Bianchini Adalto, Wood Chris M
Fundação Universidade Federal do Rio Grande, Departamento de Ciências Fisiológicas, Rua Eng. Alfredo Huch, 475, 96.201-900 Rio Grande, RS, Brazil.
Comp Biochem Physiol C Toxicol Pharmacol. 2002 Sep;133(1-2):137-45. doi: 10.1016/s1532-0456(02)00088-1.
Daphnia magna were exposed to a total concentration of 5.0+/-0.04 microg Ag/l, added as AgNO(3) (dissolved concentration, as defined by 0.45 microm filtration = 2.0+/-0.01 microg Ag/l) in moderately hard synthetic water under static conditions (total organic carbon = 4.80+/-1.32 mg/l) with daily feeding and water renewal, for 21 days. There was no mortality in control daphnids and 20% mortality in silver-exposed animals. Silver exposure caused a small but significant reduction of reproductive performance manifested as a 13.7% decrease in the number of neonates produced per adult per reproduction day over the 21-day exposure. However, silver exposed daphnids also exhibited a much more marked ionoregulatory disturbance, which was characterized by a 65% decrease in whole body Na(+) concentration, and an 81% inhibition of unidirectional whole body Na(+) uptake. Previous work on the acute toxicity of Ag(+) to daphnids has shown that Na(+) uptake inhibition is directly related to inhibition of Na(+),K(+)-ATPase activity. Therefore, we suggest that the Na(+) uptake inhibition seen in response to chronic silver exposure was explained by an inhibition of the Na(+) channels at the apical 'gill' membrane, since a 60% increase in whole body Na(+),K(+)-ATPase activity was observed in the chronically silver-exposed daphnids. Our findings demonstrate that, in broad view, the key mechanism involved in chronic silver toxicity in D. magna, the most acutely sensitive freshwater organism tested up to now, resembles that described for acute toxicity-i.e. ionoregulatory disturbance associated with inhibition of active Na(+) uptake, though the fine details may differ. Our results provide encouragement for future extension of the current acute version of the Biotic Ligand Model (BLM) to one that predicts chronic silver toxicity for environmental regulation and risk assessment. The results strongly suggest that Na(+) uptake inhibition is the best endpoint to determine sensitivity to both acute and chronic toxicity in the scope of future versions of the BLM for silver.
将大型溞暴露于总浓度为5.0±0.04微克银/升的环境中,以硝酸银形式添加(溶解浓度,经0.45微米过滤定义为2.0±0.01微克银/升),在静态条件下(总有机碳 = 4.80±1.32毫克/升)置于中等硬度的合成水中,每日投喂并更换水,持续21天。对照大型溞无死亡,而暴露于银的动物有20%死亡。银暴露导致繁殖性能出现轻微但显著的下降,表现为在21天的暴露期内,每只成年大型溞每天繁殖产生的幼体数量减少了13.7%。然而,暴露于银的大型溞还表现出更为明显的离子调节紊乱,其特征是全身钠离子浓度降低65%,以及单向全身钠离子摄取受到81%的抑制。先前关于银离子对大型溞急性毒性的研究表明,钠离子摄取抑制与钠钾ATP酶活性的抑制直接相关。因此,我们认为,长期银暴露导致的钠离子摄取抑制是由于顶端“鳃”膜上的钠离子通道受到抑制,因为在长期暴露于银的大型溞中观察到全身钠钾ATP酶活性增加了60%。我们的研究结果表明,从广义上讲,迄今测试的最急性敏感的淡水生物——大型溞中,慢性银毒性所涉及的关键机制与急性毒性所描述的机制相似,即与主动钠离子摄取抑制相关的离子调节紊乱,尽管具体细节可能有所不同。我们的结果为将当前生物配体模型(BLM)的急性版本扩展为预测环境监管和风险评估中的慢性银毒性的模型提供了鼓励。结果强烈表明,在未来版本的银BLM范围内,钠离子摄取抑制是确定对急性和慢性毒性敏感性的最佳终点。