Biological Trace Element Research最新文献

Postpartum depression (PPD) constitutes a serious mental health concern linked to behavioral disturbances. Zinc exerts a significant influence on mood states. This novel study revealed the antidepressant-like action of zinc oxide nanoparticles (ZnO NPs) and their underlying mechanisms in the PPD model through the forced swimming test (FST), emphasizing their therapeutic potential for maternal mental health. PPD was induced in female mice via intraperitoneal injection of progesterone (5 mg/kg) for 5 days, followed by 3 days withdrawal period. The depressed mice received ZnO NPs (5, 10, and 20 mg/kg) 30 min before the FST. Moreover, L-arginine (NO precursor, 750 mg/kg), L-NAME (non-specific NOS inhibitor, 10 mg/kg), WAY100635 (selective 5-HT_1A receptor antagonist, 0.1 mg/kg), caffeine (non-selective adenosine receptor antagonist, 3 mg/kg), adenosine (non-selective adenosine receptor agonist, 0.1 mg/kg), NMDA (NMDA receptor agonist, 75 mg/kg), MK-801 (NMDA receptor antagonist, 0.05 mg/kg) were used to ascertain the neural pathways implicated in the antidepressant-like response of ZnO NPs. ZnO NPs exhibited a significant and dose-dependent decrease in immobility time. Prior administration of L-arginine, WAY100635, caffeine, and NMDA suppressed the anti-immobility effect of the maximal effective dose of ZnO NPs. Pre-treatment with L-NAME, adenosine, and MK-801 amplified the decrease in immobility duration provoked by a sub-effective dose of ZnO NPs. These findings suggest that the antidepressant-like action of ZnO NPs is likely mediated through nitrergic, serotonergic, adenosinergic, and glutamatergic pathways.

Lead (Pb) is a widespread environmental metal with recognized genotoxicity, yet whether it impairs DNA damage repair via epigenetic regulation remains unclear. Here, human lymphoblastoid TK6 cells were exposed to a series of concentrations of lead acetate solutions at 0, 120, 240, 480 µM for 24 h. We quantified cell viability, oxidative stress indicators (ROS, MDA, SOD, CAT), DNA damage markers (the Comet assay indicators Tail Length, Tail DNA % and Tail Moment and γ-H2AX levels), DNA damage repair capacity using 3-AB method based on the Comet assay, cell cycle and apoptosis, and the mRNA and protein expressions of DNA repair genes (RAD51, CHEK2, BRCA1, Ku80, MSH2, LIG4). We further measured expressions of DNA methyltransferase DNMT1 and demethylase TET2, and methylation of the Ku80 promoter region by Pyrosequencing. The results suggested that Pb exposure decreased cell viability, increased ROS levels and MDA content while reduced SOD and CAT activity. Pb exposure induced dose-dependent increases in DNA single-strand breaks (SSBs) and double-strand breaks (DSBs), as evidenced by elevated Tail Length, Tail DNA%, Tail Moment and fluorescence intensity of γ-H2AX levels. G0/G1-phase arrest and apoptosis also rose with dose. In addition, DNA damage repair capacity of TK6 cells were decreased in a dose-dependent manner after Pb exposure. DNA damage repair genes showed a biphasic response-elevated at lower doses and suppressed at higher doses-at both mRNA and protein levels. The methylation level in promoter region of Ku80 increased with dose and coincided with higher DNMT1 and lower TET2 expression. Collectively, Pb exposure induces oxidative stress and DNA damage in TK6 cells; higher lead concentration inhibited DNA repair capacity, potentially via DNMT1/TET2 mediated hypermethylation of the Ku80 promoter region.

Methylmercury (MeHg) is a potent neurotoxin that disrupts neurodevelopment in offspring when exposure occurs early in life. However, to date, there is a lack of effective therapeutic strategies for MeHg toxicity. Short-chain fatty acids (SCFAs), metabolites of gut microbial fermentation, influence the gut-brain axis and offer neuroprotective effects. This study investigated the effects of a SCFA intervention on offspring cognitive impairment and gut microbiota dysbiosis following maternal MeHg exposure. The Morris water maze protocol was employed to evaluate cognitive performance in the filial generation of rats. SCFAs were quantified with gas chromatography, while microbial community profiling of the intestine was performed with high-throughput sequencing of the 16 S ribosomal RNA gene. Additionally, histopathological alterations were evaluated via hematoxylin and eosin (HE) staining. The results showed that SCFA supplementation significantly increased mercury excretion through the feces and reduced mercury accumulation in the colon and brain compared to the MeHg group. MeHg exposure markedly decreased colonic levels of acetate, propionate, and butyrate, but SCFA supplementation effectively restored these levels. Further investigations demonstrated that SCFA supplementation influenced the intestinal microbial community and restored its diversity, while HE staining revealed that SCFAs alleviated pathological damage to both the colon and brain tissues. Additionally, behavioral assessments demonstrated that MeHg exposure reduced platform crossings in offspring rats, while SCFA supplementation significantly enhanced cognitive performance. These findings highlight the potential of SCFAs in mitigating MeHg-induced damage and improving cognitive function, offering new insights into therapeutic approaches for neurotoxin exposure.

One hazardous heavy metal that causes oxidative stress is cadmium (Cd) and harms male reproductive function. Although various antioxidants have been explored for protection, the potential of Mesembryanthemum crystallinum (M. crystallinum) - a flavonoid and phenolic-rich halophyte- remains understudied in this context. According to the United Nations Sustainable Development Goals (SDGs), specifically SDG 3 on Good Health and Well-Being and SDG 12 Responsible Consumption and Production this novel research evaluated the protective potential of M. crystallinum aqueous extract (MAE) to mitigate cadmium chloride (CdCl₂)-testicular dysfunction. After acclimatization, Eight groups (n = 5) of forty male rats were allocated into groups: (1) control; (2) CdCl₂ (2 mg/kg); (3) MAE 200 mg/kg; (4) MAE 400 mg/kg; (5) CdCl₂ + MAE 200 mg/kg; (6) CdCl₂ + MAE 400 mg/kg; (7) MAE (200 mg/kg) pre-treatment + CdCl₂; (8) MAE (400 mg/kg) pre-treatment + CdCl₂. For 14 days, oral treatments were administered. HPLC profiling revealed eight major phenolic compounds in M. crystallinum like quercetin and ellagic acid. CdCl₂ exposure impaired sperm indices, reduced serum LH and testosterone and induced oxidative and histological damage with elevated caspase-3 and TNF-α expression. MAE treatment especially at 400 mg/kg restored hormonal levels, improved sperm quality, normalized antioxidant defense, and preserved testicular architecture. Molecular docking confirmed binding of hesperidin, rutin, and ellagic acid to apoptotic and inflammatory proteins. MAE may exhibit potent anti-inflammatory, antioxidant, and anti-apoptotic activity, protecting against CdCl₂-induced reproductive injury. M. crystallinum represents a sustainable, plant based therapeutic candidate aligned with SDG-driven strategies for combating environmental toxicity-related infertility.

Surface sediments, mussels, and macroalgae were collected to investigate metal accumulation, distribution, pollution levels, and sources from Gemlik Bay in the southeastern Sea of Marmara. The elements Cu, Zn, V, Co, Cr, Pb, Ni, and Mn were determined in macroalgae (Ulva lactuca Linnaeus,1753), (Ulva intestinalis, Linnaeus, 1753) and mussel (Mytilus galloprovincialis, Lamarck, 1819) samples, while Al and Fe were also determined in sediment samples in addition to these metals. Element accumulation and metal contamination levels were determined, and health risks from mussel and macroalgae consumption were assessed across age groups. The average enrichment factor (EF) calculated for sediment samples indicates that the contamination originates from anthropogenic sources, while the contamination factor (Cf) indicates that the contamination is at a low level. Additionally, the potential ecological risk (Er) and index (PERI) reveal that, except for lead (Pb), the ecological factors for other metals are low. In addition, according to the average geochemical index (Igeo) results, sediments were uncontaminated with Mn and Al, slightly contaminated with Fe, slightly to moderately with Cr and Pb, and moderately with Zn. Detected metals in mussels and macroalgae were assessed for health risks across age groups for the first time. Accordingly, the daily chronic intake (CDI) was calculated, and separate hazard index (HI) and target hazard quotient (THQ) values were determined for each age group. Children were identified as the most vulnerable group, highlighting the need for caution in their consumption of seafood, especially mussels and macroalgae.

Neuroinflammation is increasingly recognized as a critical factor in the progression of various neurological disorders, with chronic exposure to environmental toxicants like arsenic emerging as a major contributor. This review focuses on arsenic-induced neuroinflammation, highlighting its underlying molecular mechanisms and pathways, global epidemiological burden, and current strategies for effective management. Arsenic groundwater contamination, particularly prevalent in Asian countries, poses a significant health risk to millions across more than 100 nations. Chronic exposure to arsenic generates reactive oxygen species (ROS), triggering oxidative stress and activating microglia, the key drivers of neuroinflammation. This cascade promotes proinflammatory cytokine release, leading to cognitive and neurological impairments. This review examines the underlying mechanisms, including mitochondrial dysfunction, oxidative damage, and inflammatory signaling pathways. Additionally, this review highlights current therapeutic strategies aimed at mitigating arsenic-induced neurotoxicity, including chelation therapy, natural antioxidants, and supplementation with essential trace elements. By addressing the multifactorial mechanisms underlying arsenic-induced neuroinflammation, the review emphasizes the urgent need for integrated public health initiatives and targeted interventions to alleviate the neurological consequences of chronic arsenic exposure.

Painkiller medicines, either over-the-counter (non-opioid) or prescription (opioid), pose a risk of heavy metal poisoning, Heavy metal contamination of pharmaceuticals is a common and international issue; therefore, it is critical to regularly check their safety as they are connected to a variety of adverse health effects. The elemental concentration levels of (Pb, Cd, As, Cr, Cu, and Ni) of 32 over-the-counter painkillers medications; paracetamol (12 samples) and nonsteroidal anti-inflammatory, specifically diclofenac (16 samples) and ibuprofen (4 samples) from four selected countries; Jordan, United Arab Emirates, Saudi Arabia and Switzerland are evaluated in this research by comparing the results obtained using inductively coupled plasma mass spectrometry (ICP-MS) with the permissible limit of elements recommended by United States Pharmacopeia (USP). The results of Pb, As, and Cr elements were most abundant in the paracetamol group, whereas Cd, Ni, and Cu had the highest concentrations in the diclofenac group. All over-the-counter painkiller medication samples have permissible limits as recommended by the United States Pharmacopeia (USP) of examined elemental impurities except Pb and Cd in some tested Jordanian, Emirati paracetamol medication samples, as well as Cd in some diclofenac and ibuprofen medication samples from Jordanian, Saudi, Swiss sources. The validation parameters demonstrated positive results, including good accuracy and good correlation coefficient values (R²) of 0.999 and relative standard deviations (RSD) < 5%. Data were analyzed statistically by using the parametric ONE-WAY (ANOVA). A comparison among the means of the three categories of medication type for different chemical elements indicated that all p-values are ˃ 0.05 except for Ni (0.017).