Embryonic exposure to benzo(a)pyrene influences neural development and function in rockfish (Sebastiscus marmoratus)

Abstract

Benzo(a)pyrene (BaP) is known to be carcinogenic and teratogenic. Several epidemiological and animal studies report that BaP causes neurological abnormalities; however, the mechanism of BaP-induced impairment of nervous system development and function, particularly in fish, remains unclear. In this study, Sebastiscus marmoratus embryos were exposed to BaP at environmental levels (0.5, 5 and 25 nmol/L) for 7 days. The results show disruption of the cranial innervation pattern. The expression of calmodulin (CaM) and Ca(2+)/calmodulin dependent kinase II (CaMKII) was decreased in a dose-dependent manner. BaP exposure reduced the levels of ACh and ChAT and promoted the activity of AChE. In addition, BaP exposure decreased NO concentration in all treatments and increased the activity of NOS in the 0.5 and 5 nmol/L groups. These results suggest that BaP could decrease the expression CaM and CaMKII mRNA and NO, which would perturb the cholinergic system and disrupt nervous system development.