Interactive effects of naphthalene treatment and the onset of vitellogenesis on energy metabolism in liver and gonad, and plasma steroid hormones of rainbow trout Oncorhynchus mykiss

Abstract

The purpose of the study was to assess in female fish the possible interaction between treatment with a polycyclic aromatic hydrocarbon (PAH) like naphthalene and the onset of vitellogenesis. In a first experiment, female rainbow trout ( Oncorhynchus mykiss) at stages 2–3 (previtellogenesis) or 4 (early vitellogenesis) were intraperitoneally injected (2 μl g − 1 ) with vegetable oil alone (control) or containing naphthalene (50 mg kg − 1 ) to be sampled 3 h later. A second experiment was similarly designed but using fish intraperitoneally implanted (10 μl g − 1 ) with slow-release coconut oil implants alone (control) or containing 50 mg naphthalene kg − 1 body mass that were sampled 3 days after injection. On each sampling time, plasma levels of cortisol and 17β-estradiol, and several metabolic parameters in plasma, liver and gonad were assessed. In controls, early vitellogenic fish compared with previtellogenic fish displayed changes that in some cases are confirmatory of previous studies whereas in other cases provide new information in plasma (increased amino acid levels), liver (decreased capacity for exporting glucose and reduced amino acid levels) and gonad (decreased amino acid levels). Naphthalene treatment produced in previtellogenic fish decreased 17β-estradiol levels in plasma, increased plasma glucose or decreased liver gluconeogenic capacity whereas no major effects were noticed on parameters involved in lipid, amino acid and lactate metabolism. Differential effects of naphthalene treatment were noticed in early vitellogenic fish such as decreased 17β-estradiol and glucose levels in plasma, increased hexokinase and glucokinase and lack of changes in fructose 1,6-bisphosphatase activities in liver, and a lower decrease of amino acid levels in gonad. Those alterations produced by naphthalene treatment resulted in a decreased capacity for covering the energy demand of vitellogenesis in liver and gonad that could contribute to a delay and/or impairment of the onset of maturation.