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Dual impacts of elevated pCO2 on the ecological effects induced by microplastics and nanoplastics: A study with Chlamydomonas reinhardtii

Aquatic Toxicology 2025 2 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Chengwei Liang, Zhihua Jia, Tianle Xi, Tianle Xi, Zhihua Jia, Zhihua Jia, Yajing Liu, Zhihua Jia, Xiaowen Zhang, Tianle Xi, Yajing Liu, Tianle Xi, Chengwei Liang, Jia Liu, Chengwei Liang, Xiaowen Zhang, Xiaowen Zhang, Shanshan Ge, Shanshan Ge, Xiaowen Zhang, Xiaowen Zhang, Naihao Ye Naihao Ye Chengwei Liang, Zhihua Jia, Zhihua Jia, Xiaowen Zhang, Naihao Ye Naihao Ye Naihao Ye Naihao Ye Naihao Ye

Summary

Researchers examined how freshwater acidification from elevated carbon dioxide interacts with polystyrene micro- and nanoplastics to affect a common green algae species. They found that smaller nanoplastics caused greater harm than larger microplastics, primarily through oxidative stress, while acidification alone actually promoted algal growth. The study reveals that climate change and plastic pollution can interact in unexpected ways, with acidification sometimes masking or modifying the toxic effects of plastic particles.

Polymers
Study Type Environmental

Aquatic organisms face increased complexity and severity when exposed to the combined stressors of climate change and micro- and nanoplastics (MNPs), as opposed to facing these stressors individually. This study examined the effects and underlying mechanisms of elevated pCO, which leads to freshwater acidification, as well as amino-modified polystyrene MNPs (PS-NH MNPs) of varying sizes (5 μm, 300 nm, 80 nm), on Chlamydomonas reinhardtii under both individual and combined conditions. The results showed a size-dependent toxicity of PS MNPs, with the smaller nanoparticles (80 nm) causing greater toxic inhibition than the larger microparticles (5 μm and 300 nm), primarily attributed to oxidative stress-related cellular damage. In contrast, freshwater acidification (FA) appeared to promote the growth of C. reinhardtii, possibly by upregulating transcripts associated with energy metabolism. However, when C. reinhardtii was exposed to both FA and MNPs simultaneously, distinct toxic effects were observed. The co-exposure to FA and NPs induced the most severe oxidative stress, implying the greatest energetic cost. This stress resulted in the downregulation of pathways involved in fatty acid biosynthesis and protein folding, ultimately causing significant damage to cellular structure and function. The increased energy from the upregulation of the TCA cycle was mainly allocated for DNA damage repair and cell division, which induced an energy deficit necessary for stress resistance. In contrast, during co-exposure to FA and MPs, energy was redirected towards DNA replication and the synthesis of anti-stress substances, facilitating recovery and promoting growth. Our study highlighted the decisive influence of climate change and particle size in assessing the ecological effects and risks associated with MNPs.

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