Toxic effects of PFOA on Nitzschia palea and its apoptosis mechanism

Abstract

This study investigates the acute toxicity effects and apoptosis mechanisms of perfluorooctanoic acid (PFOA) on Nitzschia palea (N. palea), aiming to provide a theoretical foundation for the joint risk assessment of perfluorinated compounds (PFCs) in aquatic ecosystems. N. palea was exposed to PFOA concentrations ranging from 0 to 320 mg·L⁻¹, and the effects of exposure on cell density, Chl a, antioxidant systems, and cell morphology were analyzed. The results showed that the 96-h EC50 of PFOA-induced N. palea was 90 mg·L⁻¹. PFOA concentrations of ≤40 mg·L⁻¹ promoted algal reproduction, while higher doses inhibited growth. Optical and scanning electron microscopy revealed that some N. palea cells had distinctly raised or depressed shell edges. The increase in reactive oxygen species (ROS) and antioxidant substances (SOD, CAT, and GSH) indicated that PFOA induced oxidative stress. Based on flow cytometry and AO/EB morphological observations, PFOA was found to induce apoptosis in N. palea cells. Transcriptomic analysis and qRT-PCR results showed that PFOA promotes the expression of mitochondria-associated apoptosis-related genes (NpCyt C, NpCaspase-3, and NpCaspase-9) in N. palea. This indicates that PFOA enhances the production of ROS in N. palea. Moreover, it initiates the mitochondrial apoptosis pathway by upregulating the expression of NpCyt C.