Mercury is a highly toxic chemical element, and although it is dangerous in its elemental form, it becomes especially harmful when it is converted into methylmercury. This compound, accumulating in marine organisms, can enter the food chain and cause severe health effects, particularly impacting the neurological development of fetuses and children.

The severity lies in the fact that small amounts of methylmercury can cause permanent neurological damage. Unfortunately, methylmercury primarily enters our bodies through the consumption of fish and shellfish, where it has concentrated as it ascends the food chain. Despite scientific efforts, no effective solution has been available so far to remove this toxin from our food and the environment.

Recently, however, a group of researchers has made a significant step in understanding the processes that convert mercury into methylmercury. Using high-energy X-rays at the Stanford Synchrotron Radiation Lightsource (SSRL) of the SLAC National Accelerator Laboratory, they identified an unexpected player in this process: a molecule called S-adenosyl-L-methionine (SAM), which appears to play a key role in mercury transformation. The study’s findings, published in the journal Proceedings of the National Academy of Sciences, could open new avenues for developing remediation strategies to reduce methylmercury concentrations in the environment and food.

Dr. Riti Sarangi, a scientist with the Structural Molecular Biology program at SSRL and co-author of the study, explained that one of the major challenges was understanding how mercury methylation occurs biologically. Without this fundamental understanding, it is difficult to advance in creating effective strategies to combat the problem of methylmercury in aquatic ecosystems.

Methylmercury fishes
Gills of a fish damaged by methylmercury. Credit: Public domain / Wikimedia Commons

To address this issue, SSRL researchers focused their efforts on studying the activity of the HgcAB protein system, which is responsible for converting mercury into methylmercury in certain microorganisms. However, HgcAB is an extremely delicate protein and exists in very small quantities in microbes, making it particularly challenging to study.

After a decade of collaborative work, scientists from various universities and laboratories, under the direction of Professor Steve Ragsdale at the University of Michigan, developed a protocol that allowed them to obtain a stable amount of HgcAB. With this technique, they could bring the purified protein to SSRL, where it was studied using X-ray absorption spectroscopy, an advanced method that allows detailed observation of molecular structures. This technology was essential, as HgcAB samples are highly sensitive to light and oxygen, and any exposure could deactivate their activity.

During the SSRL experiments, the research team discovered that, contrary to previous beliefs, the methyl group involved in mercury transformation did not come from methyltetrahydrofolate, a molecule commonly involved in methyl group transfer reactions in living organisms, but from SAM. This finding was surprising, as it points to a different biochemical mechanism than previously thought and suggests that SAM plays a crucial role in methylmercury production.

Professor Ragsdale suggested that this discovery could inspire the development of SAM analogs that interfere with methylmercury production in aquatic ecosystems. The idea would be to design similar molecules that inhibit the conversion of mercury into its methylated form, which could be a promising strategy to reduce the amount of methylmercury in the environment and, consequently, in food.

SOURCES

SLAC (National Accelerator Laboratory)

K. Zheng, K.W. Rush, S.S. Date, A. Johs, et al., S-adenosyl-L-methionine is the unexpected methyl donor for the methylation of mercury by the membrane-associated HgcAB complex, Proc. Natl. Acad. Sci. U.S.A. 121 (47) e2408086121, doi.org/10.1073/pnas.2408086121

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