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Selenium (Se) is an important microelement with numerous positive effects on human health and diseases. It is important to specify that the status and consumption of Se are for a specific community as the levels of Se are extremely unpredictable between different populations and regions. Our existing paper was based on the impacts of Se on human health and disease along with data on the Se levels in Middle Eastern countries. Overall, the findings of this comprehensive review show that the consumption and levels of Se are inadequate in Middle Eastern nations. Such findings, together with the growing awareness of the importance of Se to general health, require further work primarily on creating an acceptable range of blood Se concentration or other measures to determine optimal Se consumption and, consequently, to guarantee adequate Se supplementation in populations at high risk of low Se intake.

Selenium is an essential microelement required for a number of biological functions. Selenium—and more specifically the amino acid selenocysteine—is present in at least 25 human selenoproteins involved in a wide variety of essential biological functions, ranging from the regulation of reactive oxygen species (ROS) concentration to the biosynthesis of hormones. These processes also play a central role in preventing and modulating the clinical outcome of several diseases, including cancer, diabetes, Alzheimer’s disease, mental disorders, cardiovascular disorders, fertility impairments, inflammation, and infections (including SARS-CoV-2). Over the past years, a number of studies focusing on the relationship between selenium and such pathologies have been reported. Generally, an adequate selenium nutritional state—and in some cases selenium supplementation—have been related to improved prognostic outcome and reduced risk of developing several diseases. On the other hand, supra-nutritional levels might have adverse effects. The results of recent studies focusing on these topics are summarized and discussed in this review, with particular emphasis on advances achieved in the last decade.

Mammalian cells possess a multifaceted antioxidant enzyme system, which includes superoxide dismutases, catalase, the peroxiredoxin/thioredoxin and the glutathione peroxidase systems. The dichotomous role of reactive oxygen species and antioxidant enzymes in tumorigenesis and cancer progression complicates the use of small molecule antioxidants, pro-oxidants, and targeting of antioxidant enzymes as therapeutic approaches for cancer treatment. It also highlights the need for additional studies to investigate the role and regulation of these antioxidant enzymes in cancer. The focus of this review is on glutathione peroxidase 3 (GPx3), a selenoprotein, and the only extracellular GPx of a family of oxidoreductases that catalyze the detoxification of hydro- and soluble lipid hydroperoxides by reduced glutathione. In addition to summarizing the biochemical function, regulation, and disease associations of GPx3, we specifically discuss the role and regulation of systemic and tumor cell expressed GPx3 in cancer. From this it is evident that GPx3 has a dichotomous role in different tumor types, acting as both a tumor suppressor and pro-survival protein. Further studies are needed to examine how loss or gain of GPx3 specifically affects oxidant scavenging and redox signaling in the extracellular tumor microenvironment, and how GPx3 might be targeted for therapeutic intervention.

Oxidative stress and antioxidants play an important role in obesity etiopathology. Genetic variants, including single nucleotide polymorphisms (SNPs) of the antioxidant-related genes, may impact disease risk in several populations. This preliminary study aimed to explore the association of 12 SNPs related to superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione-S-transferase (GST), and nitric oxide synthase (NOS) genes with obesity susceptibility in a Saudi population. A total of 384 unrelated participants, including 154 (40.1%) obese individuals, were enrolled. TaqMan OpenArray Genotyping assays were used. Six SNPs were significantly more prevalent in obese cohorts: (1) GSTM1 rs1056806*C/T; (2) SOD1 rs2234694*A; (3) SOD2 rs4880*G; (4) SOD3 rs2536512*A; (5) GPX1 rs1800668*A; (6) NOS3 rs1799983*G. Four SNPs were associated with higher obesity risk under heterozygote and dominant models for GSTM1 rs1056806 (C/T), homozygote model for SOD2 rs4880 (A/G), and homozygote and recessive models for GPX1 rs1800668 (A/G). In contrast, SOD3 rs2536512 (A/G) were less likely to be obese under heterozygote and dominant models. The CGAG, CAAA, TGGG, and CGAG combined genotypes showed a higher risk of obesity. In conclusion, the present results suggest that oxidative-stress-related genetic determinants could significantly associate with obesity risk in the study population.

Selenium is an essential trace element in living organisms, and is present in selenoenzymes with antioxidant activity, like glutathione peroxidase (GPx) and thioredoxin reductase (TrxR). The search for small selenium-containing molecules that mimic selenoenzymes is a strong field of research in organic and medicinal chemistry. In this review, we review the synthesis and bioassays of new and known organoselenium compounds with antioxidant activity, covering the last five years. A detailed description of the synthetic procedures and the performed in vitro and in vivo bioassays is presented, highlighting the most active compounds in each series.

Epilepsy is one of the most common symptoms of many neurological disorders. The typical excessive, synchronous and aberrant firing of neurons originating from different cerebral areas cause spontaneous recurrent epileptic seizures. Prolonged epilepsy can lead to neuronal damage and cell death. The mechanisms underlying epileptic pathogenesis and neuronal death remain unclear. Ferroptosis is a newly defined form of regulated cell death that is characterized by the overload of intracellular iron ions, leading to the accumulation of lethal lipid-based reactive oxygen species (ROS). To date, studies have mainly focused on its role in tumors and various neurological disorders, including epilepsy. Current research shows that inhibition of ferroptosis is likely to be an effective therapeutic approach for epilepsy. In this review, we outline the pathogenesis of ferroptosis, regulatory mechanisms of ferroptosis, related regulatory molecules, and their effects on epilepsy, providing a new direction for discovering new therapeutic targets in epilepsy.

Background Heavy metal contamination of agricultural soils, particularly from mining activities, poses serious risks to food safety and public health. At the Kilembe mining site in Uganda, elevated levels of heavy metals have been reported in soils where maize ( Zea mays L.) is widely cultivated. This study investigated the biochemical stress response and culturable rhizobacteria in maize grown in heavy metal-contaminated soils to understand their mechanisms of adaptation. Methods Maize seeds were planted on farms obtained at varying distances from the Kilembe mining site (0, 1, 3, and 5 km) and a control site in Bushenyi (95 km), serving as groups 1-5, respectively. Oxidative stress and hormone profiles of germinated leaves and rhizospheric bacterial composition were determined using standard analytical and microbiological methods. Results Maize plants near the site had higher malondialdehyde levels and lower antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase). Brassinosteroid levels increased at 0 km, whereas auxin and abscisic acid levels decreased significantly across all distances compared to the control. Bacillus sp. was dominant at 39.71%, and Acinetobacter sp. was the least abundant (1.47%). The 3 km site had the highest bacterial load, while the 0 km site had high counts at lower dilutions. Plant growth-promoting rhizobacteria ( Bacillus sp. , Staphylococcus sp. , and Klebsiella sp. ) were highly distributed across sites. Conclusion The study showed that the presence of plant growth-promoting rhizobacteria, such as Bacillus spp., which were dominant, provided insight into the role of these rhizospheric organisms in conferring tolerance and is a probable adaptive mechanism that ensures the survival of maize plants grown around mining-associated farmlands, as seen in Kilembe, Uganda.

AbstractSelenium is an essential immunonutrient which holds the human’s metabolic activity with its chemical bonds. The organic forms of selenium naturally present in human body are selenocysteine and selenoproteins. These forms have a unique way of synthesis and translational coding. Selenoproteins act as antioxidant warriors for thyroid regulation, male-fertility enhancement, and anti-inflammatory actions. They also participate indirectly in the mechanism of wound healing as oxidative stress reducers. Glutathione peroxidase (GPX) is the major selenoprotein present in the human body, which assists in the control of excessive production of free radical at the site of inflammation. Other than GPX, other selenoproteins include selenoprotein-S that regulates the inflammatory cytokines and selenoprotein-P that serves as an inducer of homeostasis. Previously, reports were mainly focused on the cellular and molecular mechanism of wound healing with reference to various animal models and cell lines. In this review, the role of selenium and its possible routes in translational decoding of selenocysteine, synthesis of selenoproteins, systemic action of selenoproteins and their indirect assimilation in the process of wound healing are explained in detail. Some of the selenium containing compounds which can acts as cancer preventive and therapeutics are also discussed. These compounds directly or indirectly exhibit antioxidant properties which can sustain the intracellular redox status and these activities protect the healthy cells from reactive oxygen species induced oxidative damage. Although the review covers the importance of selenium/selenoproteins in wound healing process, still some unresolved mystery persists which may be resolved in near future.Graphic abstract

Herein, we describe a simple and efficient route to access aniline-derived diselenides and evaluate their antioxidant/GPx-mimetic properties. The diselenides were obtained in good yields via ipso-substitution/reduction from the readily available 2-nitroaromatic halides (Cl, Br, I). These diselenides present GPx-mimetic properties, showing better antioxidant activity than the standard GPx-mimetic compounds, ebselen and diphenyl diselenide. DFT analysis demonstrated that the electronic properties of the substituents determine the charge delocalization and the partial charge on selenium, which correlate with the catalytic performances. The amino group concurs in the stabilization of the selenolate intermediate through a hydrogen bond with the selenium.

Diabetes mellitus (DM) is a common global metabolic disease. Oxidative stress from reactive oxygen species (ROS) contributes to its development and leads to complications like heart disease, kidney failure, and stroke. Chronic inflammation in diabetes is associated with insulin resistance and elevated glucose levels, as indicated by increased markers of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-α). This study investigates the activity and concentration of antioxidant enzymes (SOD, GPX1, CAT) and inflammatory markers (IL-6, CRP, TNF-α) in patients with type 1 and type 2 diabetes compared to healthy controls. The study included 73 patients—33 with type 1 diabetes (18 men, 15 women) and 40 with type 2 diabetes (20 men, 20 women)—and 41 healthy controls (23 men, 18 women). Antioxidant enzymes and inflammatory markers were measured using enzyme-linked immunosorbent assay (ELISA), and HbA1c levels were assessed. Program R and Statistica 13 were used to analyze the results. Group membership had a significant impact on SOD and CAT activity ( p  < 0.0001) and GPX1 ( p  < 0.001). BMI correlated with CAT concentration ( p  < 0.0001). SOD activity was affected by comorbidities, such as arthritis and urinary tract issues ( p  = 0.03). Diabetes markedly altered inflammatory markers, particularly CRP and TNF-α ( p  < 0.0001), and higher IL-6 levels were found in patients using medications other than metformin ( p  = 0.01). Type 1 and 2 diabetes significantly affect antioxidant enzyme activity and concentration. High SOD and GPX activity suggests chronic oxidative stress, while increased BMI is linked to lower enzyme levels. Additionally, TNF-α levels rise with diabetes duration, which may serve as a biomarker for disease progression and complications, potentially helping to predict diabetic complications and insulin resistance.