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<p>The chemically diverse group of nonsteroidal anti-inflammatory drugs (NSAIDs) is a significant source of aquatic pollution, inducing oxidative stress in algae. The aim of this study was to evaluate the antioxidant response of <i>Chlamydomonas reinhardtii</i> exposed to four NSAIDs differing in toxicity and structure: flufenamic acid (FFA), nabumetone (NBT), ibuprofen (IBU), and naproxen (NPX). This study demonstrated that all pharmaceuticals significantly increased H₂O₂ production, confirming redox imbalance in cells. The antioxidant defense also showed compartment- and compound-specific signatures depending on the NSAID toxicity level. Less toxic IBU and NPX induced coordinated SOD isoforms and catalase activation, while more toxic FFA and NBT triggered chloroplast-targeted H₂O₂ scavenging via APX pathways. Notably, <i>MSD3</i> transcript levels increased in all treatments, indicating its potential as an NSAID stress biomarker. IBR analysis demonstrated that antioxidant efficiency decreased with increasing NSAID toxicity. These findings demonstrate that NSAID toxicity shapes compartment- and isoform-specific antioxidant strategies in <i>C. reinhardtii.</i> We believe that future studies with a broader range of NSAIDs would enable us to investigate subcellular redox dynamics using compartment-specific ROS reporters and to identify NSAID-sensitive biomarkers for aquatic ecotoxicology monitoring.</p>

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Differential antioxidant pathways displayed by Chlamydomonas reinhardtii exposed to selected NSAIDs

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月15日

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  • Dominika Kapuścińska,
  • Monika Hejna,
  • Wojciech Pokora,
  • Anna Aksmann

摘要

The chemically diverse group of nonsteroidal anti-inflammatory drugs (NSAIDs) is a significant source of aquatic pollution, inducing oxidative stress in algae. The aim of this study was to evaluate the antioxidant response of Chlamydomonas reinhardtii exposed to four NSAIDs differing in toxicity and structure: flufenamic acid (FFA), nabumetone (NBT), ibuprofen (IBU), and naproxen (NPX). This study demonstrated that all pharmaceuticals significantly increased H₂O₂ production, confirming redox imbalance in cells. The antioxidant defense also showed compartment- and compound-specific signatures depending on the NSAID toxicity level. Less toxic IBU and NPX induced coordinated SOD isoforms and catalase activation, while more toxic FFA and NBT triggered chloroplast-targeted H₂O₂ scavenging via APX pathways. Notably, MSD3 transcript levels increased in all treatments, indicating its potential as an NSAID stress biomarker. IBR analysis demonstrated that antioxidant efficiency decreased with increasing NSAID toxicity. These findings demonstrate that NSAID toxicity shapes compartment- and isoform-specific antioxidant strategies in C. reinhardtii. We believe that future studies with a broader range of NSAIDs would enable us to investigate subcellular redox dynamics using compartment-specific ROS reporters and to identify NSAID-sensitive biomarkers for aquatic ecotoxicology monitoring.