role of selenium.

Mercury is a well-known environmental toxicant, particularly in its most common organic form, methylmercury. Consumption of fish and shellfish that contain methylmercury is a dominant source of mercury exposure in humans and piscivorous wildlife. Considerable efforts have focused on assessment of mercury and its attendant risks in the environment and food sources, including the studies reported in this issue. However, studies of mercury intoxication have frequently failed to consider the protective effects of the essential trace element, selenium. Mercury binds to selenium with extraordinarily high affinity, and high maternal exposures inhibit selenium-dependent enzyme activities in fetal brains. However, increased maternal dietary selenium intakes preserve these enzyme activities, thereby preventing the pathological effects that would otherwise arise in their absence. Recent evidence indicates that assessments of mercury exposure and tissue levels need to consider selenium intakes and tissue distributions in order to provide meaningful risk evaluations.

Selenium and mercury in pelagic fish in the central north pacific near Hawaii.

Protective effects of selenium against mercury toxicity have been demonstrated in all animal models evaluated. As interactions between selenium and mercury and their molar ratios in seafood are essential factors in evaluating risks associated with dietary mercury exposure, considering mercury content alone is inadequate. In this study, the absolute and molar concentrations of mercury and selenium were determined in edible portions from 420 individual fish representing 15 species of pelagic fish collected from the central North Pacific Ocean near Hawaii. Selenium was in molar excess of mercury in almost all fish species evaluated. The rank order of mean Se/Hg molar ratios was striped marlin (17.6) > yellowfin tuna (14.1) > mahimahi (13.1) > skipjack tuna (12.8) > spearfish (11.4) > wahoo (10.8) > sickle pomfret (6.7) > albacore tuna (5.3) > bigeye tuna (5.2) > blue marlin (4.1) > escolar (2.4) > opah (2.3) > thresher shark (1.5) > swordfish (1.2) > mako shark (0.5). With a Se/Hg molar ratio of less than 1, mako shark was the only fish containing a net molar excess of mercury. A selenium health benefit value based on the absolute amounts and relative proportions of selenium and mercury in seafood is proposed as a more comprehensive seafood safety criterion.

Importance of molar ratios in selenium-dependent protection against methylmercury toxicity.

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.