The compound BDE-47 induces apoptotic mechanisms in the rotifer Brachionus plicatilis through both lysosomal-intrinsic and extrinsic pathways
The study was conducted under experimental ecological conditions to investigate the response of the marine toxicological model organism Brachionus plicatilis to the highly toxic tetrabrominated diphenyl ether(BDE-47).Differential genes and enrichment pathways were analyzed at the transcriptome level and key gene proteins were validated,to reveal the mechanisms and pathways of stress response.The results indicated that(1)compared with the control group,582 differentially expressed genes were appeared in the treatment group after 24 hours of exposure to 0.08mg/L BDE-47;KEGG annotation showed that differentially expressed genes were mainly enriched in metabolic pathways such as ribosomes and apoptosis;the differentially expressed genes were responsible for repairing damage and inhibiting apoptosis in ribosomes and estrogen signaling pathways were significantly down-regulated,while those associated with apoptosis-related MAPK signaling pathways and apoptosis pathways were significantly up-regulated,indicated that BDE-47 stress could induce apoptosis in the rotifer.(2)BDE-47 stress increased the permeability of the lysosomal membrane of the Brachionus plicatilis,and the expression of tissue protease L(Cathepsin L)in the lysosome was significantly increased(P＜0.05),indicating the damage of lysosomal.The ratio of pro-apoptotic/anti-apoptotic factors Bax/Bcl-2 was significantly increased(P＜0.05)and the Caspase family was activated.After the addition of the Cathepsin L inhibitor leupeptin,the activity of Bax/Bcl-2and Caspase family was significantly inhibited,indicating relief from the apoptotic phenomenon.The results suggested that the release of Cathepsin L caused by lysosomal damage was involved in the apoptosis process of the roundworm.Furthermore,significant increases in reactive oxygen species(ROS)and peroxidase(POD)were observed in the body of the rotifer,indicating the elevation of ROS caused by lysosomal damage was another way to induce rotifer apoptosis.
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