ROS-mediated autophagy-apoptosis crosstalk regulates cell fate in the marine microalga Isochrysis galbana under BDE-47 stress.

Although the regulatory crosstalk between autophagy and apoptosis in response to stress has been well documented in higher multicellular eukaryotes, its functional significance in marine microalgae exposed to persistent organic pollutants (POPs) remains largely unclear. Here, we investigated the coordinated responses of these two pathways in the marine microalga Isochrysis galbana exposed to 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), a widespread coastal environmental contaminant. Exposure to BDE-47 (50-150 μg/L, 48 h) induced dose-dependent oxidative stress, characterized by excessive reactive oxygen species (ROS) accumulation, a decreased glutathione (GSH)/glutathione disulfide (GSSG) ratio, and increased malondialdehyde (MDA) content. Simultaneously, BDE-47 activated both the intrinsic apoptotic pathway, characterized by mitochondrial membrane potential (MMP) depolarization and elevated caspase-9 and caspase-3 activities, and the extrinsic pathway, reflected by the upregulation of Fas-associated death domain (FADD) and increased caspase-8 activity. Enhanced autophagic fluorescence intensity, autophagosomes formation, and upregulation of autophagy-related genes (ATGs) and proteins further confirmed that autophagy was also induced. Pharmacological inhibition assays revealed that the ROS scavenger N-acetylcysteine (NAC) markedly attenuated both autophagy and apoptosis, identifying ROS as a common upstream trigger for both processes. Inhibition of autophagy by 3-methyladenine (3-MA) exacerbated apoptotic damage, whereas blockade of apoptosis by Z-VAD-FMK promoted autophagic activity, indicating an antagonistic crosstalk in which autophagy suppresses apoptosis and vice versa. These findings demonstrate that the ROS-autophagy-apoptosis axis is functionally conserved in a marine microalga, and provide new insight into the cellular response of marine phytoplankton to organic pollutant stress.