Immunomodulatory and Anti-Inflammatory Properties of Selenium-Containing Agents: Their Role in the Regulation of Defense Mechanisms against COVID-19.

The review presents the latest data on the role of selenium-containing agents in the regulation of diseases of the immune system. We mainly considered the contributions of selenium-containing compounds such as sodium selenite, methylseleninic acid, selenomethionine, and methylselenocysteine, as well as selenoproteins and selenium nanoparticles in the regulation of defense mechanisms against various viral infections, including coronavirus infection (COVID-19). A complete description of the available data for each of the above selenium compounds and the mechanisms underlying the regulation of immune processes with the active participation of these selenium agents, as well as their therapeutic and pharmacological potential, is presented. The main purpose of this review is to systematize the available information, supplemented by data obtained in our laboratory, on the important role of selenium compounds in all of these processes. In addition, the presented information makes it possible to understand the key differences in the mechanisms of action of these compounds, depending on their chemical and physical properties, which is important for obtaining a holistic picture and prospects for creating drugs based on them.

Selenium biofortification in Hericium erinaceus (Lion's Mane mushroom) and its in vitro bioaccessibility.

Hericium erinaceus is a traditional edible mushroom. Selenium (Se) is an essential trace element for humans and other mammals. To develop a Se biofortification strategy for H. erinaceus, the effects of selenate, selenite, and selenomethionine (SeMet) on Se uptake and mushroom growth were investigated. Selenium bioaccessibility and the major Se species present in Se-enriched H. erinaceus were tested in vitro . The H. erinaceus growth was efficiently affected by SeMet than by selenite and selenate. Selenium concentrations in fruiting bodies increased with substrate Se concentration and disturbed accumulation of other microelements. Substrate Se was absorbed and transformed into organic forms. The major Se species in Se-enriched fruiting bodies was SeMet (>63.9%). During in vitro gastrointestinal digestion tests, 51% of total Se was released, and selenocystine (SeCys2 ) (90%) and Se-methylselenocysteine (MeSeCys) (76%) were more easily digested than SeMet (51%). H. erinaceus is suggested as a novel dietary source of supplemental bioavailable Se.

A general covalent binding model between cytotoxic selenocompounds and albumin revealed by mass spectrometry and X-ray absorption spectroscopy.

Selenocompounds (SeCs) are promising therapeutic agents for a wide range of diseases including cancer. The treatment results are heterogeneous and dependent on both the chemical species and the concentration of SeCs. Moreover, the mechanisms of action are poorly revealed, which most probably is due to the detection methods where the quantification is based on the total selenium as an element. To understand the mechanisms underlying the heterogeneous cytotoxicity of SeCs and to determine their pharmacokinetics, we investigated selenium speciation of six SeCs representing different categories using liquid chromatography-mass spectrometry (LC-MS) and X-ray absorption spectroscopy (XAS) and the cytotoxicity using leukemic cells. SeCs cytotoxicity was correlated with albumin binding degree as revealed by LC-MS and XAS. Further analysis corroborated the covalent binding between selenol intermediates of SeCs and albumin thiols. On basis of the Se-S model, pharmacokinetic properties of four SeCs were for the first time profiled. In summary, we have shown that cytotoxic SeCs could spontaneously transform into selenol intermediates that immediately react with albumin thiols through Se-S bond. The heterogeneous albumin binding degree may predict the variability in cytotoxicity. The present knowledge will also guide further kinetic and mechanistic investigations in both experimental and clinical settings.

Selenoneine is a major selenium species in beluga skin and red blood cells of Inuit from Nunavik.

Nunavimmiut (Inuit of Nunavik, Northern Quebec, Canada) exhibit a high selenium (Se) status because of their frequent consumption of marine mammal foods. Indirect evidence from our previous studies had suggested that selenoneine - a novel selenocompound - may be accumulating in the blood of Nunavimmiut. We used a liquid-chromatography/inductively coupled tandem mass spectrometry (LC-ICP-MS/MS) method to measure concentrations of selenoneine and its methylated metabolite Se-methylselenoneine in archived red blood cells (RBC) obtained from 210 Nunavimmiut living in communities along the Hudson Strait, where marine mammal hunting and consumption are most frequent in Nunavik. This method was adapted to quantify selenoneine and its methylated metabolite in beluga mattaaq, an Inuit delicacy consisting of the skin with the underlying layer of fat and the major dietary source of Se for Nunavimmiut. Total selenium concentration was also measured in RBC and beluga mattaaq samples by isotope dilution ICP-MS/MS. The median selenoneine concentration in RBC was 413 µg Se/L (range = 3.20-3230 µg Se/L), representing 54% (median) of total Se content (range = 1.6-91%). Quantification of selenoneine in five beluga mattaaq samples (skin layer) from Nunavik revealed a median concentration of 1.8 µg Se/g wet wt (range = 1.2-7.4 µg Se/g), constituting 54% (median) of the total Se content (range = 44-74%). Se-methylselenoneine was also detected in Inuit RBC but not in beluga mattaaq, suggesting that selenoneine undergoes methylation in humans. Selenoneine may protect Nunavimmiut from methylmecury toxicity by increasing its demethylation in RBC and in turn decreasing its distribution to target organs.

Ultrasmall Biocompatible Bi2Se3 Nanodots for Multimodal Imaging-Guided Synergistic Radiophotothermal Therapy against Cancer.

Sub-3 nm ultrasmall Bi2Se3 nanodots stabilized with bovine serum albumin were successfully synthesized through a reaction of hydroxyethylthioselenide with bismuth chloride in aqueous solution under ambient conditions. These nanodots exhibit a high photothermal conversion efficiency (η = 50.7%) due to their strong broad absorbance in the near-infrared (NIR) window and serve as a nanotheranostic agent for photoacoustic imaging and photothermal cancer therapy. In addition, they also display radioenhancement with a ratio of 6% due to their sensitivity to X-rays, which makes them a potential sensitizer for radiotherapy. These nanodots were also labled with radioactive 99mTc for quantification of their biodistribution by single-photon-emission computed tomography (SPECT)/computed tomography (CT) imaging. Our work demonstrates the potential of ultrasmall Bi2Se3 nanodots in multimodal imaging-guided synergetic radiophotothermal therapy of cancer.

Intervention in cyclophosphamide induced oxidative stress and DNA damage by a flavonyl-thiazolidinedione based organoselenocyanate and evaluation of its efficacy during adjuvant therapy in tumor bearing mice.

A novel flavonyl-thiazolidinedione based organoselenocyanate compound was synthesized and established as nontoxic at the doses of 2.5 and 5 mg/kg b.w. in mice. Oral administration of the compound in combination with cyclophosphamide (CP) resulted in an improved therapeutic efficacy which was mostly evidenced in terms of tumor burden and protection of normal cells. The adjuvant therapy was proved to be immensely significant in increasing the mean survivability of the tumor bearing hosts. Reduction in the tumor volume was manifested through the induction of apoptosis and generation of ROS in transformed cells. Moreover, the organoselenium compound could efficiently suppress CP-induced DNA damage, chromosomal aberration, hepatic damage and enhanced the activities of various antioxidant enzymes in normal cells.

Comparative excretion and tissue distribution of selenium in mice and rats following treatment with diphenyl diselenide.

The purpose of this study was to provide data about in vivo tissue distribution and excretion of diphenyl diselenide ((PhSe)2) in rats and mice through determination of selenium levels in different biological samples. (PhSe)2 (500 mg/kg, dissolved in canola oil) was administered to animals once a day per oral. After this, mice and rats were housed in metabolic cages (one animal per cage) and urine and feces were collected at specific times after treatment. Three to five animals per group (for each time-point) were anesthetized and blood samples were collected at 0 and 30 min, 24 h, at day 5, 15, and 30 after (PhSe)2 administration. The plasma and red blood cells were separated. Brain, liver, lungs, kidneys, and adipose tissue were also collected. The determination of selenium levels was performed by inductively coupled plasma atomic emission spectrometry. The main results indicate that: (1) urine is an important route of excretion of selenium originated from (PhSe)2 in mice and rats; (2) a large amount of (PhSe)2 or some of its metabolites are stored in fat; (3) the content of selenium found in plasma was low; and (4) liver and kidneys are the tissues with high amounts of selenium.

Selenium bioaccumulation and speciation in Chironomus dilutus exposed to water-borne selenate, selenite, or seleno-DL-methionine.

The objective of the present study was to describe the uptake and elimination kinetics of selenium (Se) administered in the forms of selenate, selenite, and selenomethionine (seleno-DL-methionine) in different life stages of the midge Chironomus dilutus, and to determine the relationship between Se bioavailability and Se speciation using X-ray absorption spectroscopy (XAS). Midge larvae exposed to 4.3 µg/L as dissolved selenate for 10 d of had negligible accumulation of Se (indistinguishable from control organisms). However, larvae rapidly accumulated Se over 10 d of exposure to 3.8 and 1.8 µg/L selenite and seleno-DL-methionine (Se-met), respectively. Most Se accumulated by larvae exposed to selenite or Se-met was retained after 10 d of elimination in clean water. When additional midge larvae were exposed to Se until emergence, Se accumulated during the larval stage was largely retained in the adults. Although a strong correlation was found between the adult whole-body Se concentration and the Se concentration in the exuvia after emergence, only a minor loss of Se occurred in the shed exuvia compared with larvae and adult whole-body concentrations. X-ray absorption spectroscopy analysis showed that organic selenides and diselenides, modeled as Se-met and selenocystine, respectively, were the dominant forms of Se in both the larval and adult insect stages. The proportion and concentration of organic selenides (selenomethionine) increased in larvae and adults exposed to Se-met and selenite compared with larvae exposed to selenate, whereas the concentration of diselenides (selenocystine) remained relatively constant for all treatments.

Distribution and metabolism of selenohomolanthionine labeled with a stable isotope.

The distribution and metabolism of selenohomolanthionine (4,4'-selenobis[2-aminobutanoic acid], SeHLan), a newly identified selenoamino acid in selenized Japanese pungent radish, were evaluated by administering 77Se-labeled SeHLan at a dose of 25 µg/kg body weight in rats. Exogenous 77Se of SeHLan was preferably distributed to the kidneys and remained in the intact form for up to 6 h after dosing. The accumulation in the kidneys is one of the specific characteristics of SeHLan, differing from other selenoamino acids, such as selenomethionine and Se-methylselenocysteine, which preferably accumulate in the pancreas. The intact form of SeHLan was detected in the serum and kidney supernatant but not in the urine, suggesting that the amount of exogenous Se that was distributed to the kidneys was within metabolic capacity. Indeed, the exogenous Se was converted into two urinary metabolites, Se-methylseleno-N-acetyl-galactosamine and trimethylselenonium. Exogenous Se was also detected in several selenoproteins, including selenoprotein P and extracellular glutathione peroxidase. SeHLan is expected to be a potential supplemental source of Se because its distribution differs from that of selenomethionine and Se-methylselenocysteine.

Biomimetic chromatographic analysis of selenium species: application for the estimation of their pharmacokinetic properties.

The retention behavior of selenites, selenates, seleno-DL-methionine, selenocystine, selenocystamine, selenourea, dimethyl selenide, and dimethyl diselenide was investigated by means of biomimetic liquid chromatography. For this purpose, two immobilized artificial membrane (IAM) columns, namely, IAM.PC.DD2 and IAM.PC.MG, and two immobilized plasma protein columns, human serum albumin (HSA) and alpha(1)-acid glycoprotein (AGP) columns, were employed using different mobile phase conditions in respect to pH and buffer composition. In general, satisfactory interrelations between retention factors obtained with the two IAM stationary phases and HSA/AGP columns were obtained. Large differences were observed between biomimetic retention factors and octanol-water logD values, since the latter fail to describe electrostatic interactions. In contrast, despite the column diversity, the net retention outcome on all four biomimetic columns was quite similar, especially in the presence of phosphate-buffered saline, which by its effective shielding alleviates the differences between the stationary phases. Of the two IAM columns, IAM.PC.DD2 showed better performance when compared with HSA and AGP columns as well as to octanol-water partitioning. Biomimetic chromatographic indices were further used to estimate the percentage of human oral absorption and plasma protein binding of the eight selenium species investigated, according to equations previously reported in the literature. The estimated values of human oral absorption imply moderate absorption only for dimethyl diselenide, which also may exhibit considerable plasma protein binding. Moderate affinity for plasma proteins should also be expected for dimethyl selenide and selenocystamine.

Selenium metabolism in rats with long-term ingestion of Se-methylselenocysteine using enriched stable isotopes.

Se-methylselenocysteine (MeSeCys) is not only a selenium (Se) supplement but also a more promising precursor of an anti-tumor drug containing Se than selenomethionine, which is currently used as Se supplement. In this study, the metabolism of MeSeCys labeled with an Se isotope, 82Se, in rats depleted of endogenous natural abundance isotopes with another Se isotope, 78Se, was traced for 21 days when MeSeCys was continuously and perorally ingested at a supplemental dose. The tracer experiment was performed with our improved method that utilized an inductively coupled plasma-deuterium reaction-mass spectrometer. The substitution of endogenous Se with a single isotope, 78Se, facilitated the detection of exogenous labeled Se. Exogenous Se in the form of MeSeCys preferably accumulated and/or assimilated in the liver, kidneys and testes with long-term ingestion of MeSeCys and was utilized for the synthesis of selenoproteins, i.e., extracellular and cellular glutathione peroxidases and selenoprotein P. Meanwhile, intact MeSeCys was not excreted into urine although trimethylselenonium was detected in addition to selenosugar. The results suggest that MeSeCys was transformed into selenide via methylselenol by beta-lyase. Consequently, it is surmised that MeSeCys is a precursor of methylselenol under long-term ingestion.

[Estimation of organic and inorganic selenium bioavailability in experiments with growing rats].

There was conducted a comparative study of organic and inorganic selenium forms bioavailability and of an influence of said trace elements safety on growth parameters and glutathione peroxidase activity in male wister rats. The results obtained confirmed an advance of organic selenium use (as an enzymatic yeast hydrolysate) on comparison to it's inorganic form (sodium selenite).

Low toxicity of diphenyl diselenide in rabbits: a long-term study.

Selenium compounds, like diphenyl diselenide (Ph(2)Se(2)), possess glutathione peroxidase (GSHPx)-like activities and other antioxidant properties. The aim of this study was to evaluate the effects of a long-term oral supplementation with Ph(2)Se(2) on various toxicological parameters in rabbits. Adult New Zealand male rabbits were divided into four groups: Group I served as control; Groups II, III and IV received 0.3, 3.0 and 30 p.p.m. of Ph(2)Se(2) pulverized in the chow for 8 months. A number of toxicological parameters were examined in liver, kidney, cerebral cortex and hippocampus, such as delta-aminolaevulinic acid dehydratase (delta-ALA-D), catalase (CAT), GSHPx activities, non-protein thiol (-SH), lipid peroxidation and ascorbic acid levels. The results indicated that supplementation 30 p.p.m. Ph(2)Se(2 )significantly increased delta-ALA-D activity in liver and in cerebral cortex. Non-protein -SH levels were significantly increased in liver but not in kidney, cerebral cortex and hippocampus of rabbits. Ascorbic acid content was significantly lower in the liver and cerebral cortex after supplementation with 30 p.p.m. Ph(2)Se(2). Conversely, no alterations in GSHPx and CAT activities, nor in thiobarbituric acid reactive substances levels were observed in rabbit tissues. These results indicate that oral supplementation with Ph(2)Se(2) is relatively secure in rabbits after 8 months of exposure. The findings encourage further experiments on the potential therapeutic effects of such compound.

Biological availability of selenosugars in rats.

The biological availability and metabolism of two selenosugars orally administered to rats were investigated. Two other selenium species, selenite and trimethylselenonium ion (TMSe) were included in the study as positive and negative controls, respectively. Male Wistar strain rats (three per group) at 8 weeks of age were exposed to sodium selenite, TMSe, selenosugar 1 (methyl-2-acetamido-2-deoxy-1-seleno-beta-D-galactopyranoside) or selenosugar 2 (methyl-2-acetamido-2-deoxy-1-seleno-beta-D-glucopyranoside) through drinking water for 48 h. Total selenium concentrations (ICPMS) and selenium species concentrations (HPLC/ICPMS) were determined in urine samples collected in two 24h periods during the exposure, and total selenium concentrations in liver, kidney, small intestine and blood were determined at the end of the experiment. The major species found in background urine were selenosugar 1 (major metabolite) and TMSe (minor metabolite). Rats exposed to selenite excreted large quantities of selenosugars and TMSe consistent with efficient uptake and biotransformation of selenite, whereas TMSe-exposed rats excreted large quantities of TMSe, but there was no significant increase of other selenium metabolites, consistent with TMSe being taken up and excreted unchanged. Rats exposed to selenosugars, however, excreted significant quantities of TMSe suggesting that the sugars were at least partly biologically available and biotransformed. Rats exposed to selenite accumulated selenium in the liver, kidney, small intestine and blood, whereas no accumulation was observed for the other samples except for small increases in selenium concentrations of small intestine from the two selenosugar-exposed groups.

Metabolism of 76Se-methylselenocysteine compared with that of 77Se-selenomethionine and 82Se-selenite.

Se-Methylated selenoamino acids, Se-methylselenocysteine (MeSeCys) and selenomethionine (SeMet), are chemically inert storage forms of selenium in selenium-accumulators, and a nutritional and supplemental source. The metabolic pathway for MeSeCys was precisely traced by referring to those for SeMet and selenite by applying a new tracer method involving multiple homo-elemental stable isotopes. Male Wistar rats were depleted of endogenous natural abundance selenium with a single (80)Se-enriched isotope, and then (76)Se-MeSeCys, (77)Se-SeMet and (82)Se-selenite were orally administered simultaneously at 25 microg Se/kg body weight each. Organs and body fluids were obtained at 3, 6, 9 and 12 h, and 1 and 2 days later, and subjected to speciation analysis. The main characteristics of the metabolism were as follows; MeSeCys was incorporated into selenoprotein P slightly more than or at a comparable level to that of SeMet but less than that of selenite. MeSeCys and SeMet but not selenite was taken up by organs in their intact forms. MeSeCys and SeMet were delivered specifically to the pancreas and present in a form bound to an identical or similar protein. Trimethylselenonium (TMSe) was only produced from MeSeCys, i.e., not from SeMet or selenite, in the kidneys. Both selenosugars A and B of MeSeCys, SeMet and selenite origin were detected in the liver but only selenosugar B in the kidneys. These results suggest that MeSeCys can be a similar or better selenium source than SeMet, and supplies methylselenol much more efficiently in organs than SeMet and selenite. TMSe was produced much efficiently from MeSeCys than from SeMet and selenite, suggesting a role of methylselenol through the beta-lyase reaction in the metabolism of Se-methylated selenoamino acids.

Small-molecule screening identifies the selanazal drug ebselen as a potent inhibitor of DMT1-mediated iron uptake.

HEK293T cells overexpressing divalent metal transporter-1 (DMT1) were established to screen for small-molecule inhibitors of iron uptake. Using a fluorescence-based assay, we tested 2000 known bioactive compounds to find 3 small molecules that potently block ferrous iron uptake. One of the inhibitors, ebselen, is a seleno compound used in clinical trials as a protective agent against ischemic stroke. Ebselen inhibited Fe(II) uptake (IC(50) of approximately 0.22 microM), but did not influence Fe(III) transport or DMT1-mediated manganese uptake. An unrelated antioxidant, pyrrolidine dithiobarbamate (PDTC), also inhibited DMT1 activity (IC(50) of approximately 1.54 microM). Both ebselen and PDTC increased cellular levels of reduced glutathione. These observations indicate that Fe(II) transport by DMT1 can be modulated by cellular redox status and suggest that ebselen may act therapeutically to limit iron-catalyzed damage due to transport inhibition.

Availability and metabolism of 77Se-methylseleninic acid compared simultaneously with those of three related selenocompounds.

Nutritional selenocompounds are considered to be transformed into the common intermediate selenide for utilization as selenoenzymes and/or for excretion as selenosugar and trimethylselenonium (TMSe). Therefore, selenocompounds can only be traced with a labeled selenium atom. Methylseleninic (MSA(IV)) has been proposed to be a third nutritional selenium source, the other two being inorganic selenocompounds and organic selenoamino acids, and to be a proximate selenochemical for producing the assumed biologically active form methylselenol. Here we applied a new tracer method to compare the availability and metabolism of MSA(IV) with those of three related selenocompounds under exactly identical host and tracing conditions. (82)Se-Selenite, (78)Se-selenate, (77)Se-MSA(IV) and (76)Se-methylselenonic acids (MSA(VI)) were simultaneously administered orally, each at the dose of 25 microg Se/kg body weight, to rats that had been depleted of endogenous natural abundance selenium with a single stable isotope ((80)Se). Time-related changes in the concentrations and/or distributions of the four labeled isotopes in the serum, liver, kidney, pancreas, lung and urine were determined simultaneously by inductively coupled argon plasma mass spectrometry (ICP MS) and/or HPLC-ICP MS. The availability with different isotope ratios was in the decreasing order of selenate>selenite=MSA(IV)>MSA(VI). Although selenate and MSA(VI) were distributed in organs and urine partly in their intact forms, MSA(IV) and selenite were not detected in the intact forms at all. MSA(IV) and MSA(VI) but not selenite or selenate produced TMSe in organs other than the liver, suggesting the transformation of MSA(IV) into methylselenol, and then either into selenide for the synthesis of selenoproteins and selenosugar or directly into TMSe. Thus, selenosugar and TMSe were produced widely in the organs. However, TMSe was not detected in the liver. The organ- and selenium source-specific production of TMSe was discussed as to the differences in selenium sources, and demethylation and methylation activity.

Distribution and reuse of 76Se-selenosugar in selenium-deficient rats.

Nutritional selenium compounds are transformed to the common intermediate selenide and then utilized for selenoprotein synthesis or excreted in urine mostly as 1beta-methylseleno-N-acetyl-Dd-galactosamine (selenosugar). Since the biological significance of selenosugar formation is unknown, we investigated their role in the formation of selenoenzymes in selenium deficiency. Rats were depleted of endogenous natural abundance selenium with a single stable isotope ((82)Se) and then made Se-deficient. (76)Se-Selenosugar was administered intravenously to the rats and their urine, serum, liver, kidneys and testes were subjected to speciation analysis with HPLC inductively coupled argon plasma mass spectrometry. Most (76)Se was recovered in its intact form (approximately 80% of dose) in urine within 1 h. Speciation analysis revealed that residual endogenous natural abundance selenium estimated by (77)Se and (78)Se was negligible and distinct distributions of the labeled (76)Se were detected in the body fluids and organs without interference from the endogenous natural abundance stable isotope. Namely, intact (76)Se-selenosugar was distributed to organs after the injection, and (76)Se was used for selenoprotein synthesis. Oxidation to methylseleninic acid and/or hydrolysis of the selenoacetal group to methylselenol were proposed to the transformation of selenosugar for the reuse. Effective use of an enriched stable isotope as an absolute label in hosts depleted of natural abundance isotopes was discussed for application in tracer experiments.

Metabolic transformation of methylseleninic acid through key selenium intermediate selenide.

Methylseleninic acid (MSA(IV)) [CH(3)Se(O)OH] is readily reducible to methylselenol [CH(3)SeH], the assumed lyase metabolite and the proposed biologically active form of methylated selenoamino acids. At the same time, MSA(IV) is an oxidation product of the major urinary metabolite selenosugar. (77)Se-Enriched MSA(IV) was injected intravenously into rats (25 microg Se/kg body weight), and urine, blood and liver were obtained at five time points after the injection. Time-related changes in the concentration of (77)Se were determined together with speciation analysis of the labeled metabolites. (77)Se was mostly moved into red blood cells (RBCs) within 10 min, and then redistributed into organs within 30 min. Excessive (77)Se taken up by the liver was first detected as selenosugar A and then as B, suggesting that MSA(IV) was transformed to selenide, and then to selenosugar A followed by methylation to selenosugar B (urinary metabolite). (77)Se was incorporated also into selenoproteins (most efficiently to plasma selenoprotein P that is synthesized in liver), suggesting that MSA(IV) is utilized for the synthesis of selenosugar (for excretion) and selenoproteins (for utilization) through selenide. In vitro experiments with simultaneous incubation of (77)Se-MSA(IV) and (82)Se-selenite in a RBC suspension revealed the precise difference in the metabolism between MSA(IV) and selenite in RBCs. (77)Se excreted into the urine was mostly detected as selenosugar but with a distinct amount of trimethylselenonium, suggesting that selenosugar and trimethylselenonium are produced depending on the capacity to transform methylselenol to selenide. MSA(IV) was suggested to be reduced to methylselenol (allowing the production of a proposed active form of selenium), and then transformed (demethylated) to selenide for utilization and excretion.

Effect of organic selenium in quail diet on its accumulation in tissues and transfer to the progeny.

1. The aim of the present study was to investigate the effects on the eggs and hatchlings (up to 2 weeks post-hatch) of feeding a relatively large amount of so-called organic selenium to breeder quail. 2. Two groups of quail (3 families in each group consisting of 4 females and 1 male) were formed at the beginning of their reproductive period. The quail were fed on a commercial maize-based diet containing 0.096 mg/kg feed-derived selenium (Se), supplemented with 0.2 mg/kg selenite (control group) or 0.5 mg/kg organic selenium in the form of Sel-Plex (Alltech Ltd, USA) for 6 months. Eggs were collected at 6 months of age and Se in the egg yolk, egg white and shell was analysed. Five quail at 1, 7 and 14 d post-hatch were killed to provide samples of liver, brain, breast and leg muscles for Se analysis. After egg collection for analysis and incubation, adult quail were killed and liver, kidney, lung, brain, breast and leg muscles were collected for Se analyses. 3. Inclusion of high doses (0.5 mg/kg) of organic Se in the quail diet was associated with a significant increase in Se concentration in all tissues studied of adult quail as well as in egg yolk, egg albumin and eggshell. 4. Increased Se concentration in the quail egg was associated with increased Se concentration in the liver, breast and leg muscles and brain of newly hatched quail. This difference was shown to be significant for 2 weeks post-hatch. Therefore, it has been suggested that the maternal effect of dietary selenium can be seen beyond the hatching time and more emphasis should be given to this effect in future. 5. It was shown that it is possible to produce Se-enriched quail meat and eggs by adding organic selenium to the diet.