Understanding the Ecotoxicity of Diclofenac on the Freshwater Cyanobacterium Arthrospira platensis through Growth Kinetics, Primary Biocomponents, Oxidative Metabolism, and Molecular Docking
摘要
The increasing presence of pharmaceutical pollutants, such as diclofenac (DFN), in aquatic environments poses significant ecological risks. However, their toxicity to microalgae remains poorly understood. The study examined the influence of DFN (0–100 mg L−1) on the freshwater cyanobacterium Arthrospira platensis for 7 days. The outcome revealed that biomass formation was increasingly suppressed in a time and dose dependent manner with maximum effects observed at higher doses (100 mg L−1). DNF exposure caused oxidative stress, with enhanced levels of malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) levels. Besides, there was a considerable reduction in the level of antioxidant and detoxification enzyme activities, namely catalase (CAT), peroxidase (POD), glutathione S-transferase (GST), and ascorbate peroxidase (APX). Composition of pigments was affected by a 39% decrease in chlorophyll a level at 100 mg L⁻1 DFN, as well as conspicuous reductions in lipids and carbohydrate content. Molecular docking analysis further revealed that DFN interacts with all four enzymes (APX, GPX, GST, and POD) with binding energies ranging from –6.4 to –8.0 kcal/mol. These interactions were stabilized through hydrogen bonds, pi-pi stacking, and hydrophobic contacts, with unique features such as a pi-sulfur bond in the POD complex and extensive aromatic interactions in the APX and GST complexes. The relatively uniform affinity across different enzymes suggests that DFN disrupts redox homeostasis via a multi-target mechanism. These results highlight the ecotoxicological hazard of DFN to aquatic life and affirm the necessity of research on the molecular basis for these responses. This work adds to improved comprehension of pharmaceutical pollution's environmental impact and serves as a basis for future ecotoxicological risk assessment.