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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Nanoplastics Sign in to save

Distinct responses of Pseudomonas aeruginosa PAO1 exposed to different levels of polystyrene nanoplastics

The Science of The Total Environment 2022 36 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 50 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Yuxin Hu, Yuanyuan Kang, Yuanyuan Kang, Xu Zhou Shu-Hong Gao, Yuanyuan Kang, Yuanyuan Kang, Shu-Hong Gao, Fang Huang, Yuanyuan Kang, Yuanyuan Kang, Yuanyuan Kang, Yuanyuan Kang, Shu-Hong Gao, Yiyi Su, Yuanyuan Kang, Yuanyuan Kang, Yuanyuan Kang, Yuanyuan Kang, Aijie Wang, Shu-Hong Gao, Xu Zhou Xu Zhou Xu Zhou Yuanyuan Kang, Aijie Wang, Yuanyuan Kang, Xu Zhou Shu-Hong Gao, Aijie Wang, Aijie Wang, Xu Zhou Aijie Wang, Shu-Hong Gao, Aijie Wang, Aijie Wang, Aijie Wang, Aijie Wang, Aijie Wang, Aijie Wang, Shu-Hong Gao, Xu Zhou

Summary

Researchers examined the molecular mechanisms by which polystyrene nanoplastics affect Pseudomonas aeruginosa, finding dose-dependent responses in growth, metabolism, and virulence gene expression that reveal how nanoplastics interact with environmentally relevant bacteria.

Polymers

Large amounts of discarded plastics in the environment can be aged into microplastics and nanoplastics, which are not easily removed, posing potential nonnegligible risks to the ecosystem and human health. Although previous studies have revealed that nanoplastics have detrimental impacts on microorganisms, the potential molecular mechanisms of nanoplastic particles' effect on microbial growth and metabolism are still lacking. Here, multiple responses of Pseudomonas aeruginosa PAO1 (PAO1) to different levels of polystyrene nanoplastics (PS NPs) exposure were investigated by physiological experiments, live/dead staining, redox status, and genome-wide RNA sequencing. The results showed that PS NPs had dual effects on PAO1, and different concentrations of PS NPs demonstrated different effects on the growth and metabolism of PAO1. All levels of PS NPs had no obvious biocidal effect on PAO1. The production and consumption of ROS were in dynamic equilibrium and could be regulated genetically to ensure that the ROS level was in the biotolerable range. 20 and 50 mg/L of PS NPs severely inhibited the nitrate reduction, while 0.1 mg/L of PS NPs promoted the denitrification and TCA cycle. Meanwhile, 20 and 50 mg/L of PS NPs resulted in intense down-regulation of genes involved in denitrification. In contrast, the expression of genes involved in respiration is promoted with generated energy to withstand stress from high-level PS NPs, coinciding with the physiological results. In addition, our results showed that PS NPs concentrations of 20 and 50 mg/L exposure substantially up-regulated the expression of genes encoding for flagellar biosynthesis and biofilm formation to tackle the stress. Our findings would provide new insights into the interactions between environmental bacteria and PS NPs at the transcriptional level, thereby enhancing our understanding of the potential risks of PS NPs to microbial ecosystems and public health.

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