Pedroso Mariana S, Pinho Grasiela L L, Rodrigues Sandra C, Bianchini Adalto
Programa de Pós-Graduação em Ciências Fisiológicas, Fisiologia Animal Comparada, Fundação Universidade Federal do Rio Grande, Av. Itália km 8, 96.201-900 Rio Grande, RS, Brazil.
Aquat Toxicol. 2007 May 15;82(3):173-80. doi: 10.1016/j.aquatox.2007.02.009. Epub 2007 Feb 23.
Acute silver effects on whole-body ion regulation and Na(+),K(+)-ATPase activity were evaluated in the euryhaline copepod Acartia tonsa. Experiments were run at 20 degrees C, three different salinities (5, 15 and 30 ppt), in either the absence or the presence of food (diatom Thalassiosira weissflogii; 2 x 10(4)cells/mL). Standard static-renewal procedures were used. Copepods were acutely (48 h) exposed to silver (AgNO(3)) concentrations equivalent to the 48-h EC10 (dissolved Ag=3, 49, and 94 microg/L), 48-h EC30 (dissolved Ag=5, 71, and 125 microg/L) or 48-h EC50 (dissolved Ag=7, 83, and 173 microg/L) values in the absence of food or to the 48-h EC50 (dissolved Ag=35, 90, and 178 microg/L) values in the presence of food. These values were previously determined under the same experimental conditions at salinities 5, 15 and 30 ppt, respectively. Endpoints analyzed were whole-body ion concentrations (Na(+), Cl(-), and Mg(2+)) and Na(+),K(+)-ATPase activity. In starved copepods, lower whole-body Na(+) and Mg(2+) concentrations were observed in salinities 5 and 30 ppt, respectively. Also a higher whole-body Na(+),K(+)-ATPase activity was observed in all salinities tested. Data from fed copepods indicate that all these salinity effects were completely associated with starvation. Silver exposure induced a decrease in the whole-body Mg(2+) concentration in starved copepods in salinities 5 and 30 ppt and a Na(+),K(+)-ATPase inhibition in both starved and fed copepods in all salinities tested. Thus, food addition in the experimental media completely protected against silver effects on Mg(2+) concentration, but not against those on Na(+),K(+)-ATPase activity. In starved copepods, enzyme inhibition was dependent on silver concentration and a relationship between this parameter and mortality was observed in all salinities tested. Therefore, Na(+),K(+)-ATPase molecules seem to be a key site for acute silver toxicity in marine invertebrates, as reported for freshwater fish and crustaceans.
在广盐性桡足类中华哲水蚤中评估了银对全身离子调节以及钠钾 - ATP 酶活性的急性影响。实验在 20 摄氏度、三种不同盐度(5、15 和 30 盐度单位)下进行,实验中要么有食物(硅藻威氏海链藻;2×10⁴ 个细胞/毫升),要么无食物。采用标准的静态更新程序。将桡足类动物急性(48 小时)暴露于相当于无食物情况下 48 小时 EC10(溶解态银 = 3、49 和 94 微克/升)、48 小时 EC30(溶解态银 = 5、71 和 125 微克/升)或 48 小时 EC50(溶解态银 = 7、83 和 173 微克/升)的值,或者有食物情况下 48 小时 EC50(溶解态银 = 35、90 和 178 微克/升)的值。这些值先前分别在盐度为 5、15 和 30 盐度单位的相同实验条件下测定。分析的终点指标为全身离子浓度(钠、氯和镁)以及钠钾 - ATP 酶活性。在饥饿的桡足类动物中,分别在盐度 5 和 30 盐度单位下观察到全身钠和镁浓度较低。在所有测试盐度下还观察到全身钠钾 - ATP 酶活性较高。来自喂食桡足类动物的数据表明,所有这些盐度影响都与饥饿完全相关。银暴露导致盐度 5 和 30 盐度单位下饥饿桡足类动物的全身镁浓度降低,并且在所有测试盐度下,饥饿和喂食的桡足类动物的钠钾 - ATP 酶均受到抑制。因此,在实验介质中添加食物完全防止了银对镁浓度的影响,但未防止对钠钾 - ATP 酶活性的影响。在饥饿的桡足类动物中,酶抑制取决于银浓度,并且在所有测试盐度下都观察到该参数与死亡率之间的关系。因此,钠钾 - ATP 酶分子似乎是海洋无脊椎动物中银急性毒性的关键位点,正如在淡水鱼和甲壳类动物中所报道的那样。