The objective of this study was to evaluate the effect of salinity on the acute and sub-chronic toxicity of silver nanoparticles (AgNPs) in Persian sturgeon. This was evaluated by exposing Persian sturgeon to AgNPs in three salinities: freshwater (F: 0.4 ppt), brackish water 1 (B1: 6 ± 0.2 ppt), and brackish water 2 (B2: 12 ± 0.3 ppt) for 14 days, which was followed by analysis of alterations in plasma chemistry and histopathology of the gills, liver, and intestine. Values of 96-h median lethal concentration (LC50) were calculated as 0.89 mg/L in F, 2.07 mg/L in B1, and 1.59 mg/L in B2. After sub-chronic exposures, plasma cortisol, glucose, potassium, and sodium levels illustrated no significant changes within each salinity level. In F, 0.2 mg/L AgNP caused the highest levels of alkaline phosphatase and osmolality levels. In B1, 0.6 mg/L AgNP induced the highest level of alkaline phosphatase and elevated plasma osmolality was recorded in all AgNP-exposed treatments in comparison with the controls. The B2 treatment combined with 0.6 mg/L AgNP significantly reduced plasma chloride level. The results showed elevating salinity significantly increased osmolality, chloride, sodium, and potassium levels of plasma in the fish exposed to AgNPs. The abundance of the tissue lesions was AgNP concentration-dependent, where the highest number of damages was observed in the gills, followed by liver and intestine, respectively. The histopathological study also confirmed alterations such as degeneration of lamella, lifting of lamellar epithelium, hepatic vacuolation, pyknotic nuclei, and cellular infiltration of the lamina propria elicited by AgNPs in the gills, liver, and intestine of Persian sturgeon. In conclusion, the stability of AgNPs in aquatic environments can be regulated by changing the salinity, noting that AgNPs are more stable in low salinity waters.

中文翻译：

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盐度可调节波斯波斯st（Acipenser persicus）中银纳米颗粒引起的生化和组织病理学变化。

这项研究的目的是评估盐度对波斯st鱼中银纳米颗粒（AgNPs）的急性和亚慢性毒性的影响。通过在三种盐度下将波斯st鱼暴露于AgNPs进行评估：淡水（F：0.4 ppt），微咸水1（B1：6±0.2 ppt）和微咸水2（B2：12±0.3 ppt），持续14天。随后分析plasma，肝和肠的血浆化学和组织病理学变化。96小时中位致死浓度（LC50）的值计算为：F中为0.89 mg / L，B1中为2.07 mg / L，B2中为1.59 mg / L。在亚慢性暴露后，血浆皮质醇，葡萄糖，钾和钠水平表明在每个盐度水平内均无显着变化。在F中，0.2 mg / L AgNP导致碱性磷酸酶和渗透压浓度最高。在B1中，0。与对照组相比，在所有暴露于AgNP的处理中，6 mg / L AgNP诱导的碱性磷酸酶水平最高，并且血浆渗透压升高。B2处理与0.6 mg / L AgNP结合可显着降低血浆氯化物水平。结果表明，盐度升高显着增加了暴露于AgNPs的鱼类的渗透压，氯离子，钠离子和钾离子水平。组织损伤的丰度是AgNP浓度依赖性的，在where中观察到最多的损伤，其次是肝脏和肠。组织病理学研究还证实了由NP，肝脏、,管中的AgNPs引起的片状细胞变性，层状上皮抬升，肝空泡，粘滞性核以及固有层的细胞浸润等改变。和波斯st的肠子。总之，可以通过改变盐度来调节AgNP在水生环境中的稳定性，并指出AgNP在低盐度水中更稳定。