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Title of Presentation
Title of Conference Presenter
Date
Selenium’s Pivotal Roles in Relation to Mercury Exposure Risks
PROMOTING HEALTHY COMMUNITIES: Developing and Exploring Linkages Between Public Health Indicators, Exposure and Hazard Data
September 26, 2011
Nicholas Ralston Ph.D.
University of North Dakota
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CHEMICAL CONTEXT
1b 2b 3a 4a 5a 6a 7a 0
He
B C N O F Ne
Al Si P S Cl Ar
Cu Zn Ga Ge As Se Br Kr
Ag Cd In Sn Sb Te I Xe
Au Hg Ti Pb Bi Po At Rn
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Se-PHYSIOLOGY BACKGROUND
• Selenium is an essential nutrient that is abundant in seafoods.
• Selenium-dependent enzymes perform vital functions in brain tissues.
• Selenoenzymes are genetically unique and functionally elite.
• It was thought that there were only 20 genetically encoded amino acids.
• Selenoenzymes employ selenocysteine, the 21st genetically encoded amino acid—which is the most powerful intracellular nucleophile.
• Selenoenzymes recycle vitamin C and other vital molecules that detoxify dangerous oxygen species, thus preventing oxidative damage.
• All forms of life that have recognizable brains have selenoenzymes present to protect their brains.
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WHAT MAKES A SELENIUM PHYSIOLOGIST GET INTO MERCURY TOXICOLOGY?
• The only environmental challenge that significantly impairs brain selenoenzymes is mercury exposure, especially if it occurs during fetal growth. Studies have found that developing children can be harmed if their mothers eat seafoods that contain more mercury than selenium.
• Pilot whale meats (source of >90% of Hg exposure in the Faroes study), have Hg:Se molar ratios of 4:1!
• Although the Hg:Se ratios in king mackerel and tilefish have not been assessed, but sharks have ratios of 2:1 or even higher, swordfish; 1:1. These seafoods should be avoided during pregnancy as recommended by the 2004 FDA/EPA advisory.
• Ocean fish generally contain far more Se than Hg, and protect against rather than contribute to causing Hg toxicity.
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SELENOPROTEIN W mRNA IN BRAIN TISSUES
Allen Brain Institute
Selenoprotein W
Gene Expression
Map
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SELENOPROTEIN M mRNA in BRAIN TISSUES
Allen Brain Institute
Selenoprotein M
Gene Expression
Map
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METHYLMERCURY TOXICITY • Toxic effects of high MeHg exposures are well established.
• Implications of low level MeHg exposure had been uncertain.
• Human and animal studies demonstrate that MeHg exposure is
increasingly hazardous as Hg:Se molar ratios increase.
• Selenium’s protective effect against MeHg toxicity has been demonstrated in all species studied
• Selenium is not a “tonic”, it is the “target” of MeHg toxicity.
• MeHg irreversibly inhibits selenoenzyme activities in brain.
• Selenoenzyme activities in the fetal brain are extremely sensitive to maternal MeHg exposure.
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DIETARY SELENIUM AND GROWTH
100
200
300
400
500
0 14 28 42 56 70 84 98 112 126Study Day
Bod
y W
eigh
t (g
)
0.1 µmol Se/kg1.0 µmol Se/kg10 µmol Se/kg
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SELENIUM’S PROTECTIVE EFFECT (AGAINST MeHg TOXICITY)
100
200
300
400
500
0 14 28 42 56 70 84 98 112 126
Study Day
Bod
y W
eigh
t (g)
0.1 µmol Se; 50µmol MeHg/kg1.0 µmol Se; 50 µmol MeHg/kg10 µmol Se; 50 µmol MeHg/kg
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SELENIUM’S ROLE IN THE MERCURY ISSUE • The effects of mercury toxicity correspond with the effects expected to
accompany loss of selenoenzyme activities in brain and other tissues.
• Previous approaches to evaluating risks related to mercury exposures appear to have been overly simplistic (Imagine evaluating bankruptcy risks, but only considering debts and ignoring debt:income ratios. This approach could not reliably provide accurate predictions of risk).
• Consumption of selenium-rich ocean fish enriches the selenium status of the consumer, protecting them against mercury toxicity rather than increasing their risks.
• However, consumption of fresh water fish that have high mercury, but poor selenium contents may pose far greater risks of toxicity than has previously been expected.
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DISTRIBUTION OF SELENIUM IN U.S. SOILS
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IN SUMMATION
Methylmercury is the only challenge that impairs brain selenoenzyme activities.
This is your brain
This is your brain without selenoenzymes…
Any questions?