Nick Ralston has spent many years doing research into the interaction between selenium and mercury in the human body. He is a research scientist and adjunct professor in the Department of Earth System Sciences and Policy at the University of North Dakota. His research has changed how scientists and regulators think about mercury’s impact on human health. Now, scientists regard selenium status as a central factor in determining the risk of mercury toxicity [Ralston 2018; Ralston 2010].
Previously, the most common explanation of mercury toxicity was that mercury exposure directly caused oxidative stress. Selenium’s binding with mercury, it was thought, reduced the risk of oxidative stress and reduced the risk of mercury toxicity.
Yes, it is true that selenium sequesters mercury. And, yes, that is a good thing. However, Ralston realized that the relationship also works the other way around. Equally, mercury sequesters selenium [Raymond & Ralston 2020].
This is the important point. The depletion of selenium in the body and in the brain, once bound to mercury and made inactive, that is the decisive phenomenon. Selenium depletion results in the damaging effects of oxidative stress. Accordingly, it is the effect of this oxidative stress that we know as mercury poisoning or mercury toxicity [Raymond & Ralston 2020; Ralston 2018].
What is the Mercury and Selenium Interaction?
Here, step by step, is Ralston’s thinking about the relationship of selenium status to mercury toxicity [Ralston 2018]:
Selenium a component of selenocysteine
Selenium is the indispensable component of the amino acid selenocysteine.
Selenocysteine is the most important building block of 25-30 selenoproteins.
Several of these selenoproteins are antioxidant selenoenzymes that prevent and neutralize oxidative damage. For example, the glutathione peroxidases are among the most researched antioxidant selenoenzymes.
Brain tissue needing antioxidant protection
The human brain is largely composed of fatty acids. The fatty acids in the brain are especially vulnerable to oxidative stress. In consuming oxygen, the brain produces harmful reactive oxygen species free radicals as a by-product.
Fortunately, the human brain is preferentially supplied with selenium. The hierarchical distribution of selenium from food and supplements should ensure that the brain always has enough to synthesize the selenoenzymes. The brain needs these selenoenzymes to protect brain cells and tissues against oxidative damage by the reactive oxygen species.
Mercury binding to selenium depletes selenium
However, high exposure to mercury from industrial chemicals or from foods that contain more mercury than selenium irreversibly inhibits and impairs the synthesis of selenoenzymes. Without an adequate supply of selenoenzymes, the brain will lose its protection against oxidative stress.
Note: Oxidative stress is an imbalance between harmful free radicals and protective antioxidants. This imbalance leads to damage of cells and tissues.
What Does Ralston Conclude about Selenium and Mercury?
Ralston concludes that selenium in the brain is the molecular target of the mercury. When mercury binds selenium and stops the synthesis of protective selenoenzymes, the brain is more vulnerable to oxidative damage. The key concept in Ralston’s work is that mercury preferentially targets selenium-containing enzymes. Mercury’s aim is to impair antioxidant defense in the brain [Ralston 2018].
When mercury and other toxic metals bind to selenium, the supply of selenium is depleted. The synthesis of important antioxidant enzymes is disrupted. The assault of harmful free radicals causes irreversible damage [Ralston 2018].
In other words, mercury toxicity occurs not so much because of what mercury does directly. According to Ralston, what we know as mercury toxicity is the extensive oxidative damage that occurs because mercury binds to selenium. Mercury’s binding to selenium keeps the selenium from being incorporated into selenocysteine. It is the resultant oxidative stress that causes the cell damage that we associate with mercury toxicity [Ralston 2018].
How Dangerous is Mercury in the Fish We Eat?
In a future article, we will summarize Nick Ralston’s writing about the mercury in the fish that we eat.
Conclusions: Selenium and Mercury Interaction?
Selenium status is a central factor in determining the risk of mercury poisoning.
Selenium binds and neutralizes mercury.
Mercury toxicity occurs because mercury targets and depletes the supply of selenium to the brain.
A surplus of selenium over mercury is necessary for antioxidant selenoenzymes to form and provide antioxidant protection in the brain.
The molar mercury:selenium ratio plays a pivotal role in determining the benefits and risks associated with eating seafood.
Sources
Ralston NVC, Raymond LJ. Mercury’s neurotoxicity is characterized by its disruption of selenium biochemistry. Biochim Biophys Acta Gen Subj. 2018;1862(11):2405-2416.
Ralston NVC, Raymond LJ. Dietary selenium’s protective effects against methylmercury toxicity. Toxicology. 2010;278(1):112-123.
Raymond LJ & Ralston NVC. Mercury: selenium interactions and health implications.
NeuroToxicology. 2020;81:294-299.
The information provided in this review article is not intended as medical advice. It should not be used as such.