Adenovirus (HAdV) can cause severe respiratory infections in children and immunocompromised patients. There is a lack of specific therapeutic drugs for HAdV infection, and the study of anti-adenoviral drugs has far-reaching clinical implications. Elemental selenium can play a specific role as an antioxidant in the human immune cycle by non-specifically binding to the amino acid methionine in body proteins. Methods: The antiviral mechanism of selenomethionine was explored by measuring cell membrane status, intracellular DNA status, cytokine secretion, mitochondrial membrane potential, and ROS production. Conclusions: Selenomethionine improved the regulation of ROS-mediated apoptosis by modulating the expression of Jak1/2, STAT3, and BCL-XL, which led to the inhibition of apoptosis. It is anticipated that selenomethionine will offer a new anti-adenoviral therapeutic alternative.

N-acetyl-selenomethionine (NASeLM), a representative of the selenium compounds, failed to convince in clinical studies and cell cultures that it neither inhibits cancer growth nor has a chemoprotective effect. This study aims to find out whether NASeLM shows a growth-inhibiting property compared to the carrier substance N-Acetyl-L-methionine (NALM) on two different cancer cells, namely Jurkat cells and MTC-SK cells.
METHODS: Jurkat and MTC-SK cells were cultured in the absence or presence of varying concentrations (0-500 µg/mL) of NASeLM and NALM solutions. After 0, 24, 48, and 72 h, mitochondrial activity, cancer cell membrane CP levels, cell growth, and caspase-3 activity were assessed in aliquots of Jurkat and MTC-SK cells.
RESULTS: Both substances, NASeLM and NALM, were similarly able to inhibit cell growth and mitochondrial activity of Jurkat cells in a concentration-dependent and time-dependent manner up to 70%. Only the determination of caspase activity showed that only NASeLM was able to increase this to almost 40% compared to the control as well as the same lack of NALM. However, the experiments on MTC-SK cells showed a clear difference in favor of NASeLM compared to NALM. While NASeLM was able to reduce cell growth to up to 55%, the same amount of NALM was only at around 15%, which turned out to be highly significant (p < 0.001). The same could also be measured for the reduction in MTC-SK mitochondrial activity. Time dependence could also be recognized: the longer both substances, NASeLM and NALM, were incubated, the higher the effect on cell growth and mitochondrial activity, in favour of NASeLM. Only NASeLM was able to increase caspase-3 activity in MTC-SK cells: at 250 µg/mL NASeLM, caspase-3 activity increased significantly to 28% after 24 and 48 h compared to the control (14%) or the same NALM concentration (14%). After 72 h, this could still increase to 37%. A further increase in the NASeLM concentration did not result in higher caspase-3 activity.
CONCLUSIONS: NASeLM could clearly increase caspase-3 activity in both cell types, Jurkat or MTC-SK cells, and thus induce cell death. NALM and NASeLM showed a reduction in cell growth and mitochondrial activity in both cell lines: While NALM and NASeLM showed almost identical measurements on Jurkat cells, NASeLM was much more effective on MTC-SK than the non-selenium-containing carrier, indicating that it has additional anti-chemoprotective effects.

Selenium is an essential trace element co-translationally incorporated into selenoproteins with important biological functions. Health benefits have long been associated with selenium supplementation. However, cytotoxicity is observed upon excessive selenium intake. The aim of this study is to investigate the metabolic pathways underlying the response to the selenium-containing amino acids selenomethionine and selenocysteine in a normal human breast epithelial cell model. We show that both selenomethionine and selenocystine inhibit the proliferation of non-cancerous MCF-10A cells in the same concentration range as cancerous MCF-7 and Hela cells, which results in apoptotic cell death. Selenocystine exposure in MCF-10A cells caused a severe depletion of free low molecular weight thiols, which might explain the observed upregulation of the expression of the oxidative stress pathway transcription factor NRF2. Both selenomethionine and selenocystine induced the expression of target genes of the unfolded protein response (GRP78, ATF4, CHOP). Using a redox-sensitive fluorescent probe targeted to the endoplasmic reticulum (ER), we show that both selenoamino acids shifted the ER redox balance towards an even more oxidizing environment. These results suggest that alteration of the redox state of the ER may disrupt protein folding and cause ER stress-induced apoptosis in MCF-10A cells exposed to selenoamino acids.

Previously, insulin resistance and hepatic oxidative stress with increased expressions of glutathione peroxidase (GPx) 1 and selenoprotein P (SelP) were induced in NSY mice, a diabetic mouse model, by administrating a high fat diet (HFD) and seleno-L-methionine (SeMet) for 12 weeks. In this study we developed an analysis method for serum selenoproteins using LC-tandem mass spectrometry (LC-MS/MS) and investigated the effects of supplementary selenium on serum concentrations of selenoproteins as well as protein expression in skeletal muscle as a major insulin target tissue under the same experimental condition. The glucose area under the curves for oral glucose tolerance and insulin tolerance tests indicated that the HFD induced insulin resistance, whereas the treatment of SeMet + HFD showed insignificant promotion compared with the HFD-induced insulin resistance. Although the expressions of GPx1 in gastrocnemius and soleus were not significantly induced by supplementary SeMet nor HFD administration, the expressions of SelP in both skeletal muscles were significantly induced by the treatment of SeMet + HFD. There were also significant increases in serum concentrations of SelP by supplementary SeMet + HFD administration, whereas GPx3 was augmented by supplementary SeMet only. These results indicated that the HFD intake under the sufficient selenium status augmented the blood secretion of SelP, which may participate in the reduction of insulin sensitivity in skeletal muscles as well as liver or adipose tissues, and it is a better indicator of deterioration than GPx3 as it is a major selenoprotein in serum.

UNASSIGNED: Selenium (Se) deficiency, stemming from malnutrition in humans and animals, has the potential to disrupt many vital physiological processes, particularly those reliant on specific selenoproteins. Agronomic biofortification of crops through the application of Se-containing sprays provides an efficient method to enhance the Se content in the harvested biomass. An optimal candidate for systematic enrichment, guaranteeing a broad trophic impact, must meet several criteria: (i) efficient accumulation of Se without compromising crop yield, (ii) effective conversion of mineral Se fertilizer into usable organically bound Se forms (Seorg), (iii) acceptance of a Se-enriched crop as livestock feed, and (iv), interest from the food processing industry in utilization of Se-enriched outputs. Hence, priority should be given to high-protein leafy crops, such as soybean.
UNASSIGNED: A three-year study in the Czech Republic was conducted to investigate the response of field-grown soybean plants to foliar application of Na2SeO4 solutions (0, 15, 40, and 100 g/ha Se); measured outcomes included crop yield, Se distribution in aboveground biomass, and the chemical speciation of Se in seeds.
UNASSIGNED: Seed yield was unaffected by applied SeO4 2-, with Se content reaching levels as high as 16.2 mg/kg. The relationship between SeO4 2-dose and Se content in seeds followed a linear regression model. Notably, the soybeans demonstrated an impressive 73% average recovery of Se in seeds. Selenomethionine was identified as the predominant species of Se in enzymatic hydrolysates of soybean, constituting up to 95% of Seorg in seeds. Minor Se species, such as selenocystine, selenite, and selenate, were also detected. The timing of Se spraying influenced both plant SeO4 2- biotransformation and total content in seeds, emphasizing the critical importance of optimizing the biofortification protocol. Future research should explore the economic viability, long-term ecological sustainability, and the broad nutritional implications of incorporating Se-enriched soybeans into food for humans and animals.

Selenium (Se) is a vital trace element, essential for growth and other biological functions in fish. Its significance lies in its role as a fundamental component of selenoproteins, which are crucial for optimal functioning of the organism. The inclusion of Se in the diets of farmed animals, including fish, has proved invaluable in mitigating the challenges arising from elemental deficiencies experienced in captivity conditions due to limitations in the content of fishmeal. Supplementing diets with Se enhances physiological responses, particularly mitigates the effects of the continuous presence of environmental stress factors. Organic Se has been shown to have higher absorption rates and a greater impact on bioavailability and overall health than inorganic forms. A characteristic feature of yeasts is their rapid proliferation and growth, marked by efficient mineral assimilation. Most of the selenized yeasts currently available in the market, and used predominantly in animal production and aquaculture, are based on Saccharomyces cerevisiae, which contains selenomethionine (Se-Met). The object of this review is to highlight the importance of selenized yeasts. In addition, it presents metabolic and productive aspects of other yeast genera that are important potential sources of organic selenium. Some yeast strains discussed produce metabolites of interest such as lipids, pigments, and amino acids, which could have applications in aquaculture and further enrich their usefulness.

Selenium (Se) is an essential trace mineral that plays an important role in physiological processes by regulating the antioxidant defense system and enhancing immunity. Chromium is an essential mineral involved in carbohydrate and lipid metabolism and also plays a role in maintaining normal insulin function. Based on these advantages, we hypothesized that the addition of selenomethionine (SeMet) and organic chromium (OC) to broiler diets would increase Se deposition, antioxidant capacity and immune response in meat. Therefore, this study analyzed the effects of OC and SeMet on growh performance, nutrients digestibility, blood profiles, intestinal morphology, meat quality characteristics, and taxonomic analysis of broilers. A total of 168 one-day-old broiler chicken (Arbor Acres) were randomly allotted to 3 groups based on the initial body weight of 37.33 ± 0.24 g with 7 replicate per 8 birds (mixed sex). The experiments period was 28 days. Dietary treatments were folloewd: Basal diets based on corn-soybean meal (CON), basal diet supplemented with 0.2 ppm OC and 0.2 ppm SeMet (CS4), and basal diet supplemented with 0.4 ppm OC and 0.4 ppm SeMet (CS8). Supplementation of OC and SeMet did not affect on growth performance, nutrient digestibility. However, CS8 supplementation increased in duodenum villus height and villus height : crypt depth, and increased in breast meat Se deposition. In addition, CS8 group showed higher uric acid and total antioxidant status than CON group. Taxonomic analysis at phylum level revealed that Proteobacteria and Firmicutes of CS4 and CS8 were lower than CON group. In genus level, the relative abundance of fecal Lactobacillus and Enterococcus of CS4 and CS8 groups were higher than CON group. In short, 0.4 ppm OC and 0.4 ppm SeMet supplementation to broiler diet supporitng positive gut microbiome change, also enhancing antioxidant capacity, and Se deposition in breast meat.

Extracellular vesicles (EVs) derived from Mesenchymal Stromal Cells (MSCs) have shown promising therapeutic potential for multiple diseases, including intervertebral disc degeneration (IDD). Nevertheless, the limited production and unstable quality of EVs hindered the clinical application of EVs in IDD. Selenomethionine (Se-Met), the major form of organic selenium present in the cereal diet, showed various beneficial effects, including antioxidant, immunomodulatory and anti-apoptotic effects. In the current study, Se-Met was employed to treat MSCs to investigate whether Se-Met can facilitate the secretion of EVs by MSCs and optimize their therapeutic effects on IDD. On the one hand, Se-Met promoted the production of EVs by enhancing the autophagy activity of MSCs. On the other hand, Se-Met pretreated MSC-derived EVs (Se-EVs) exhibited an enhanced protective effects on alleviating nucleus pulposus cells (NPCs) senescence and attenuating IDD compared with EVs isolated from control MSCs (C-EVs) in vitro and in vivo. Moreover, we performed a miRNA microarray sequencing analysis on EVs to explore the potential mechanism of the protective effects of EVs. The result indicated that miR-125a-5p is markedly enriched in Se-EVs compared to C-EVs. Further in vitro and in vivo experiments revealed that knockdown of miR-125a-5p in Se-EVs (miRKD-Se-EVs) impeded the protective effects of Se-EVs, while overexpression of miR-125a-5p (miROE-Se-EVs) boosted the protective effects. In conclusion, Se-Met facilitated the MSC-derived EVs production and increased miR-125a-5p delivery in Se-EVs, thereby improving the protective effects of MSC-derived EVs on alleviating NPCs senescence and attenuating IDD.

The objective of this study was to investigate the effects of two different organic selenium (Se) supplements, selenomethionine (Se-Met) and selenohomolanthionine (Se-Hlan), on the serum biochemical parameters and Se status of dairy cows. Different dietary Se supplementation treatments were set as follows: a control group (CON, adding sodium selenite at 0.3 mg Se/kg dry matter [DM]), 0.3 and 0.5 Se-Met (adding Se-Met at 0.3 and 0.5 mg Se/kg DM, respectively), as well as 0.3 and 0.5 Se-Hlan (adding Se-Hlan at 0.3 and 0.5 mg Se/kg DM, respectively). The experiment lasted 8 weeks. The serum measurements showed that both organic Se treatments resulted in higher uric acid than CON. Se-Met produced higher aspartate aminotransferase, glucose, urea, low-density lipoprotein cholesterol, and lactate dehydrogenase than Se-Hlan. Regarding the Se status, the highest milk Se values appeared in 0.5 Se-Met, with intermediate values in 0.3 Se-Met and 0.5 Se-Hlan, whereas the highest and lowest serum Se levels were presented in 0.5 Se-Met and 0.3 Se-Hlan, respectively. Our results suggest that Se-Hlan was not as efficient in boosting serum or milk Se as Se-Met and differences in serum biomarkers between Se-Met and Se-Hlan may be associated with distinct metabolic pathways for different forms of organic Se.

The aim of this study was to investigate the alleviating effect of selenomethionine (SeMet) on aflatoxin B1 (AFB1)-induced testicular injury in rabbits. Twenty-five 90-d-old rabbits were randomly divided into 5 groups (the control group, the AFB1 group, the 0.2 mg/kg SeMet + AFB1 group, the 0.4 mg/kg SeMet + AFB1 group and the 0.6 mg/kg SeMet + AFB1 group). After 1 d of the experiment, the SeMet-treated groups were fed 0.2 mg/kg SeMet, 0.4 mg/kg SeMet, or 0.6 mg/kg SeMet daily, and the remaining two groups were fed a normal diet for 30 d. On Day 31, all rabbits in the model group and the three treatment groups were fed 0.5 mg/kg AFB1 for 21 d. The levels of testosterone (T), luteinizing hormone (LH) and follicle stimulating hormone (FSH) in rabbit plasma were detected. Rabbit semen was collected, and its quality was evaluated. Pathological changes in rabbit testes were observed by hematoxylin-eosin (HE) staining. The expression of related proteins in testicular tissue was detected by immunohistochemistry, immunofluorescence and western blot (WB) analysis. Enzyme-linked immunosorbent assays (ELISAs) were used to detect oxidative stress-related indices and inflammatory factors in testicular tissue. The results showed that AFB1 can induce oxidative stress and inflammation to activate the p38/MSK/NF-κB signalling pathway, mediate apoptosis, inhibit the proliferation and differentiation of testicular cells, destroy the integrity of the blood-testis barrier (BTB) and the normal structure of the testis, and reduce the content of sex hormones and semen quality. SeMet pretreatment significantly alleviated testicular injury oxidative stress, and the inflammatory response in rabbits. Thus, we demonstrated that SeMet restores AFB1-induced testicular toxicity by inhibiting the p38/MSK/NF-κB signalling pathway. In addition, in this study, 0.4 mg/kg SeMet had the most impactful effect.