Abstract

Selenium is an essential micronutrient and its metabolism is closely linked to the methionine cycle and transsulfuration pathway. The present study evaluated the effect of two different selenium supplements in the diet of rainbow trout (Onchorhynchus mykiss) broodstock on the one-carbon metabolism and the hepatic DNA methylation pattern in the progeny. Offspring of three parental groups of rainbow trout, fed either a control diet (NC, basal Se level: 0.3 mg/kg) or a diet supplemented with sodium selenite (SS, 0.8 mg Se/kg) or hydroxy-selenomethionine (SO, 0.7 mg Se/kg), were collected at swim-up fry stage. Our findings suggest that parental selenium nutrition impacted the methionine cycle with lower free methionine and S-adenosylmethionine (SAM) and higher methionine synthase (mtr) mRNA levels in both selenium-supplemented treatments. DNA methylation profiling by reduced representation bisulfite sequencing (RRBS) identified differentially methylated cytosines (DMCs) in offspring livers. These DMCs were related to 6535 differentially methylated genes in SS:NC, 6890 in SO:NC and 7428 in SO:SS, respectively. Genes with the highest methylation difference relate, among others, to the neuronal or signal transmitting and immune system which represent potential targets for future studies.

Highlights

  • Selenium (Se) is an essential micronutrient in humans and animals, with selenoproteins exerting various metabolic functions [1]

  • The ongoing replacement of Se-rich fishmeal with plant protein sources [3,4] is associated with a decrease in dietary Se level provided to farmed fish reared over a long period [5,6]

  • The present study aims to make a comparison between the use of sodium selenite and hydroxy-selenomethionine (OH-SeMet), a pure form of the hydroxy-analogue of selenomethionine, as dietary supplements in plant protein-rich feeds for rainbow trout broodstock on the 1C metabolism and the hepatic DNA methylation pattern of the progeny

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Summary

Introduction

Selenium (Se) is an essential micronutrient in humans and animals, with selenoproteins exerting various metabolic functions [1]. The ongoing replacement of Se-rich fishmeal with plant protein sources [3,4] is associated with a decrease in dietary Se level provided to farmed fish reared over a long period [5,6]. Many of the characterized selenoproteins are known to influence antioxidant metabolism, but knowledge on the effects of dietary Se on other metabolic pathways is not well characterized [7]. In the case of a Se deficiency, an increase in glutathione levels possibly relates to a feedback mechanism by changes in redox state [8,9]. The major source for glutathione is cysteine, Life 2020, 10, 121; doi:10.3390/life10080121 www.mdpi.com/journal/life

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