Key Laboratory of Integrated Regulation and Resources Development on Shallow Lakes, Ministry of Education, Hohai University, Nanjing 210098, PR China; College of Environment, Hohai University, Nanjing 210098, PR China.
Key Laboratory of Integrated Regulation and Resources Development on Shallow Lakes, Ministry of Education, Hohai University, Nanjing 210098, PR China; College of Environment, Hohai University, Nanjing 210098, PR China.
Aquat Toxicol. 2024 Jun;271:106937. doi: 10.1016/j.aquatox.2024.106937. Epub 2024 May 6.
In aquaculture around the world, sulfamonomethoxine (SMM), a long-acting antibiotic that harms microalgae, is widely employed in combination with trimethoprim (TMP), a synergist. However, their combined toxicity to microalgae under long-term exposures at environmentally relevant concentrations remains poorly understood. Therefore, we studied the effects of SMM single-exposures and co-exposures (SMM:TMP=5:1) at concentrations of 5 μg/L and 500 μg/L on Chlorella pyrenoidosa within one aquacultural drainage cycle (15 days). Photosynthetic activity and N assimilating enzyme activities were employed to evaluate microalgal nutrient assimilation. Oxidative stress and flow cytometry analysis for microalgal proliferation and death jointly revealed mechanisms of inhibition and subsequent self-adaptation. Results showed that exposures at 5 μg/L significantly inhibited microalgal nutrient assimilation and induced oxidative stress on day 7, with a recovery to levels comparable to the control by day 15. This self-adaptation and over 95 % removal of antibiotics jointly contributed to promoting microalgal growth and proliferation while reducing membrane-damaged cells. Under 500 μg/L SMM single-exposure, microalgae self-adapted to interferences on nutrient assimilation, maintaining unaffected growth and proliferation. However, over 60 % of SMM remained, leading to sustained oxidative stress and apoptosis. Remarkably, under 500 μg/L SMM-TMP co-exposure, the synergistic toxicity of SMM and TMP significantly impaired microalgal nutrient assimilation, reducing the degradation efficiency of SMM to about 20 %. Consequently, microalgal growth and proliferation were markedly inhibited, with rates of 9.15 % and 17.7 %, respectively, and a 1.36-fold increase in the proportion of cells with damaged membranes was observed. Sustained and severe oxidative stress was identified as the primary cause of these adverse effects. These findings shed light on the potential impacts of antibiotic mixtures at environmental concentrations on microalgae, facilitating responsible evaluation of the ecological risks of antibiotics in aquaculture ponds.
在全球水产养殖中，广泛使用长效抗生素磺胺甲噁唑（SMM）与增效剂甲氧苄啶（TMP）联合使用。然而，在环境相关浓度下长期暴露时，它们对微藻的联合毒性仍知之甚少。因此，我们研究了磺胺甲噁唑单一暴露和共暴露（SMM:TMP=5:1）在 5μg/L 和 500μg/L 浓度下对一个水产养殖排水周期（15 天）内的蛋白核小球藻的影响。我们利用光合作用活性和氮同化酶活性来评估微藻的营养吸收。氧化应激和流式细胞术分析微藻的增殖和死亡共同揭示了抑制和随后的自我适应的机制。结果表明，在 5μg/L 时，暴露显著抑制了微藻的营养吸收，并在第 7 天引起了氧化应激，到第 15 天恢复到与对照相当的水平。这种自我适应和抗生素的去除率超过 95%共同促进了微藻的生长和增殖，同时减少了受损细胞膜的细胞数量。在 500μg/L 的磺胺甲噁唑单一暴露下，微藻适应了对营养吸收的干扰，保持了不受影响的生长和增殖。然而，超过 60%的磺胺甲噁唑仍然存在，导致持续的氧化应激和细胞凋亡。值得注意的是，在 500μg/L 的磺胺甲噁唑-甲氧苄啶共暴露下，磺胺甲噁唑和甲氧苄啶的协同毒性显著损害了微藻的营养吸收，将磺胺甲噁唑的降解效率降低到约 20%。因此，微藻的生长和增殖受到明显抑制，分别为 9.15%和 17.7%，并且受损细胞膜的细胞比例增加了 1.36 倍。持续和严重的氧化应激被认为是这些不利影响的主要原因。这些发现揭示了抗生素混合物在环境浓度下对微藻的潜在影响，有助于对水产养殖池塘中抗生素的生态风险进行负责任的评估。
