Biological Trace Element Research最新文献

Lead (Pb) is an environmental metal with toxic effects primarily targeting the central nervous system (CNS). Early-life exposure is linked to long-term behavioral and cognitive impairments. This study aims to evaluate the behavioral effects of Pb exposure during gestation and lactation and investigate the neuroprotective effect of the aqueous extract of Ononis natrix (AEON), a medicinal plant recognized for its antioxidant and anti-inflammatory properties, selected for its potential to counteract Pb-induced neurological damage. Pregnant mice were assigned to four groups: control, Pb-exposed (1 g/L in drinking water), and two groups receiving AEON (100 mg/kg and 500 mg/kg) by oral gavage alongside Pb from the first day of gestation until the end of lactation. Reproductive parameters were measured, such as fertility rate, gestation period, and offspring viability. Sensorimotor development was assessed using negative geotaxis, surface righting reflex, cliff avoidance, and suspension test. In adulthood, neurobehavioral functions such as anxiety-related behavior, locomotion, memory, depression-like behavior, and motor performance were assessed. We also measured markers of oxidative stress, notably catalase (CAT) and malondialdehyde (MDA), in the whole brain, hippocampus, and prefrontal cortex. Our results showed that Pb exposure led to a significant reduction in gestation period in pregnant females and considerably disrupted sensorimotor development in the offspring. In adulthood, Pb-exposed mice exhibited pronounced anxiety-like behavior and depressive-like symptoms, along with hyperactivity and impaired motor coordination. These dysfunctions were correlated with increased CAT activity and MDA levels in different brain regions. However, co-administration of AEON improved reproductive parameters, enhanced sensorimotor functions, normalized neurobehavioral performance in adulthood, and restored disrupted oxidative stress markers. These findings provide the first evidence of AEON's efficacy in mitigating developmental Pb-induced neurotoxicity, highlighting its potential as a novel neuroprotective agent and paving the way for future therapeutic strategies.

One of the atypical antipsychotic drugs is olanzapine (OLZ). Enhancing metabolic and detoxifying activities requires zinc (Zn). Thus, the objective of the current study was to determine if Zn supplementation might effectively reduce hepatic lesions induced by OLZ. The oxidative stress, inflammatory, and fibrotic indicators of the liver tissues were evaluated, and electrophoretic methods were used to analyze the native protein and isoenzyme patterns. Furthermore, the liver tissues were examined histopathologically. The dynamic motion of the extracted hemoglobin was also examined. In addition to the serious damage identified histopathologically, our results show that OLZ treatment altered the liver tissue's antioxidant and inflammatory indicators. The zinc sulfate (ZnSO₄) salt solution, given in a dose-dependent fashion, reduced these changes. Additionally, the ZnSO₄ salt solution enhanced the natural protein, lipid, and calcium moieties of the protein pattern that were electrophoretically detected and changed by OLZ. In terms of the isoenzyme patterns, the ZnSO₄ salt solution reduced the electrophoretic catalase (CAT), peroxidase (POX), and β-esterase (β-EST) isoenzyme patterns that were hampered by OLZ in a dose-dependent manner. Rats treated with OLZ in addition to ZnSO₄ showed an increase in heme-heme interactions, suggesting that zinc therapy stabilized oxyhemoglobin. This promotes a more effective folding process that improves the use of oxygen. A dosage of 100 mg/kg of ZnSO₄ was shown to normalize physiological, histological, and biochemical markers. It also improved interactions between heme molecules.

Selenium is one of the essential trace elements in humans and animals. It is incorporated in the redox-active selenocysteine (Sec), the 21st proteinogenic amino acid, which is found in a limited number of proteins/enzymes. The reactivity of the Sec residue in these proteins allows them to perform diverse functions such as reducing oxidative stress, maintaining redox homeostasis, and thyroid hormone metabolism. An important family of biomolecules is derived from pyridyl-based systems (e.g., 2-pyridinol, 2-nicotinamide). Several of these molecules are also responsible for a wide range of biological activities like redox reactions (e.g., NAD ⇌ NADH; NADP⁺ ⇌ NADPH). Due to their presence in natural systems, these scaffolds are widely used as pharmaceutical motifs in drug design and development. This is supported by the FDA database which reveals that over 60% of small molecule drugs contain N-heterocycles. Thus, a variety of selenium-incorporated pyridyl derivatives with reference to their antioxidant activity have been synthesized and studied. Antioxidant activity and cytotoxicity of these compounds have also been investigated in cellular models. The nature of the substituent at the C-3 position of the pyridine ring significantly influences the structure of the molecule as well as its antioxidant activity and cytotoxic properties. In this article, the work published by us and other groups on pyridyl selenium compounds is reviewed.

Selenium (Se) is a vital trace element for aquatic organisms. This study investigated the impact of dietary nano-selenium (Nano-Se) on growth, muscle nutritional quality, protein deposition, and selenoprotein gene expression in channel catfish (Ictalurus punctatus). A total of 12,000 catfish (85.74 ± 5.75 g) were randomly allocated into four groups (0, 1.5, 3.5, and 5.0 mg/kg Nano-Se) for 60 days. Optimal Nano-Se supplementation (3.5 mg/kg) significantly improved weight gain rate (WGR), specific growth rate (SGR), and feed conversion ratio (FCR) compared to the control. Additionally, Nano-Se enhanced muscle protein, lipid content, and free amino acid levels while modulating fatty acid composition, indicating improved flesh quality. Histological analysis revealed increased myofiber diameter, suggesting muscle growth promotion. Mechanistically, Nano-Se enhanced protein deposition by activating the PI3K/AKT/TOR pathway, stimulating protein synthesis, while simultaneously inhibiting proteolytic pathways (ubiquitin-proteasome and autophagy-lysosome systems). Furthermore, Nano-Se upregulated 17 key selenoprotein genes (Gpx1a, Gpx2, Gpx3, Gpx9, Selenoh, Selenoi, Selenok, Selenom, Selenop, Selenot1a, Selenot2, Selenow1, Selenow2, Selenoe, Selenoo1, Dio2, and Dio3b), implicating their roles in muscle development and oxidative stress regulation. The above results indicate that adding Nano-Se to feed can improve growth performance, flesh nutritional quality, muscle protein deposition, and selenoprotein genes expression of channel catfish.

Hexavalent chromium [Cr(VI)] is a hazardous heavy metal that poses serious toxicity to humans, in particular nephrotoxicity. The current work explored the potential nephroprotective impact of chrysin against Cr(VI)-induced nephrotoxicity. Chrysin significantly improved renal functions in the Cr(VI)-treated rats as indicated by decreased levels of urinary protein loss, serum creatinine and urea, and renal lipocalin-2, together with improved renal histopathological picture. Mechanistically, chrysin upregulated AMPK signaling as evidenced by a significant increase in phospho-AMPK and its downstream target SIRT1. These findings were accompanied by a significant decrease in the acetylated (active) forms of NF-κB and p53 the transcription factors that control inflammation and apoptosis. Additionally, chrysin inhibited NF-κB nuclear translocation, increased level of its cytosolic inhibitory protein IκB, and reduced levels of its responsive inflammatory molecules interleukin-6 and cyclooxygenase-2. Moreover, it modulated levels of p53-responsive apoptotic proteins BAX and Bcl2. Interestingly, chrysin boosted the master regulator of mitochondrial biogenesis PGC-1α, modulated its responsive proteins DRP1 and MFN2, increased activity of the antioxidant enzymes catalase and thioredoxin reductase, together with inhibition of lipid hydroperoxidation and DNA oxidation. Collectively, these findings highlight the mitigating activity of chrysin against Cr(VI)-induced nephrotoxicity and underscore AMPK, SIRT1, NF-κB, p53, and PGC-1α as underlying molecular targets.

In this study, we explored the efficacy of the probiotic Lactobacillus curvatus in growth performance, chemical composition, hematological characteristics, serum biochemical parameters, and immune response of Caspian Kutum (Rutilus frisii) under HMs stress. Fish with an average initial weight of 8.05 ± 1.58 g were allocated to 40-L polyethylene tanks, with six fish per tank. These fish were divided into six treatment groups: a control group, a Lactobacillus curvatus only group (10⁸ CFU/g), a Pb exposure group (12 mg/L), a Cd exposure group (4 mg/L), a Pb + Lactobacillus curvatus group (10⁸ CFU/g with Pb), and a Cadmium + Lactobacillus curvatus group (10⁸ CFU/g with Cadmium). Each treatment was conducted in triplicate, with the fish being fed three times daily at 6% of their body weight over. The outcomes demonstrated that growth indices in fish treated with probiotic strain had a considerable enhancement compared with the control treatment (p < 0.05). The addition of 3 g of probiotics to the diet caused a remarkable growth in white blood cells, neutrophils, a reduction in lysozyme and complement, which showed a significant difference compared with the control treatment. In general, probiotic Lactobacillus curvatus have a considerable effect on the growth, blood, and immunity, and it plays an effective role in reducing injuries caused by lead and cadmium poisoning of Caspian Sea fish fingerlings (Rutilus frisii). The administration of Lactobacillus curvatus resulted in significant improvements in growth parameters compared to the control group (p < 0.05). Lactobacillus curvatus treatment Pb to a substantial increase in white blood cells and neutrophils, along with a reduction in lysozyme and complement levels, indicating an enhanced immune response. Moreover, Lactobacillus curvatus effectively mitigated the adverse effects of Pb and Cd exposure, underscoring its potential as a protective agent against heavy metal toxicity in Caspian kutum.

Fetal growth restriction (FGR) or small for gestational age (SGA) is a serious birth outcome affected by environmental factors. Animal studies have shown that prenatal chromium (Cr) exposure leads to intrauterine growth restriction and reduced birth weight in fetal rats. However, evidence remains limited in human studies. Our study aimed to examine the association between maternal urinary Cr levels during pregnancy and also investigated possible sex-dependent response. Our cross-sectional study included 1,220 women with singleton pregnancies in the third trimester (38.31 ± 1.82 weeks). Maternal urinary Cr levels were quantified using inductively coupled plasma mass spectrometry (ICP-MS). Subsequently, the relationship between Cr exposure and SGA was evaluated using logistic regression analysis. Our investigation has found that the incidence of SGA was 13.2% in the high-exposure group (urinary Cr ≥ 14.76 µg/L; n = 305) compared to 4.6% in the low-exposure group (urinary Cr < 14.76 µg/L; n = 915; P = 0.004). The risk of SGA increased 6.2-fold for each unit increase in the normalized Cr levels in the newborns when the maternal urinary Cr concentration was > 26.15 µg/L. After adjusting for covariates, disparities were observed in the urinary Cr exposure among SGA infants based on their sex. Specifically, male infants with high Cr exposure had a higher risk of SGA than those with low exposure (odds ratio, 3.2; 95% confidence interval: 1.73, 6.04). Study found that maternal Cr exposure can affect SGA. Moreover, sex-specific implications of Cr on fetal development were observed, with male infants showing a higher susceptibility than the female.

Delayed healing of diabetic wounds is one of the major complications of diabetes mellitus, which increases the rate of amputation and mortality in patients. The impairment of vascular endothelial cells in a high-glucose environment is one of the main reasons for the delayed healing of diabetic wounds. Orthosilicic acid (OSA), the primary bioavailable form of silicon, has not yet been investigated for its potential role in the delayed healing of diabetic wounds. The CCK-8 experiment confirmed that 30 μM was the optimal concentration for OSA to affect the proliferation of human umbilical vein endothelial cells (HUVECs). EdU, Transwell, and cell-scratch experiments verified that OSA promoted the proliferation and migration ability of HUVECs under a high-glucose environment. The result of the tube-formation experiment demonstrated that OSA rescued the inhibition of HUVECs angiogenesis caused by a high-glucose environment. TUNEL and flow cytometry revealed that OSA inhibited the apoptosis of HUVECs induced by a high-glucose environment. In vivo experiments revealed that OSA could promote the healing of skin wounds in db/db mice through the PI3K/AKT/mTOR pathway. Our findings suggested that OSA promoted angiogenesis in HUVECs via the PI3K-AKT/mTOR pathway and emphasized that OSA is a potential therapeutic strategy for treating diabetic wounds.

Arsenic exposure has been implicated in various malignancies, including head and neck cancers (HNCs). However, the association between arsenic exposure and HNC development remains unclear. This systematic review aimed to assess the relationship between arsenic exposure and the risk of developing HNCs. This study adhered to PRISMA guidelines. A systematic search of PubMed, Embase, Scopus, and Web of Science was conducted from inception to January 2025 to identify relevant studies. Observational studies reporting the association between arsenic and HNCs were included. Two independent reviewers performed study selection, data extraction, and risk of bias assessment using the NIH criteria. A total of 24 studies met the eligibility criteria, including 35,641 cases and 4,631 controls. The mean age of cases was 50.3 years, while controls had a mean age of 57.7 years. Nineteen studies assessed nasopharyngeal/laryngeal cancers, and 13 investigated oral cancers. Environmental/occupational arsenic exposure was reported in 14 studies, while 11 studies measured arsenic levels in biological samples. Geographical differences in exposure outcomes were observed, with significant associations reported in studies from Tunisia, Chile, Brazil, and Taiwan, while studies from the UK, Finland, and a multicenter European study found no significant relationship. Blood, hair, soil, and drinking water arsenic concentrations varied across studies, with inconsistent findings. The findings suggest a potential link between arsenic exposure and HNCs, particularly in regions with high environmental contamination. However, heterogeneity in exposure assessment and study design limits definitive conclusions. Further well-controlled studies are needed to clarify the association and underlying mechanisms.

Lead is a major environmental pollutant and a poisonous substance that induces oxidative stress. It is responsible for several serious diseases associated with its toxicity. Its presence in the environment mostly affects children, mining workers, and pregnant women. Multiple studies are underway to investigate the mechanisms of lead-induced renal damage and associated diseases. Several mechanisms contribute to lead-induced nephrotoxicity, resulting in nephron damage and eventually inducing acute kidney injury (AKI) and chronic kidney disease (CKD). Chelation therapy is currently the main approach for the treatment of lead toxicity. However, recent research is increasingly exploring the potential of naturally occurring bioactive compounds, plant-derived extracts, and nanotechnology-based strategies as alternative treatments for lead poisoning. This review focuses on the mechanistic effects of toxicity and the various categories of compounds that have a beneficial impact on lead-induced renal toxicity. Plant extracts are significant in mitigating lead intoxication. A combination of phyto-bioactive and chelating agents is used for the treatment of lead toxicity. Cerium- and selenium-derived nanoparticles are used for therapeutic purposes. Further research is required to investigate the therapeutic potential of these therapeutic interventions.