Biological Trace Element Research最新文献

Contamination of aquatic ecosystems by toxic metals and metalloids poses potential health risks to fishing communities with high fish consumption. This study assessed arsenic (As), mercury (Hg), chromium (Cr), and copper (Cu) concentrations in paired hair and nail samples from 50 fishermen on Lake Hawassa, Ethiopia, using MP-AES. Descriptive statistics, Wilcoxon signed-rank tests, correlation analyses, and multiple linear regression were applied to evaluate elemental concentrations, relationships between biomarkers, and the influence of age and fishing experience. Nails generally showed higher elemental levels than hair. Median concentrations in hair and nails were 0.15 and 0.42 µg/g for As, 0.18 and 0.35 µg/g for Hg, 0.43 and 0.70 µg/g for Cr, and 8.73 and 7.73 µg/g for Cu, respectively. Significant differences between biomarkers were found for As (p = 0.029) and Hg (p = 0.038), but not for Cr and Cu. Elevated levels above reference values were more frequent in nails, especially for As (36%), Hg (30%), and Cr (30%). Hair and nail concentrations correlated positively for As (R²=0.15, p = 0.005) and Hg (R²=0.22, p < 0.001). Age and fishing experience were not major determinants, though fishing experience negatively correlated with hair Cr (β=-0.547, p = 0.004), and age with nail Cu (β=-0.511, p = 0.034). The findings confirm measurable exposure to toxic elements and suggest nails may be a more sensitive long-term biomarker than hair. This establishes baseline data and underscores the need for ongoing environmental and health surveillance in the region.

People from all over the world use cosmetics to enhance their physical appearance, seeking social acceptance. Most locally produced skin-lightening creams used in developing countries are a mixture of fat and water applied to the skin surface. These Skin Lightening creams may pose a potential health risk due to their inclusion of various highly toxic active ingredients like hydroquinone, mercury, and steroids. This study quantifies the levels of these toxic substances in ten commonly used SLC brands in Pakistan and their associated health risks in samples marketed in Lahore. To determine the concentration levels of various ingredients, including hydroquinone, steroids (Betamethasone, Dexamethasone, Hydrocortisone, and Prednisolone), and mercury, high-performance liquid chromatography, ultra violet- high-performance liquid chromatography, and a direct mercury analyzer were used, respectively. Health risks were assessed by calculating Chronic Daily Intake (CDI) and Hazard Quotient (HQ). Results showed that some samples exceeded international limits for hydroquinone (up to 5.56%) and mercury (up to 4.9 ppm), surpassing U.S Food and Drug Administration (USFDA), Pakistan Standards and Quality Control Authority (PSQCA), and World Health Organization (WHO) standards. The analysis also revealed undeclared corticosteroids in several samples: betamethasone (0.6-1.8% in 30% of samples), dexamethasone (1.4-6.4% in 20% of samples), hydrocortisone (0.4-8.5% in 50% of samples), and prednisolone (0.3-1.6% in 30% of samples). These findings suggest the need for improved regulatory enforcement in developing countries along with enhanced monitoring of Pakistan's cosmetic industry to effectively protect public health from the cumulative toxicity of hydroquinone, mercury, and corticosteroids.

Fluoride exposure through drinking water is an independent risk factor for cardiovascular disease. Terminalia arjuna is well known for its cardioprotective properties, including positive inotropic effects, hypolipidemic activity and coronary vasodilation. This study aimed to evaluate the effect of T. arjuna bark nanosuspension on fluoride-induced cardiotoxicity in rats. The nanosuspension was prepared using polysorbate-80 as an aqueous stabilizer and exhibited uniform particles with a mean size of 118.0 nm. Forty rats were divided into five groups: Group I served as the control, while the other four groups were exposed to sodium fluoride (100 ppm) daily through drinking water for 28 days. Group III received 200 mg/kg T. arjuna bark extract, while Groups IV and V were administered T. arjuna bark nanosuspension at doses of 100 mg/kg and 50 mg/kg, respectively. Fluoride administration caused significant increases in blood pressure and serum biochemical markers, along with decreased cardiac antioxidant defenses, in rats compared with the control group. Fluoride exposure also increased angiotensin-converting enzyme (ACE), nuclear factor kappa B (NF-κB), and tumor necrosis factor alpha (TNF-α) levels, as well as altered the histology and immunohistochemical expression (Bcl-2 and caspase-9) of cardiac tissue. Treatment with T. arjuna bark nanosuspension significantly attenuated these fluoride-mediated cardiotoxic effects and preserved the normal histological architecture of the cardiac tissue. However, the magnitude of these effects indicates that T. arjuna bark nanosuspension at a dose of 100 mg/kg has greater ameliorative potential.

Cyanate-based compounds have received increasing attention due to their neuroprotective and antioxidant properties, which can be further enhanced by the incorporation of selenium, a key element in redox regulation. In this study, five selenocyanate derivatives (1-5), differing by alkyl or aryl groups, were synthesized and systematically evaluated using an integrated in silico, in vitro, and in vivo approach to explore their pharmacological and toxicological potential. Computational analyses included predictions of pharmacokinetic and toxicological parameters (ADME/T), as well as molecular docking studies targeting neurotransmitter-related enzymes, namely acetylcholinesterase (AChE) and monoamine oxidases (MAO-A and B). Antioxidant activity was evaluated using multiple complementary in vitro assays, including DPPH, ABTS, FRAP, GST-like, and SOD-like, as well as cerebral reactive species (RS). Cerebral AChE, MAO-A, and MAO-B activities were also measured in vitro. In vivo experiments involved evaluating acute oral toxicity in female Swiss mice. In silico results indicated favorable ADME/T profiles and affinity of selenocyanates for the target neurochemical enzymes. In vitro assays revealed antioxidant capacity for selenocyanates, particularly for compounds 1, 4, and 5. All compounds inhibited cerebral AChE and MAO isoforms in vitro, with particular emphasis on compounds 2 and 4 as AChE inhibitors. Therefore, compounds 2 and 4 were tested in vivo and showed no acute toxicity at an oral dose of 50 mg/kg; however, at 300 mg/kg, compound 2 showed signs of toxicity, whereas compound 4 remained non-lethal. Taken together, these results highlight organoselenocyanates, especially compound 4, as promising candidates for the development of antioxidant and neuroprotective agents.

Titanium dioxide nanoparticles (TiO₂-NPs) are extensively used in industrial and biomedical applications and have been reported to induce hepato-renal toxicity through oxidative stress and inflammation. This study evaluated the protective effects of virgin olive oil (VOO) against TiO₂-NP-induced damage, while characterizing its chemical composition and exploring the molecular interactions of its bioactive compounds. VOO composition was analyzed by UV-visible spectrophotometry, HPLC-PDA, and GC-FID, and its antioxidant activity was assessed using the DPPH assay. Twenty-four male Wistar rats were divided into four groups (n = 6): a control group and three TiO₂-NP-exposed groups, two of which received VOO at 2 and 4 g/kg body weight, respectively, starting 24 h post-exposure. After six weeks, hematological, biochemical, oxidative stress, and histopathological parameters were evaluated. Molecular docking was performed to explore interactions between identified phenolics and key antioxidant and inflammatory enzymes (GSTP1-1, COX-2, CAT, and 5-LOX). VOO exhibited notable antioxidant activity (DPPH inhibition: 54.80%) and a high content of phenolic compounds, including quercetin, rutin, and 4-hydroxybenzoic acid. TiO₂-NP exposure induced significant oxidative stress, evidenced by increased malondialdehyde levels, decreased glutathione content, reduced antioxidant enzyme activities (GPx, GST, and CAT), and altered hematological parameters. VOO supplementation significantly attenuated these alterations in a dose-dependent manner, partially restored antioxidant defenses, and improved biochemical and hematological profiles, while helping to preserve tissue architecture. Docking analysis revealed notable binding affinities of phenolic compounds toward target enzymes, suggesting interactions consistent with the in vivo findings. In conclusion, VOO may mitigate TiO₂-NP-induced hepato-renal toxicity in rats, possibly through antioxidant and anti-inflammatory mechanisms. These effects are likely associated with its phenolic compounds, as suggested by both in-vivo and in silico findings.

Serum selenium (Se) is a core indicator for evaluating human selenium nutritional status. In Shaanxi Province, considerable geographical variation in selenium environment distribution limits the applicability of generalized reference intervals, which do not account for regional or physiological differences. This study aimed to establish stratified serum/hair Se reference intervals for populations with different physiological statuses across high-Se, adequate-Se, and low-Se regions in Shaanxi Province, China, and to identify key influencing factors, thereby providing region-specific evidence for selenium monitoring and intervention. This study integrated multiple datasets from Shaanxi Province, China, including pregnant women, healthy adults, hospitalized patients, and children aged 7-12 years, and comprised two components: (1) a multicenter observational analysis to establish stratified serum and hair selenium reference intervals and evaluate environmental factors, and (2) a selenium supplementation intervention in children from a low-selenium region to assess changes in hair selenium after supplementation. Multiple sets of stratified reference intervals were established: 32.7-96.5 µg/L for healthy adults (adequate-Se), 30.1-86.7 µg/L for healthy women, 32.8-89.7 µg/L for pregnant women (high-Se), 33.1-68.2 µg/L for pregnant women (medium-to-high Se composite), 35.2-88.2 µg/L for elderly hospitalized patients (adequate-Se), and 0.2-0.5 µg/g for hair Se in supplemented children (low-Se). Region, age, and liver/kidney function were identified as core influencing factors. Hair Se levels in children from low-Se regions were significantly increased after Se supplementation. This study established stratified Se reference intervals for populations with different Se environments and health/physiological statuses in Shaanxi Province, China, providing region-specific evidence for selenium assessment and for cautiously tailored nutritional intervention in comparable settings.

Arsenic contamination poses a significant environmental health risk, yet the mechanisms underlying its induction of hepatic fibrosis remain incompletely elucidated.Our previous clinical studies in arsenic poisoning areas found that serum inflammatory factors (such as IL-6, IL-1β, TNF-α) levels were significantly elevated, but there were no significant differences in liver function and fibrosis markers, suggesting that the inflammatory response precedes detectable typical pathological alterations. Established theories suggest that persistent inflammation is a key factor in the initiation of hepatic fibrosis. PINK1, a key initiator of mitophagy, was found to be downregulated in the livers of arsenic-exposed mice.Based on this, we propose a scientific hypothesis: arsenic exposure induces a persistent inflammatory response by inhibiting PINK1/Parkin-mediated mitophagy, thereby driving hepatic stellate cells (HSCs) activation and the fibrosis process. Experimental validation demonstrated that arsenic exposure significantly inhibited the PINK1/Parkin pathway, impaired mitophagy, and upregulated the expression of fibrosis markers and inflammatory factors in both liver tissues and cells. Conversely, PINK1 overexpression reversed these pathological phenotypes. In summary, dysregulation of the PINK1/Parkin pathway is a pivotal mechanism connecting arsenic exposure to chronic inflammation and the initiation of hepatic fibrosis, providing new insights for early recognition and targeted intervention of arsenic-related liver diseases.

Endothelial dysfunction is one of the important pathological bases of atherosclerosis, and cardiovascular diseases caused by atherosclerosis are the first major cause of human death. Our previous studies indicated that selenium nanoparticles (SeNPs) could prevent experimental atherosclerosis in animals, while their association with endothelial dysfunction remain unclear. Meanwhile, the size and surface properties of nanomaterials have a great influence on their biological functions. In this study, we prepared SeNPs with different sizes and surface charges to study their effects on H₂O₂-induced endothelial dysfunction in endothelial cells and the possible mechanisms. The results showed that SeNPs pretreatment significantly reduced the endothelial cell injury and dysfunction caused by H₂O₂. SeNPs pretreatment also significantly inhibited H₂O₂-induced oxidative stress, probably by enhancing cellular Se content and antioxidant selenoprotein expression in endothelial cells. Additionally, SeNPs pretreatment reversed H₂O₂-induced changes of Nrf2/Keap1 pathway. Moreover, SeNPs with middle size (around 40 nm) exhibited advantage in increasing cellular Se uptake and expression of antioxidant selenoproteins compared with smaller size (around 20 nm) or larger size (around 80 nm). Overall, SeNPs protect endothelial cells from H₂O₂-induced endothelial dysfunction by alleviating oxidative stress, and this activity may be dependent on their particle size. These results provided a deeper understanding of the anti-endothelial dysfunction activity of SeNPs and contribute to the potential use of SeNPs as a therapeutic agent against atherosclerosis in the future.

This study investigated the effects of reducing soybean meal (SBM) with balanced essential amino acids (EAAs) and supplementing non-essential amino acids (NEAAs) on organ development and mineral deposition in weaned piglets. In Experiment 1, forty-nine 28-day-old piglets (Duroc × Landrace × Large White) were randomly assigned to seven groups (n = 7) and fed corn-soybean meal diets with varying SBM inclusion levels (30% to 0%) with balanced EAAs (Lys, Met, Thr, Trp, Val, Ile, Leu, Arg, His, and Phe). In Experiment 2, twenty-eight piglets were allocated to four groups (n = 7) and fed SBM-free diets balanced for EAAs and supplemented with high, medium, or low levels of NEAAs. The results showed that reducing SBM balanced with EAAs did not impair growth performance while significantly altered mineral deposition. Calcium (Ca) concentrations in the heart, liver, and carcass, alongside carcass phosphorus (P) and serum zinc (Zn) were declined linearly. Conversely, liver Zn, kidney P, serum alanine aminotransferase (ALT) activities and and alkaline phosphatase (ALP) were increased. Serum iron (Fe) and albumin levels were exhibited U-shaped trends, reaching their nadir at moderate SBM levels. Moreover, based on the above diet, balancing NEAA significantly enhanced mineral deposition, and partially ameliorated hepatic stress indicators. These results suggest that although SBM reduction maintains growth, it disrupts mineral deposition and organ health. Our findings provide a strategy that supplementing with high dosage NEAAs in EAA-balanced low-protein diets is recommended to maintain mineral homeostasis.

Sub-chronic lead (Pb) exposure induces multi-organ toxicity through oxidative stress and inflammation. Dietary interventions have shown promise, but their effects are often organ nonspecific. This study investigated whether fermentation of a millet-based beverage could differentially direct its protective efficacy against Pb-induced injury in specific organs.Male Wistar rats were exposed to 1 ppm lead acetate in drinking water for 8 weeks and co-administered either: a fermented mix of skimmed milk and malted millet milk (F-Mix), fermented skimmed milk (FSM), or unfermented malted millet milk (UFMM). Hematological, hepatic, renal, inflammatory (TNF-α), hippocampal oxidative stress (Nrf2, GSH, SOD, CAT), acetylcholine, and histopathological parameters were assessed.Pb exposure significantly reduced hemoglobin, increased serum creatinine and BUN, elevated TNF-α, depleted hippocampal antioxidants, and impaired organ histology (p < 0.05 vs. control). Notably, UFMM attenuated Pb-induced hippocampal Nrf2 depletion by 63%, restored GSH by 71%, and preserved hepatic architecture with minimal necrosis. In contrast, F-Mix reduced serum TNF-α by 58% (p < 0.01 vs. Pb group), lowered creatinine by 44%, and BUN by 39%, with preserved renal tubular integrity. Fermented beverages (FSM and F-Mix) showed superior renal protection, while unfermented UFMM was more effective in liver and brain. Fermentation status critically redirects the organ-protective effects of millet-based beverages against Pb toxicity. Unfermented millet milk preferentially activates Nrf2-mediated antioxidant pathways in the brain and liver, while fermentation shifts protection toward the kidneys and systemic inflammation. These findings support the concept that food processing can be leveraged to design targeted nutritional interventions against heavy metal toxicity.