由于水中抗病毒药物的增加而导致的环境风险在很大程度上是未知的,尤其是在富营养化的湖泊中,藻类和药物之间复杂的相互作用会改变危害。在这里,全面考察了抗病毒药物阿比多对铜绿微囊藻生长和代谢的环境风险,以及藻类的生物转化机制。结果表明,阿比多醇在48h内对铜绿微囊藻具有毒性,降低了细胞密度,叶绿素a,和ATP含量。氧化应激的激活增加了活性氧的水平,导致脂质过氧化和膜损伤。此外,阿比多促进了微囊藻毒素的合成和释放。幸运的是,阿比多醇主要通过生物降解被铜绿微囊藻有效去除(1.0mg/L阿比多醇48h时50.5%),而生物吸附和生物积累的作用是有限的。arbidol的生物降解主要是通过苯硫酚的损失和氧化,藻类细胞内P450酶,较高的阿比多醇浓度促进了降解速率。有趣的是,藻类生物降解后,阿比多尔的毒性降低,大多数降解产物的毒性低于阿比多醇。这项研究揭示了藻类中阿比多的环境风险和转化行为。
The environmental risks resulting from the increasing antivirals in water are largely unknown, especially in eutrophic lakes, where the complex interactions between algae and drugs would alter hazards. Herein, the environmental risks of the antiviral drug arbidol towards the growth and metabolism of Microcystis aeruginosa were comprehensively investigated, as well as its biotransformation mechanism by algae. The results indicated that
arbidol was toxic to Microcystis aeruginosa within 48 h, which decreased the cell density, chlorophyll-a, and ATP content. The activation of oxidative stress increased the levels of reactive oxygen species, which caused lipid peroxidation and membrane damage. Additionally, the synthesis and release of microcystins were promoted by
arbidol. Fortunately, arbidol can be effectively removed by Microcystis aeruginosa mainly through biodegradation (50.5% at 48 h for 1.0 mg/L arbidol), whereas the roles of bioadsorption and bioaccumulation were limited. The biodegradation of
arbidol was dominated by algal intracellular P450 enzymes via loss of thiophenol and oxidation, and a higher
arbidol concentration facilitated the degradation rate. Interestingly, the toxicity of arbidol was reduced after algal biodegradation, and most of the degradation products exhibited lower toxicity than
arbidol. This study revealed the environmental risks and transformation behavior of arbidol in algal bloom waters.