Gene ontology analysis of expanded porcine blastocysts from gilts fed organic or inorganic selenium combined with pyridoxine

Abstract

BackgroundGene ontology analysis using the microarray database generated in a previous study by this laboratory was used to further evaluate how maternal dietary supplementation with pyridoxine combined with different sources of selenium (Se) affected global gene expression of expanded porcine blastocysts. Data were generated from 18 gilts randomly assigned to one of three experimental diets (n = 6 per treatment): i) basal diet without supplemental Se or pyridoxine (CONT); ii) CONT + 0.3 mg/kg of Na-selenite and 10 mg/kg of HCl-pyridoxine (MSeB610); and iii) CONT + 0.3 mg/kg of Se-enriched yeast and 10 mg/kg of HCl-pyridoxine (OSeB610). All gilts were inseminated at their fifth post-pubertal estrus and euthanized 5 days later for embryo harvesting. Differential gene expression between MSeB610 vs CONT, OSeB610 vs CONT and OSeB610 vs MSeB610 was performed using a porcine embryo-specific microarray.ResultsThere were 559, 2458, and 1547 differentially expressed genes for MSeB610 vs CONT, OSeB610 vs CONT and OSeB610 vs MSeB610, respectively. MSeB610 vs CONT stimulated 13 biological processes with a strict effect on RNA binding and translation initiation. OSeB610 vs CONT and OSeB610 vs MSeB610 impacted 188 and 66 biological processes, respectively, with very similar effects on genome stability, ceramide biosynthesis, protein trafficking and epigenetic events. The stimulation of genes related with these processes was confirmed by quantitative real-time RT-PCR.ConclusionsGene expression of embryos from OSeB610 supplemented gilts was more impacted than those from MSeB610 supplemented gilts. Whereas maternal OSeB610 supplementation influenced crucial aspects of embryo development, maternal MSeB610 supplementation was restricted to binding activity.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-5237-1) contains supplementary material, which is available to authorized users.

From “Every Day” Hormonal to Oxidative Stress Biomarkers in Blood and Follicular Fluid, to Embryo Quality and Pregnancy Success?

“…and that high antioxidant levels may help improve embryo quality, the only sensible conclusion is that embryos do synthesize antioxidant enzymes themselves even in in vitro conditions that may avoid some of the physiological mechanisms for maternal selenium transfer regulation. Therefore, we tend to believe that the effects of selenium on embryo development are mainly due to the effects on genomic stability, intracellular ceramides synthesis, and peptides trafficking (as concluded in [52]), rather than because of all antioxidant activity. In fact, in the article [53], it has been shown that in vivo other complementary antioxidant mechanisms were upregulated by selenium supplementation, but not the GPX system.…”

Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice

“…It has also been suggested that regardless of the source of maternal dietary Se, Se content in embryos would come from an organic metabolite: either from SeMet pool of oocytes and/or oocyte selenoproteins [47]. Therefore, it can be hypothesized that oocyte (maternal) selenoproteins provide a common source of SeCys for embryo selenoprotein synthesis [47].…”

“…It has also been suggested that regardless of the source of maternal dietary Se, Se content in embryos would come from an organic metabolite: either from SeMet pool of oocytes and/or oocyte selenoproteins [47]. Therefore, it can be hypothesized that oocyte (maternal) selenoproteins provide a common source of SeCys for embryo selenoprotein synthesis [47]. Interestingly, this hypothesis is partly supported by the findings of two recent studies, where higher Se level and GPX activities were observed in embryos harvested from Se-supplemented gilts, reinforcing the notion that embryos, regardless of maternal dietary Se source, may obtain their Se content from a common intermediary Se metabolite [83,84].…”

“…It was shown that Se was implicated in regulating the physiology of uterine smooth muscles potentially via modulating the expression of Selenon, Selenot, and Selenow [41,42], and the G protein Rho (RhoA)/Rho kinase (ROCK) signaling pathway in mice [43]. However, only recently have researchers paid attention to potential role of Se in ovarian physiology and embryo development [9,28,[44][45][46][47][48][49][50]. Interestingly, when exploring the mainstream literature, with the exclusion of one study reporting the beneficial effects of Se supplementation on sperm parameters in aging mice [51], no study has yet elucidated how Se might ameliorate the reproductive function in aging mammalian models, let alone the aged females.…”

The Possible Mechanism of Physiological Adaptation to the Low-Se Diet and Its Health Risk in the Traditional Endemic Areas of Keshan Diseases

“…Sec needs to be broken down by the specific enzyme selenocysteine lyase (Scly) into l -alanine and HSe − (SeMet → Sec → HSe − ) [ 69 – 71 ]. Historically, more attention has been paid to the effect of vitamin B6 on the catalyzation in the Scly step [ 72 – 76 ] rather than the essential role of serine [ 77 ].…”