The remarkable Osorezan dace is a cyprinid fish that spends most of its life in the extremely acidic waters of Lake Osorezan in Japan, where the pH can vary anywhere from 3.8 down to 3.4! For most fish, long-term acid exposure is terminal, dramatically affecting the gill, which results in an acute drop in plasma pH, loss of salts and eventually death. However, the Osorezan dace has the ability to rapidly correct plasma pH and sodium disturbances caused by acid exposure, which allows this fish to move easily between its neutral spawning waters and the lake's acidic conditions. The present study by Hiratam and co-workers used an impressive range of techniques to determine the mechanisms by which this fish is able to survive in such a severe environment and found that it can rapidly switch on a battery of powerful pumps that protect it from certain death.
The gill is very important in fish as it is not only the site of respiratory gas exchange but is also responsible for ion regulation and is thought to function like the mammalian kidney by protecting the fish from metabolic acid/base disturbances. In order to determine the mechanisms that underlie the Osorezan dace's remarkable ability to tolerate acidic conditions,the authors identified and cloned seven key genes that respond to acid exposure. They tracked the mRNA levels in the gill for most of these proteins and found that the levels for most of them had increased within 1 day of acid exposure.
The authors first looked at protein and mRNA expression patterns of the H+-ATPase. The H+-ATPase is usually responsible for acid–base regulation in most other fish by actively pumping acid out of the fish. However, its levels hardly changed with changes in pH, suggesting that this pump does not play a major role in the acid tolerance of the Osorezan dace.
By contrast, they found that both the Na+/H+-exchanger, which moves acid out of the fish in exchange for much needed Na+, and the Na+/HCO3– cotransporter, which moves both Na+ and basic HCO3– into the blood of the fish, were upregulated in response to acid exposure.
Using antibodies to locate the different transporters and enzymes, the authors found that the chloride cell of the gill appeared to be the site of acid regulation. The Na+/H+-exchanger, was found on the apical membrane of these cells, while the Na+/HCO3– cotransporter, the water channel protein, aquaporin 3, and the Na+/K+-ATPase were on the basolateral membrane of these same cells. In addition, the enzyme carbonic anhydrase, which converts carbon dioxide and water into H+and HCO3–, was found within chloride cells, and it is likely that it helps to feed the Na+/H+-exchanger and the Na+/HCO3– cotransporter.
The presence of these four transport mechanisms and carbonic anhydrase within the gill chloride cells suggests that these cells play a major role in the acid tolerance observed in the dace. It appears that the rapid upregulation of these pumping mechanisms within the gill chloride cell helps to correct plasma pH and sodium disturbances caused by acid exposure and allows the dace to survive incredibly low pH.