Sex-steroids and hypolipidemic chemicals impacts on brown trout lipid and peroxisome signaling - Molecular, biochemical and morphological insights.

摘要: Lipid metabolism involves complex pathways, which are regulated in a similar way across vertebrates. Hormonal and hypolipidemic deregulations cause lipid imbalance from fish to humans, but the underlying mechanisms far understood. This study explores potential of using juvenile brown trout evaluate vivo interferences caused by estrogenic (17α-ethinylestradiol - EE2), androgenic (testosterone T), (clofibrate CLF) compounds lipidic and/or peroxisomal pathways. Studied endpoints were blood/plasma biochemistry, plasma fatty acid profile, ultrastructure hepatocytes abundance their peroxisomes mRNA expression liver. Both T CLF minimal effects when compared EE2. Estrogenized had significantly higher hepatosomatic indexes, increased triglycerides very-low density lipoproteins (VLDL) plasma, with solvent control. Morphologically, EE2 showed droplets hepatocytes, reduced volume relation hepatic parenchyma. Polyunsaturated acids (PUFA) namely n-3 PUFA, animals levels vitellogenin A (VtgA), estrogen receptor alpha (ERα), peroxisome proliferator-activated (PPARα), PPARαBa acyl-CoA long chain synthetase 1 (Acsl1), while ERβ-1, oxidase 1-3I (Acox1-3I), Acox3, PPARγ, catalase (Cat), urate (Uox), binding protein (Fabp1) apolipoprotein AI (ApoAI) down-regulated. In summary, exposure altered dynamics trout, changing several genes. Our model can be used possible organism-level impacts, viz. gonadogenesis.