Effects of life-time exposure to waterborne copper on the somatotropic axis of the viviparous fish Poecilia vivipara

Reduced fish growth following chronic exposure to dissolved copper (Cu) is well reported in the literature. Nevertheless, information on the mechanism(s) involved in this process is scarce. Therefore, we evaluated growth, gene expression and concentrations of proteins related to growth regulation in the viviparous guppy Poecilia vivipara chronically exposed to dissolved Cu. Newborn (<24 h after birth) fish were kept under control conditions or exposed to environmentally relevant concentrations of Cu (5 and 9 mu g/L) in salt water (24 ppt) for 345 days. After exposure, fish growth was evaluated based on body weight and length. Also, growth hormone (gh) mRNA expression was evaluated in brain, while growth hormone receptor 1 (ghr1) and 2 (ghr2) mRNA expressions were analyzed in brain, skeletal muscle and liver. In turn, insulin-like growth factor 1 (igf1) and 2 (igf2) mRNA expressions were evaluated in skeletal muscle and liver. Additionally, Gh concentration was assessed in brain, while Ghr concentration was evaluated in skeletal muscle and liver. Exposure to 9 mu g/L Cu reduced fish body weigh and length. Metal exposure affected mRNA expression only in skeletal muscle. Reduced ghr2 mRNA expression was observed in guppies exposed to 5 and 9 mu g/L Cu. Additionally, reduced igf1 and igf2 mRNA expressions were observed in guppies exposed to 9 mu g/L Cu. However, no significant change in Ghr concentration was observed. The reduced ghr2 mRNA expression suggests that chronic Cu exposure induced an insensitivity of the skeletal muscle to Gh, thus resulting in reduced igf1 and igf2 mRNA expression which lead to reduced fish growth. These findings indicate that chronic exposure to dissolved Cu disrupts the somatotropic axis regulation, thus helping to elucidate the mechanism underlying the Cu-dependent inhibition of growth observed in the viviparous fish P. vivipara. (C) 2018 Elsevier Ltd. All rights reserved.