Bianchini Adalto, Playle Richard C, Wood Chris M, Walsh Patrick J
Departamento de Ciências Fisiológicas, Fundação Universidade Federal do Rio Grande, Campus Carreiros, Av. Itália, km 8, Rio Grande 96201-900, RS, Brazil.
Aquat Toxicol. 2005 Mar 25;72(1-2):67-82. doi: 10.1016/j.aquatox.2004.11.012. Epub 2004 Dec 29.
In freshwater crustaceans and in both freshwater and marine fish, the key mechanism of acute silver toxicity involves ionoregulatory impairment. An inhibition of the Na+ ,K+-ATPase located at the basolateral membrane of the gill epithelium seems to be the key site for silver toxicity. However, studies to determine if the same mechanism of toxicity is occurring in marine invertebrates, which also are ionoregulators, had not been done. Thus, the present study was carried out to determine acute silver effects on hemolymph osmo- and ionoregulation in three marine invertebrates: the shrimp Penaeus duorarum, the sea hare Aplysia californica, and the sea urchin Diadema antillarum. Animals were exposed to silver (1 or 10 microg/L), as silver nitrate, in seawater for 48 h. Results show that acute silver exposure did not affect hemolymph osmolality or ion concentration (Na+, Cl-, K+, Ca2+ and Mg2+) in the three species studied. However, silver induced significant changes in the water content in shrimp gill and sea hare gill and hepatopancreas. Silver also caused significant changes in Na+ ,K+-ATPase activity and in both total and intracellular ion (Cl-, Na+, K+, Mg2+, and Ca2+) concentrations in different tissues of the three species studied. Overall, these results show that the key mechanism of acute silver toxicity in marine invertebrates is not associated with an osmotic or ionoregulatory impairment at the hemolymph level, as observed in freshwater fish and crustaceans and in seawater fish. However, they indicate that acute waterborne silver induces significant changes in Na+ ,K(+)-ATPase activity and probably affects other mechanisms involved in water and ion transport at the cell membrane level, inducing impairments in water and ion regulation at the cellular level in different tissues of marine invertebrates. These results indicate the need to consider other "toxic sites" than gills in any future extension of the biotic ligand model (BLM) for seawater.
在淡水甲壳类动物以及淡水和海水鱼类中，银的急性毒性的关键机制涉及离子调节受损。位于鳃上皮基底外侧膜的钠钾ATP酶受到抑制似乎是银毒性的关键位点。然而，尚未开展研究来确定同样的毒性机制是否也发生在同样作为离子调节者的海洋无脊椎动物中。因此，开展了本研究以确定银对三种海洋无脊椎动物血淋巴渗透压和离子调节的急性影响：杜氏对虾、加州海兔和加勒比海胆。将动物置于含有硝酸银形式的银（1或10微克/升）的海水中暴露48小时。结果表明，急性银暴露并未影响所研究的这三种物种的血淋巴渗透压或离子浓度（钠、氯、钾、钙和镁）。然而，银导致了对虾鳃、海兔鳃和肝胰腺中的含水量发生显著变化。银还使所研究的三种物种不同组织中的钠钾ATP酶活性以及总离子和细胞内离子（氯、钠、钾、镁和钙）浓度发生了显著变化。总体而言，这些结果表明，海洋无脊椎动物中银的急性毒性的关键机制与淡水鱼、甲壳类动物和海水鱼中所观察到的血淋巴水平的渗透或离子调节受损无关。然而，它们表明，急性水体银暴露会导致钠钾ATP酶活性发生显著变化，并且可能会影响细胞膜水平上参与水和离子运输的其他机制，从而在海洋无脊椎动物的不同组织的细胞水平上导致水和离子调节受损。这些结果表明，在未来对海水生物配体模型（BLM）进行任何扩展时，都需要考虑鳃以外的其他“毒性位点”。
