文摘
The present study analyses the network that regulates and guards against oxidative imbalances in common dentex, poorly adapted to culture conditions, in comparison to the successfully cultured and closely related gilthead sea bream. Both sparid fish were grown from fingerlings to market size, and several molecular and metabolic biomarkers were analysed in fish sampled at the end of the trial. For such purpose, partial cDNA sequences coding for tumour necrosis factor-α (TNFα), interleukin-1β (IL-1β), growth hormone receptors (GHR-I and II), insulin-like growth factors (IGF-I and II), cytochrome P450 1A1 (CYP1A1), glucose regulated protein-75 (GRP75), metallothionein (MT), glutathione reductase (GR) and glutathione peroxidase (GPX-1) were first PCR amplified and sequenced in common dentex. The hepatic gene expression profile was then analysed by real-time PCR assays, using β-actin as housekeeping gene. Metabolic biomarkers included total plasma antioxidant capacity, ROS production, and circulating levels of GH, IGF-I, cortisol, glucose and blood lactate. Overall growth rates to attain market size were similar in both species. However, common dentex exhibited accelerated growth over the course of larval and initial juvenile stages that was not retained thereafter. They also exhibited higher levels of plasma peroxidases and secondary stress metabolites (glucose, lactate) in combination with an increased expression of pro-inflammatory cytokines (TNFα, IL-1β), which is in accordance with an inflammatory over activity in chronically stressed fish. The activity of oxidative CYP1A1 and GH/IGF pathways was down-regulated in common dentex, possibly to equilibrate this oxidative pressure. In the same way, hepatic transcripts of enzymatic (GPX-1) and non-enzymatic (GRP75, MT) antioxidant genes were up-regulated, remaining the total plasma antioxidant capacity within the reference values of gilthead sea bream. Thus, common dentex seems to orchestrate in the last juvenile stages several biological strategies, which may serve to preserve redox homeostasis at the expense of reduced growth and low detoxifying capacity for pollutants and endogenous substrates.
