Search

Halobenzoquinones (HBQs) are emerging and widespread disinfection byproducts (DBPs), but their toxicological mechanisms to aquatic organisms remain elusive. Herein, we evaluated oxidative stress, cardiac toxicity, and cerebral toxicity after 2, 6-dichloro-1, 4-benzoquinone (2,6-DCBQ) exposure in zebrafish. Adult zebrafish were respectively exposed to 0.25, 0.5, and 1 μM 2,6-DCBQ for 96 h. The mortality rate of 2,6-DCBQ (1 μM) was 10%, while the LC50 value was 1.532 μM. Besides, 2,6-DCBQ exposure caused irregularity and elimination of myocardial fiber in the heart, and the pyknosis of nuclears and the agglutination of chromatin in the brain. We measured the 2,6-DCBQ-induced oxidative stresses in the heart and brain. Additionally, the glutathione (GSH) content, superoxide dismutase (SOD) activity, catalase (CAT) activity, and total antioxidant capacity (T-AOC) were significantly inhibited. To better understand the potential toxicity of 2,6-DCBQ, transcriptomic analysis was performed in the control and 1 μM group after 96 h exposure. As a result, 545 and 1228 differentially expressed genes (DEGs) were detected in the heart and brain, respectively. GO analysis revealed that these DEGs were primarily enriched in blood vessel development, vasculature development, and oxidoreductase activity in the heart; response to stimulus, nervous system development, and oxidoreductase activity in the brain. KEGG enrichment analysis indicated that the DEGs were mainly enriched in VEGF signaling pathway and vascular smooth muscle contraction pathway in the heart; neuroactive ligand-receptor interaction, and NOD-like receptor signaling pathway in the brain. These findings exposed the underlying toxicity mechanism of 2,6-DCBQ exposure on zebrafish cardiovascular and brain systems.