by Marine fish live in highly saline environments with ionic concentrations very different from blood plasmas. Seawater contains several types of toxic ions that can build up in the body if the fish do not expel them. An example of this is boric acid, which – in small quantities – is a vital micronutrient for animals but can be extremely toxic. Therefore, marine fish must develop physiological methods to excrete boric acid. However, how they do this is still unknown. Now, an international team led by researchers from the Tokyo Institute of Technology (Tokyo Tech) has uncovered and demonstrated the molecular mechanisms underlying boric acid secretion in marine pufferfish.
Associate Professor Akira Kato of Tokyo Tech is the lead author of the published study. Journal of Biological Chemistry. It tells us more. “We compared euryhaline puffer fish (pufferfish that can survive in varying salinity levels) accustomed to salt water, brackish water and fresh water. Comparing fish from these three habitats, we found that the urine of a seawater puffer fish (Takifugu puffer fish) contains 300 from the blood of the puffer fish. times, 60 times more boric acid than seawater.” The urine of freshwater fish contains almost 1000 times less boric acid than that of seawater puffer fish. These findings revealed that Takifugu puffer fish living in sea water secrete boric acid in its urine. Just like in humans, the urinary excretion process in puffer fish is mediated by the kidneys.
So how did this boric acid get into the kidney tubules?
The team found that the Takifugu puffer fish expressed an uncharacterized gene. Slc4a11A, in the renal tubules. This gene encodes a protein homologous to BOR1, a boric acid transporter found in plants.
A detailed electrophysiological analysis of puffer fish Slc4a11A function revealed that Slc4a11A functions as an active or electrogenic boric acid transporter,” explains Dr. Kato.
This basically means that Slc4a11A can transport boric acid against a concentration gradient and its function is independent of other ions such as sodium. This is particularly important as this is the first report of an active boric acid transport mechanism in an animal species.
Mammals also have the Slc4a11 gene, which raises the question of whether they can function this way too. Although we know that mammalian Slc4a11 does not carry boric acid, human mutations Slc4a11 The gene causes visual disturbances such as congenital hereditary endothelial corneal dystrophy and Fuchs endothelial corneal dystrophy. Further investigation of the activities of Slc4a11 in different vertebrate species will reveal whether mammalian Slc4a11 lost boric acid transport activity with evolution or whether marine fish Slc4a11A acquired it as it evolved.
In any case, this resounding work opens new avenues for understanding boric acid transport in animals and unraveling the mysteries that genetics lurks.
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materials provided by Tokyo Institute of Technology. Note: Content can be edited for style and length.
