Mechanisms of Mercury Transfer across Rainbow Trout (Oncorhychus mykiss) Intestine

Mercury occurs naturally in the environment and exists in several forms, all of which are toxic to organisms at varying degrees depending on which form they are exposed to. The most common natural forms of mercury include methylmercury and mercuric chloride. These forms of mercury are of particular concern as they have been found to bioaccumulate through trophic levels, leading to ingestion by humans of considerably high levels of mercury, mainly through the consumption of fish. There have been many studies of the toxic effects of mercury in the body and regional accumulation, but very few on the cellular uptake mechisms of mercury. As the main exposure to mercury for a variety of organisms is through the digestive tract this is where this study focuses. This study aimed to identify possible uptake mechanisms for dietary exposure to mercury. In fish the regions of the gut involved in Hg absorption are relatively unknown. Everted gut sacs and isolated perfused intestine of Oncorhychus mykiss were used to explore HgCl2 absorption (at l8°C). Gut sacs exposed to 100µmol 1ˉ¹ mucosal solution HgCl2 showed that Hg was mostly absorbed in the middle and hind intestine. Most of the Hg was located in the mucosa. In perfused intestines tissue accumulation of Hg and sersoal perfusate [Hg] showed a dose dependant elevation. The combination of the Na channel blocker amiloride and Hg exposure showed that Hg is almost entirely reliant on Na channels for apical uptake, and Hg also blocks apical Ca uptake. Exposures with a combination of EGT A and Hg, and cyanide and Hg, suggested that it may use Ca/Na channel to exit tissue at the basolateral membrane, and that mercury uptake is not reliant on active transport. Preliminary exposures suggested the use of Na/K exit through the basolateral membrane, the cyanide and EGTA exposures supported these findings