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Comprehensive study on the interaction of estrogen and Microcystis aeruginosa with coexisting of microplastics
Summary
Scientists found that when a synthetic hormone found in birth control pills (EE2) ends up in lake water alongside plastic pollution, it can make harmful algae grow faster and release more toxins at high pollution levels—raising concerns for drinking water safety. The good news: the algae can also break down some of this hormone into less toxic byproducts, though this natural cleanup process has limits. This matters because lakes contaminated with both plastic waste and hormone pollution (from wastewater, pharmaceuticals, etc.) may pose greater health risks than either pollutant alone, especially as algal blooms become more common.
The increasing occurrence and concentration of emerging contaminants, particularly in eutrophic lakes, raises concerns. These pollutants, including estrogens, microplastics, and algae, interact in complex ways, which could alter environmental risks. However, these interactions and risks are not yet fully understood. This study investigated the environmental risks of 17α-ethinylestradiol (EE2) on the growth and metabolism of Microcystis aeruginosa, as well as its biotransformation mechanisms in the presence of polyethylene terephthalate (PET), using controlled algal exposure experiments combined with physiological assays, chemical analysis (UPLC-MS/MS), and molecular docking. The results show that low to moderate concentrations (0.01-1 mg/L) of EE2 combined with PET promote cell density, chlorophyll-a content, and photosynthetic efficiency (Fv/Fm) of M. aeruginosa. At higher EE2 concentrations (5.0 mg/L), PET co-exposure enhances EE2 toxicity, inducing oxidative stress as evidenced by increased reactive oxygen species levels and lipid peroxidation. These physiological changes are accompanied by stimulated production and release of microcystins, potentially increasing water toxicity. On the other hand, EE2 was biodegraded by M. aeruginosa, with 8.03% to 56.81% removal rate after 96 h. The contributions of abiotic factors, bioadsorption, and bioaccumulation were limited. The biodegradation process is driven by enzymatic activity, with molecular docking and enzyme inhibition results indicating that cytochrome P450 plays a pivotal role, exhibiting the lowest binding energy with EE2 and the highest number of hydrogen bonds and hydrophobic interactions. After biodegradation, the degradation products are less toxic than that of original EE2. This study highlights the combined environmental risks of EE2 mediated by M. aeruginosa and the influence of PET in algal blooms and clarifies EE2 transformation by algae.