Inhibition mechanisms of nanoplastics and ofloxacin on marine Synechococcus: Evidence from coupled physiological and transcriptomic assessments.

Abstract

The co-occurrence of nanoplastics (NPs) and antibiotics in marine environments poses complex threats to primary producers, yet the multi-level mechanisms of their combined toxicity remain poorly understood. In this study, we systematically investigated the physiological, biochemical, and transcriptomic responses of the marine cyanobacterium Synechococcus sp. WH8102 to single and combined exposure of polystyrene NPs and ofloxacin (OFL). Interestingly, Independent Action analysis based on population growth indicated an apparent antagonistic interaction, which may be associated with altered OFL availability in the presence of NPs. In contrast, ultrastructural and biochemical analyses revealed pronounced cellular damage under combined exposure. The adherence of NPs to the cell surface was accompanied by compromised membrane integrity, elevated ROS accumulation, and enhanced cellular impairment. This extreme oxidative stress triggered a systemic collapse of the photosynthetic apparatus, drastically inhibiting photochemical efficiency. Consequently, the resulting ATP and NADPH supply crisis propagated to the core metabolic networks, severely inhibiting key enzymes in both carbon fixation and nitrogen assimilation. Transcriptomic profiling further elucidated a critical regulatory shift: whereas single OFL exposure induced compensatory repair mechanisms-upregulating carbon metabolism and ribosomal genes-combined stress suppressed these defenses. This forced a global transcriptional shutdown of photosynthesis, the TCA cycle, and protein synthesis as a failed "energy conservation" strategy. Ultimately, this study highlights the critical disparity between macroscopic population antagonism and microscopic cellular impairment, providing profound mechanistic insights into the profound ecological risks of combined emerging contaminants.