Aroclor 1254 inhibits vasotocinergic pathways related to osmoregulation function in the gilthead sea bream (Sparus aurata)

Abstract

The present study assesses the response of vasotocinergic system in the gilthead sea bream (Sparus aurata)after administeringthe PCB(polychlorinated biphenyl) Aroclor 1254and submits the fish to ahyperosmoticchange(transfer from seawater, SW, to high salinity water, HSW).Specimens were injected intraperitoneally with slow-release implants (5 μL·g-1fresh weight) of coconut oil alone (control group)or containing two different doses ofAroclor (15 μg·g-1fresh weight, AROCLOR 15 group;and 50 μg·g-1fresh weight, AROCLOR 50 group). Sevendayspost-injection, 8specimensof eachexperimental group were sampled, and the remaining were transferred from SW(38 ppt salinity)to HSW(55pptsalinity)and sampled 3dayspost-transfer. Plasma and hepatic metabolites, pituitary and plasma arginine vasotocin (AVT), as well mRNA expression levels of their specific receptors (avtrtype v1a2, avtrtype v2) in gills were assessed.In addition, mRNA levels of branchial Na+,K+-ATPase(nka) and cystic fibrosis transmembrane conductance regulator (cftr)were also evaluated. Aroclor 1254 treatment affected plasma lactate and triglycerides levels,hepatic glucose and glycogen values, as well as AVT storage and release. Specimens ofcontrol group significantly enhancedbranchialavtr v2-type, nkaandcftrmRNA expressionlevelsafter hyperosmotic transfer, while group treated with Araclor 1254 remained unchanged. In addition,salinity challenge down-regulatedbranchialavtrv1a2-type gene expressionin fish tested with thiscompound.Our results demonstratedthat Aroclor 1254inhibitedthe response of vasotocinergic system, compromising hypoosmoregulatory capacity of S. aurataspecimensafterhyperosmotic challenge.