Single-cell elemental analysis using inductively coupled plasma-mass spectrometry (ICP-MS) is a rapidly developing field within metallomics, offering the ability to quantify elemental contents in individual cells. Pioneering works have developed diverse sample introduction systems coupled with ICP-MS, enabling high-throughput, precise, and accurate elemental analysis at the single-cell level. These advancements have facilitated applications across medicine and biology, providing insights into elemental metabolism and toxicity. Two prominent approaches have emerged: fast time-resolved analysis of cell suspensions, applicable to a broad range of cell types (bacterial, fungal, plant, and mammalian cells), and laser ablation (LA) for generating aerosols from individual cells. LA is particularly well suited for adherent cultured cells and allows for selective analysis based on cell morphology and size. These complementary techniques provide powerful tools for elucidating the complex interplay between elements and biological systems.

This review highlights the unique chemistry of π-bond compounds consisting of both selenium and other heavier main-group element, which exhibit intriguing reactivity and potential applications in catalysis, materials science, and bioinorganic chemistry. While selenium shares similarities with sulfur, its larger atomic size and greater polarizability give Se-containing double bonds distinctive characteristics that often result in higher reactivity. This review will focus on recent advancements of compounds that contain a π-bond containing selenium and other heavier main-group elements as well as unique π-conjugated systems, rather than on well-established compounds such selenoketones and selenoamides.

Selenium (Se) is one of the essential trace elements in the body. Se is present in proteins in the form of selenocysteine (Sec), in which the sulfur of cysteine (Cys) is replaced by Se. These proteins are referred to as selenoproteins. There are 25 selenoproteins in the human genome, and they play important roles in various physiological functions, including as an antioxidant and in the synthesis of thyroid hormones. Sec is inserted into selenoproteins using the Sec insertion sequence (SECIS), which is located in the 3′ untranslated region. We have identified an antisense long noncoding RNA, CCDC152, which binds mRNA of selenoprotein P (SELENOP), one of the plasma selenoproteins. CCDC152 inhibits the binding of SECIS binding protein 2 (SBP2), which is a key protein for selenoprotein translation, to SECIS by direct interaction with SELENOP mRNA. Inhibiting the formation of the SBP2 and SECIS complex by CCDC152 reduces the binding of ribosomes to SELENOP mRNA and suppresses the translation step of SELENOP. As a result, CCDC152 causes a decrease in SELENOP protein levels independent of SELENOP mRNA levels. No impact was observed on the protein and mRNA expression levels of other selenoproteins. This review describes the mechanism of SELENOP protein suppression by CCDC152.

Selenoneine (SEN) is one of the major organic selenium (Se) species present in fish and was initially identified in the blood of bluefin tuna. SEN is a selenium analog of ergothioneine (EGT), which is well known as a radical scavenger, with SEN exhibiting greater radical scavenging capacity than EGT. SEN is expected to have beneficial health functions due to its radical scavenging capacity, and elucidation of its biochemical and physiological functions in vivo may reveal additionally unknown functions. Herein, we systematically review previous SEN studies and comprehensively discuss SEN concentrations observed in various organisms including humans. Moreover, we describe the chemical, biochemical and biological properties of SEN. The current limitations of the research on SEN are shown to indicate the future studies required on understanding SEN.

It has been demonstrated that selenium (Se) and arsenic (As) interact in living organisms. The elucidation of the interaction mechanisms of these toxic metalloids is believed to be of great importance for understanding their effects on humans and animals. The seleno-bis(S-glutathionyl) arsinium ion [(GS)₂AsSe]⁻ has been identified as the major As metabolite present in the bile of rabbits and rats co-treated with selenite (iSeIV) and arsenite (iAsIII). Selenide (HSe⁻), a reduced form of iSeIV, is a crucial component in the As-Se-GSH conjugate formation. This study aimed to shed light on HSe⁻ released from erythrocytes and propose a novel mechanism for the uptake of As and Se into erythrocytes via Se-As complexes, in addition to a previously reported mechanism for [(GS)₂AsSe]⁻ formation. Erythrocytes from rats that had been fed As-depleted rodent chow for at least 7 weeks after weaning were used in the experiments. iAsIII and/or iSeIV were added to the erythrocyte suspension (final 10%) and incubated at 37℃ for up to 180 min or 10 min. The uptake of both elements into the erythrocytes was assessed by measuring the attenuation of each element in the supernatant. HSe⁻ was detected by measuring the syn-(methyl,-methyl) bimane produced from the reaction of monochlorobimane with HSe⁻. We observed that iAsIII was slightly taken up by erythrocytes. Furthermore, iSeIV was rapidly taken up by erythrocytes. Simultaneous exposure to both iSeIV and iAsIII increased Se and As uptake by erythrocytes. In addition, a temporal delay occurred in the uptake of both compounds. In conclusion, our study revealed that HSe⁻ release is more pronounced in selenite-treated erythrocytes and successfully proposed a novel mechanism for Se and As uptake.

Alzheimer’s disease (AD) is a chronic neurodegenerative disease and characterized by deposition of the amyloid-β (Aβ) peptide in the brain. Reactive oxygen species (ROS) are thought to be associated with the onset and/or progression of AD. Selenium-dependent glutathione peroxidases (GPxs) play a critical role in the brain in the extinction of ROS. The selenium concentration in the brain is kept higher than those of other organs/tissues even when dietary selenium is limited, which suggests the importance of this element in the brain. We previously reported that a dietary selenium deficiency caused the elevated deposition of Aβ plaques in the brain of Tg2576 transgenic mice, which is frequently used as a model of AD. In this study, we analyzed the GPx activity and lipid peroxidation of brain tissues after the feeding of a selenium-deficient diet to Tg2576 transgenic mice. We also investigated the effect of seleno-l-methionine (SeMet) supplementation on the Aβ plaque deposition in the brain. After feeding for 72 weeks, the selenium concentration and GPx activity in the brain of the selenium-deficient diet-fed mice was lower than those in the selenium-adequate diet-fed mice and SeMet-supplemented diet-fed mice. The deposition of Aβ plaques and lipid peroxidation in the SeMet-supplemented diet-fed mice brain appeared to decrease compared to those in the selenium-deficient diet-fed mice. Supplementation of SeMet might have a suppressive effect on the brain Aβ plaque deposition in theTg2576 transgenic mice.

In this study, Pteris vittata L. was cultivated via hydroponics by incorporating inorganic selenate (selenium concentration of 5 mg/kg or 50 mg/kg). The growth of the plants was not impaired when they were grown for three weeks with a selenium concentration of 5 ppm. Furthermore, selenium accumulated in the roots (389 mg/kg), stems (85 mg/kg), and leaves (166 mg/kg). Selenium accumulation and metabolism were observed in the roots. As the cultivation period increased, the proportion of Se(-II) in the above-ground parts increased. After three weeks, more than 80 % of the accumulated selenium had been metabolized into Se(-II) compounds. This phenomenon was particularly pronounced under conditions of low selenium concentration, with 5 mg/kg added. Moreover, an analysis conducted using a synchrotron radiation X-ray microbeam demonstrated that the metabolized selenium was present in specific tissues, including the root epidermis and central cylinder. Conversely, the extraction of selenium compounds from each tissue revealed the presence of Se-methyl selenocysteine and selenomethionine as soluble components among the selenium compounds produced by metabolism. It is hypothesized that these methylated selenium compounds accumulate in the plant body as low-toxicity chemical species. The extraction rate of selenium in the above-ground parts, such as stems and leaves, was relatively low, and it is postulated that it was metabolized into chemical species, such as selenium-containing proteins.

Trivalent phosphorus compounds are widely used for the reduction of biologically relevant sulfur- and selenium-containing species due to its strong redox potential, broad pH stability, and ability to minimize unwanted side reactions or competitive interactions with other thiol- or selenol-containing compounds. Selenocysteine selenenyl iodides (Sec–SeIs) have attracted increasing attention as key intermediates in the enzymatic functions of iodothyronine deiodinases. Investigating whether Sec–SeIs can serve as substrates for reduction by trivalent phosphorus compounds could provide valuable insights into the existence and behavior of Sec–SeI in proteins. However, to date, there have been no studies examining the reactivity between trivalent phosphorus compounds and selenenyl iodides. In this study, phosphine-mediated reduction of a selenocysteine selenenyl iodide to a selenocysteine selenol was developed using isolable model compounds stabilized by nanosized molecular cradle. The present study demonstrates that phosphines serve as excellent non-thiol reducing agents for selenenyl iodides, particularly in terms of their high reduction efficiency and lack of interfering thiol or selenol groups.