Selenium (Se), an essential trace element for human health, mainly exerts its biological function via selenoproteins. Among the 25 selenoproteins identified in human, selenoprotein P (SelP) is the only one that contains multiple selenocysteines (Sec) in the sequence, and has been suggested to function as a Se transporter. Upon feeding a selenium-deficient diet, mice lacking SelP develop severe neurological dysfunction and exhibit widespread brainstem neurodegeneration, indicating an important role of SelP in normal brain function. To further elucidate the function of SelP in the brain, SelP was screened by the yeast two-hybrid system from a human fetal brain cDNA library for interactive proteins. Our results demonstrated that SelP interacts with tubulin, alpha 1a (TUBA1A). The interaction between SelP and tubulin was verified by fluorescence resonance energy transfer (FRET) and co-immunoprecipitation (co-IP) assays. We further found that SelP interacts with the C-terminus of tubulin by its His-rich domain, as demonstrated by FRET and Isothermal Titration Calorimetry (ITC) assays. The implications of the interaction between SelP and tubulin in the brain and in Alzheimer’s disease are discussed.

Selenium, an essential trace element for human health, mainly exerts its biological function through selenoproteins. Selenoprotein M (SelM) is one of the highly expressed selenoproteins in the brain, but its biological effect and molecular mechanism remain unclear. Thus, the interactive protein of SelM was investigated in this paper to guide further study. In order to avoid protein translational stop, the selenocysteine-encoding UGA inside the open reading frame of SelM was site-directly changed to the cysteine-encoding UGC to generate the SelM' mutant. Meanwhile, its N terminal transmembrane signal peptide was also cut off. This truncated SelM' was used to screen a human fetal brain cDNA library by the yeast two-hybrid system. A new interactive protein of SelM' was found to be galectin-1 (Gal-1). This protein-protein interaction was further verified by the results of fluorescence resonance energy transfer techniques, glutathione S-transferase pull-down and co-immunoprecipitation assays. As Gal-1 plays important roles in preventing neurodegeneration and promoting neuroprotection in the brain, the interaction between SelM' and Gal-1 displays a new direction for studying the biological function of SelM in the human brain.

Apoptosis, as a programmed cell death process, is essential for the maintenance of tissue function in organisms. Alteration of this process is linked to many diseases. Over-expression of clusterin (Clu) can antagonize apoptosis in various cells. Selenium (Se) is an essential trace element for human health. Its biological function is also associated with cell apoptosis. To explore the function of Clu and the impact of Se in the process of apoptosis, several short-hairpin RNAs (shRNA) were designed for the construction of two sets of recombinant plasmids: one set for plasmid-transfection of mouse neuroblastoma N2a cells (N2a cells); and the other set for lentiviral infection of human neuroblastoma SH-SY5Y cells (SH-SY5Y cells). These shRNAs specifically and efficiently interfered with the intracellular expression of Clu at both the mRNA and protein levels. The Clu-knockdown cells showed apoptosis-related features, including down-regulation of antioxidative capacity and the Bcl-2/Bax ratio and up-regulation of caspase-8 activity. Se-methylselenocysteine (MSC) at an optimum concentration of 1 μM could reverse the alteration in antioxidative capacity, Bcl2/Bax ratio and caspase-8 activity caused by Clu-knockdown, thus inhibiting apoptosis and maintaining cell viability. The results hereby imply the potentiality of Clu and Se in neuroprotection.

Background/Objectives: As a hyperaccumulator of selenium (Se), Cardamine violifolia (Cv) and its peptide extract could ameliorate the negative effects of a high-fat diet (HFD). However, the effects of the coaccumulation of cadmium (Cd) in Se-enriched Cv (Cv2) and the potential confounding effect on the roles of enriched Se remain unknown. We aimed to investigate whether Cv2 could alleviate HFD-induced lipid disorder and liver damage. Methods: Three groups of 31-week-old female mice were fed for 41 weeks (n = 10–12) with a control Cv-supplemented diet (Cv1D, 0.15 mg Se/kg, 30 µg Cd/kg, and 10% fat calories), a control Cv-supplemented HFD (Cv1HFD, 45% fat calories), and a Cv2-supplemented HFD (Cv2HFD, 1.5 mg Se/kg, 0.29 mg Cd/kg, and 45% fat calories). Liver and serum were collected to determine the element concentrations, markers of liver injury and lipid disorder, and mRNA and/or protein expression of lipid metabolism factors, heavy metal detoxification factors, and selenoproteins. Results: Both Cv1HFD and Cv2HFD induced obesity, and Cv2HFD downregulated Selenoi and upregulated Dio3 compared with Cv1D. When comparing Cv2HFD against Cv1HFD, Cv2 increased the liver Se and Cd, the protein abundance of Selenoh, and the mRNA abundance of 10 selenoproteins; reduced the serum TG, TC, and AST; reduced the liver TG, lipid droplets, malondialdehyde, and mRNA abundance of Mtf1 and Mt2; and differentially regulated the mRNA levels of lipid metabolism factors. Conclusions: Cv2 alleviated HFD-induced lipid dysregulation and liver damage, which was probably associated with its unique Se speciation. However, further research is needed to explore the interaction of plant-coenriched Se and Cd and its effects on health.

Background: Iodine deficiency during pregnancy remains a leading cause of preventable neurodevelopmental impairment worldwide, yet quantitative characterization of the dose–response relationship between maternal iodine status and child neurodevelopment is lacking. Methods: A systematic search of PubMed, Embase, the Cochrane Library, and Web of Science was conducted for prospective cohort studies published up to February 2026 reporting associations between maternal iodine status and child neurodevelopmental outcomes across at least three exposure categories. All continuous effect estimates were converted to standardized mean differences (Hedges’ g) to permit pooling across heterogeneous assessment instruments, and meta-analyses were stratified by neurodevelopmental domain (cognitive, language, motor, behavior, academic). A two-stage dose–response meta-analysis was used to characterize non-linearity. Risk of bias was evaluated using the Newcastle–Ottawa Scale (NOS). Results: Ten prospective cohort publications corresponding to eight independent cohorts were included. After converting all continuous effect estimates to standardized mean differences (Hedges’ g) and consolidating the three overlapping MoBa publications into a single cohort, the pooled analysis revealed a significant negative association between suboptimal maternal iodine status and child neurodevelopmental performance (Hedges’ g = −0.13, 95% CI: −0.20 to −0.06, p < 0.001; I² = 95.2%). Domain-stratified analysis identified cognitive outcomes as most consistently affected (g = −0.22, 95% CI: −0.30 to −0.14; I² = 37.5%), followed by motor (g = −0.17; I² = 0%) and language outcomes (g = −0.16; I² = 92.5%), with between-domain heterogeneity explaining 38.6% of the total variance (p = 0.012). Binary outcome analysis confirmed increased odds of adverse neurodevelopmental outcomes (OR = 1.19, 95% CI: 1.03 to 1.39, p = 0.026). Subgroup analysis by iodine exposure indicator showed directionally consistent negative effects across dietary intake (g = −0.11), UIC (g = −0.11) and UI/Cr (g = −0.28), with no significant between-subgroup difference (p = 0.237). Exploratory dose–response modeling on the Hedges’ g scale suggested that neurodevelopmental performance in the fitted curves approached its maximum within a mid-range of dietary iodine intake (approximately 150–300 µg/d); however, the quadratic non-linearity terms did not reach statistical significance after cohort consolidation (p = 0.612 for dietary intake; p = 0.436 for UI/Cr), and these findings should therefore be interpreted as exploratory. Conclusions: Suboptimal maternal iodine status during pregnancy was associated with modest decrements in child neurodevelopmental performance, with exploratory dose–response analyses suggesting that the fitted curves approached their maximum within a mid-range of dietary iodine intake. Although statistical evidence for quadratic non-linearity was attenuated after consolidating overlapping cohorts, the directional pattern across indicators remained consistent with an inverted U-shaped relationship, supporting maintenance of adequate but not excessive iodine nutrition during pregnancy.