Sex Hormone-Binding Globulin expression during oogenesis. Its regulation by xenosteroids in pejerrey fish.

ANELISA GONZÁLEZ; JUAN I. FERNANDINO; TOMÁS CHALDE; MARIANO ELISIO; LEANDRO A. MIRANDA; GUSTAVO M. SOMOZA

Buenos Aires

Congreso; SETAC Latin America 11th Biennial Meeting.; 2015

SETAC-LA

Sex hormone-binding globulins (SHBGs) are carrier serum proteins involved inthe transport of sex steroids in blood. SHBGs are related to reproductionbecause they regulate the plasma metabolic clearance rate of sex steroids bycontrolling its bioavailability. It is known that the main expression site ofSHBG in teleost fish is the liver, but there is little knowledge about itsregulation. In female fish, one of the most important reproductive processes isvitellogenesis, and this process is mainly regulated by the sex steroid 17β-estradiol (E2) synthetized in the ovary. However, the involvement of sexsteroids in the regulation of SHBG expression is still under debate in teleosts.Additionally, it is well known that xenoestrogens can mimic the actions ofendogenous estrogens. In this context, the main objective of this study was toanalyze if natural and/or synthetic sex steroids can regulate shbg geneexpression. First, shbg-mRNA abundance was assessed in liver duringoogenesis in wild fish throughout one sex cycle. Then we assessed the in vitroexposure of vitellogenic female liver slices to the following estrogens: E2 and17α-ethinylestradiol (EE2), and the androgens: testosterone (T) and 5α-dihydrotestosterone (DHT). All steroids were tested at the followingconcentrations: 0.05, 0.5, 5 and 50 ng/ml. The results showed that shbg-mRNAabundance varied throughout pejerrey oogenesis, with the highest levels at previtellogenesis and lowest at advanced vitellogenesis stages. The expression of shbg showed negative correlations with plasmatic sex steroids levels (R=0.8 for E2 and R=0.58 for T), indicating that these steroid could be involved in anegative feedback mechanism. On the other hand, in vitro culture ofvitellogenic female liver slices, showed that E2, EE2 and DHT but not T,increased shbg-mRNA abundance, being E2 the most potent steroid (increasing10 times with respect to basal levels at all concentrations tested). Takentogether, these results suggest that shbg gene expression can be regulated by sex steroid and xenosteroids. Thus, the presence of these compounds in theenvironment could modulate the steroids bioavailability through the regulationof SHBG expression.