This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
Plutonium has a half-life of about 24,000 years. And scientists have known for decades that even in small doses, it is highly toxic, leading to radiation illness, cancer and often to death. After the March nuclear disaster at the Fukushima Daiichi nuclear power plant in Japan, people the world over worried that plutonium poisoning might affect those near the compromised plant—and beyond.
Inhaled plutonium can land in the lungs, where it can lead to cancer, but it—and any that is ingested—can also find its way into the blood stream where it is slowly absorbed into the body.
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New details about this toxic process are now emerging. "Plutonium is a toxic synthetic element with no natural biological functions," Mark Jensen, of the Argonne National Laboratory, and his colleagues wrote in a new paper, published online June 26 in Nature Chemical Biology (Scientific American is part of Nature Publishing Group). Not only is it useless to the body, "it is strongly retained by humans when ingested," primarily lodging in bone and liver cells, where it can release harmful alpha radiation.
But just how the body absorbed this toxic element remained a matter of speculation.
Scientists had noticed that the most prevalent plutonium ion (Pu 4+) had some similarities to more common metal ions, including iron (Fe 3+), which has a slightly smaller atomic radius but a similar ratio of radius to charge.
Jensen and his team used small-angle x-ray scattering and synchrotron x-ray fluorescence microscopy to peer into rat adrenal gland cells that had been extracted and exposed to Pu 4+.
The researchers were able to see for the first time some of the "molecular mechanisms organisms use to distinguish between metal ions," they reported. Jensen and his team found that one of the receptors that is usually charged with bringing iron into cells(known as the transport protein serum transferrin, or Tf) was also transporting the plutonium ions. The pathway has two binding sites, and in order for it to cross into the cell, both need to be filled with an iron-like ion.
But the cellular pathway didn't gobble up the plutonium and bring it into the cell wholesale. Only one of the two binding sites—the C lobe—would take on a plutonium ion. And in order for the transfer to take place, an iron ion needed to be locked into the protein's other lobe, the N lobe. And "the differences between the two lobes restricted, but did not eliminate, cellular Pu uptake," the researchers noted. The transferrin even seemed to have a slight tendency to take up more iron ions than plutonium.
Given that the cellular pathways are already partly discriminating between plutonium and iron—and partially preferring the latter—the findings could help "enable new treatments for Pu poisoning," the researchers noted.
Current plutonium-exposure therapies address circulating plutonium but cannot disarm the ions that have already been taken up by the body's cells and tissues. But future treatments could make use of the preference for iron—and the partial resistance to plutonium uptake—to develop targeted drugs for humans in case of future nuclear accidents or attacks.
Image courtesy of iStockphoto/narvikk
