Atlantic bluefin tuna show up in menus and headlines for the same reason. They are big, powerful fish that sit high on ocean food chains, and they often carry mercury.
Public health advice tells you to be mindful about mercury in seafood, but it rarely explains how the metal actually behaves inside a fish.
This work was led by Alain Manceau of CNRS and the ESRF, with collaborators at ENS Lyon and Norway’s Institute of Marine Research (IMR).
Mercury in the ocean does not start out in the most dangerous form. It becomes methylmercury, an organic compound made by certain bacteria, which moves into fish and binds to proteins in tissue.
Because tuna eat other fish, the metal can build up along the food chain. That process is called biomagnification, and it helps explain why large, older predators tend to carry more mercury than smaller species with short lifespans.
Not all mercury in fish is equally risky. Its chemical form, or speciation, matters for toxicity and for how the body handles it.
The researchers used high energy resolution X-ray absorption spectroscopy to track mercury’s chemical forms in Atlantic Bluefin tuna tissues.
The team worked at a synchrotron, a facility that accelerates electrons to make intense X-rays, then used X-ray absorption spectroscopy to identify how mercury atoms were bound inside different organs.
They found a notable share of mercury in edible muscle as a tetraselenolate complex known as Hg(Sec)4. That complex is linked to selenocysteine, a selenium bearing amino acid that is part of a transport protein involved in metal handling.
In the spleen and some other organs, the complex can transform further into mercury selenide, a mineral-like substance that is far less reactive in tissue.
Many marine mammals and seabirds degrade methylmercury mostly in the liver. Atlantic bluefin tuna appear to lean on the spleen instead, with the liver playing a smaller role.
That shift changes how mercury moves within the body. It also changes where less toxic residues end up after the fish have processed part of their load.
The work points to a more nuanced picture of detoxification in fish. The same contaminant can take different routes in different species.
Selenium is an essential nutrient, but in this story it does more than support enzymes. It can bind mercury, lowering the amount that stays in the most toxic forms in tissues.
Independent research shows selenium can influence mercury isotope patterns in marine fish and is linked with demethylation, which fits the strong selenium chemistry seen in the tuna tissues.
A key player here is selenoprotein P (SeP), a selenium rich protein that ferries selenium around the body. It contains multiple selenocysteine residues that can coordinate mercury, allowing clusters to form that later give way to mercury selenide.
This is not a free pass to ignore mercury. It is a biochemical path that helps explain why total mercury is not the whole story.
“When evaluating toxicity, we should measure the concentration of methylmercury, not total mercury, since other forms can be harmless to the body,” said Manceau.
“The muscle lacks mercury selenide simply because levels there are too low, and while one generally assumes all mercury in fish is methylated, our results show that is not always the case.”
Public health advice emphasizes the benefits of seafood while guiding people toward lower mercury species.
The FDA’s current guidance lists best choices, good choices, and choices to avoid, with serving frequencies for people who are pregnant or may become pregnant, those who are breastfeeding, and children.
This new work supports more precise testing that distinguishes toxic methylmercury from less reactive selenium bound forms. It also supports reporting methylmercury concentrations alongside or instead of totals when the goal is to estimate risk from a meal.
The data do not say bluefin tuna are low in mercury. They say a nontrivial share of the mercury in their muscle is tied up in forms that are less available to the human body.
Not all tuna are alike. Smaller species like albacore and skipjack tend to carry lower mercury levels because they feed lower on food chains and grow quickly.
Other large predators can show even stronger demethylation in muscle. In blue marlin, a peer-reviewed paper reported that muscle mercury was almost completely demethylated in the samples tested, pointing to a very high fraction of mercury in selenium bound forms.
Those species differences matter for both science and policy. They hint that monitoring should prioritize methylmercury rather than total mercury to better reflect actual exposure.
When labs measure total mercury only, they may overestimate the amount that will circulate after a meal. Measuring methylmercury directly provides a cleaner link to potential dose.
This is especially relevant for people who eat a lot of seafood or who rely on specific species. The numbers that guide their choices should match what the body actually encounters.
Better speciation data can also improve risk communication. Clearer numbers reduce confusion and keep attention on who needs to be careful and why.
The study does not erase long standing advice to limit high mercury fish. It adds chemical detail that helps match risk estimates to reality.
It also explains why some very large fish do not deliver exclusively methylmercury. Chemistry inside the fish shifts part of the load into less active forms.
That shift depends on species, age, diet, and organ level processing. It is a science story worth watching as speciation methods become more routine.
The study is published in the journal Environmental Science & Technology.
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