Effects of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) on the Peripheral Nervous System in Developing Red Seabream (Pagrus major) Embryos

Bony fish is highly sensitive to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure, especially at early developmental stages. TCDD induces various toxic effects including yolk sac edema, craniofacial malformation and neural damage in developing fish embryos. However, the effects of TCDD on the peripheral nervous system (PNS) of fish remain unclear. To clarify whether TCDD affects the morphological abnormality of PNS, the present study investigated the development of PNS in TCDD-treated red seabream (Pagrus major) embryos using a fluorescein isothiocyanate (FITC) anti-acetylated tubulin antibody. The embryos at 10 hrs post-fertilization (hpf) were exposed to 0, 0.1, 0.4 or 1.7 μg/L of TCDD in seawater for 80 min. The PNS in each exposed group was observed at 48, 78, 120 and 136 hpf. The axon guidance of posterior lateral line nerve (PLLN) was less affected by 0.1 or 0.4 μg/L of TCDD exposure, but slightly damaged by 1.7 μg/L of TCDD. On the other hand, the craniofacial distribution of PNS was notably disrupted in 1.7 μg/L TCDD-treated embryos at 120 and 136 hpf. The glossopharyngeal nerve (IX) and vagus nerve (X) were abolished by TCDD in a dose-dependent manner. At 120 hpf and 136 hpf, 1.7 μg/L TCDD exposure also affected the spinal nerve (SN), and inhibited the formation of nerve fascicle. These observations showed that TCDD produces specific effects on the development of craniofacial PNS in red seabream embryos even at low concentration (0.1 μg/L).