Biological Trace Element Research最新文献

AS3MT, GSTO2, and GSTP1 genes play important roles in the arsenic biotransformation pathway, while CYP2E1 gene has a prominent role in the metabolic activation of xenobiotics. Hence, polymorphisms of these genes might have an effect on arsenic biotransformation and could impact susceptibility to arsenical skin lesions in individuals of chronic arsenic toxicity. The present case-control study, comprising 148 subjects, attempted to evaluate genetic association between nine polymorphisms of AS3MT, GSTO2, GSTP1 and CYP2E1 genes and arsenical skin lesions in a West Bengal (WB) population. A statistically significant association was found between rs11191439 (AS3MT) and arsenical skin lesions (OR = 5.50, P-value = 0.01) using logistic regression with age and gender as covariates. Among non-genetic risk factors, age and groundwater arsenic were found to be significantly associated with skin lesions (P-value < 0.05). When haplotypes among the intragenic polymorphisms of AS3MT, CYP2E1 and GSTO2 genes were analyzed, 'ATA' and 'ACG' haplotypes of the AS3MT gene showed significant difference between the case and control. Multifactor dimensionality reduction (MDR) analysis was performed on the nine polymorphisms and groundwater and urinary arsenic for studying gene-environment interactions. Strong association was observed between groundwater arsenic and skin lesions relative to the SNPs (P-value < 10^-5). The best model with maximum testing accuracy included one SNP from the AS3MT (rs11191439) and groundwater arsenic (P-value < 0.0001). The present study documents the first report about the association of AS3MT gene variant with skin lesions in an arsenic exposed population of WB. Presumably, this is also the first study that has used MDR to investigate gene-environment interactions in arsenic-induced toxicity.

Fish is a significant source of animal protein for humans; however, it has a tendency to bioaccumulate toxicants from the environment. The present study assessed the health risks associated with potential toxic metals (PTMs) in differently processed catfish (Clarias gariepinus) from four markets in Abeokuta metropolis, southwestern Nigeria. A total of 60 samples were collected and analyzed for PTMs using an Atomic Absorption Spectrophotometer. The health risk assessment was evaluated based on the hazard quotient (HQ), hazard index (HI), and cancer risk (CR). Iron concentrations ranged from 8.10 ± 6.80 to 70.7 ± 30.8 mg/kg, making it the highest measured metal in the fish samples. The mean chromium (Cr) levels (0.25 ± 0.25 to 28.4 ± 14.5 mg/kg), and lead concentrations (< 0.08 to 0.80 ± 0.70 mg/kg) exceeded the permissible limits set by the joint FAO/WHO, in most of the differently processed fish samples. Principal component analysis identified two likely sources of metal contamination in the fish samples as pond/river runoff and vehicular emissions. The health risk assessment revealed a HQ for Cr exceeding the permissible limit of 1.0 across all processed catfish consumed by both adults and children. Similarly, the CR values for Cr surpassed the threshold of 1.0 × 10⁻4 in both age groups. Chromium accounted for 43% to 98% of the contributions to both carcinogenic and non-carcinogenic health risks. The findings indicated that children are more susceptible to the adverse health effects of PTMs than adults through the consumption of variously processed catfish.

The total content of heavy metals (Cd, Co, Cr, Cu, Fe, Mn, Ni, Pb and Zn) in chamomile sample, metals content in water chamomile infusions and water infusions with additions of ascorbic acid and lemon juice at different temperatures (70, 80, and 100 °C) and steeping times (3, 5, and 7 min), were determined. The content of heavy metals was determined by flame atomic absorption spectrometry (FAAS). Mean total concentrations of Cd, Co, Cr, Cu, Fe, Mn, Ni, Pb and Zn were 0.563, 0.624, 0.254, 8.277, 32.17, 113.5, 5.102, 3.470, 30.34 μg/g, respectively. Mn, Ni and Zn were mostly extracted in pure water, up to 100%, while lemon juice showed a significant role in the extraction of Cd, Fe and Pb. Fe was relatively poor extracted in all infusions, the highest Fe extraction percentages were obtained with the addition of lemon juice (4.07-25.7%), at all applied temperatures. For most metals, the lowest extraction percentages were obtained with the addition of ascorbic acid. Non-carcinogenic hazard quotient (HQ) was less than 1 for analyzed metals in all infusions, for adults and children.

Male infertility is a common complication of diabetes. Diabetes leads to the decrease of zinc (Zn) content, which is a necessary trace element to maintain the normal structure and function of reproductive organs and spermatogenesis. The purpose of this study was to investigate the effect of metformin combined with zinc on testis and sperm in diabetic mice. 10 of 50 male mice were randomly divided into control group (group C), and the remaining 40 mice were randomly divided into untreated diabetes group (group D), diabetes + zinc group (group Z, 10 mg/(kg • d)), diabetes + metformin group (group M, 200 mg/(kg • d)), and diabetes + zinc + metformin group (group ZM, Z 10 mg/(kg • d) + M 200 mg/(kg • d)), with 10 mice in each group. Mice fasted overnight were killed, and testes and sperm were collected for further experiments. In group D, the structure of testis was disordered, and the structure of sperm tail was destroyed and the deformity rate increased. In group D, total zinc, free zinc ions, metallothionein (MT), and metal transcription factor (MTF1) in testis were significantly decreased, while the expressions of zinc transporters ZNT7, ZIP13, and ZIP14 were significantly increased. In group D, the fluorescence intensity of free zinc in sperm tail, the expression of MT2, and MTF1 mRNA decreased significantly, while the expression of ZNT7, ZIP13, and ZIP14 mRNA increased significantly. Estrogen (E2) levels, steroid synthesis-related proteins (including CYP19A1, 3β-HSD, LHR, and STAR), and PI3K/AKT/mTOR pathway-related proteins (PI3K, p-AKT/AKT, p-mTOR/mTOR) expression were significantly decreased in group D. In addition, zinc combined with metformin activates PI3K/AKT/mTOR pathway, corrects zinc homeostasis imbalance in testis and sperm, and improves testosterone synthesis and semen quality in male type 2 diabetic mice.

Chronic fluorosis is often accompanied by neurological symptoms, leading to attention, memory and learning ability decline and causing tension, anxiety, depression, and other mental symptoms. In the present study, we analyzed the molecular mechanisms of SIRT1-BDNF regulation of PI3K-AKT, MAPK, and FOXO1A in F-treated BV2 cells. The cytotoxic effect of sodium fluoride (NaF) on BV2 cells was assessed using Cell Counting Kit-8 (CCK-8), crystal violet, and 5-ethynyl-2'-deoxyuridine (EdU) staining. Cell cycle progression and apoptosis were evaluated through flow cytometry and western blotting. Reactive oxygen species (ROS) levels, oxidative stress, and inflammatory markers were measured by ROS staining, microplate reader assays, and western blotting. The role of SIRT1 in fluoride-induced toxicity for glial cells was determined using the SIRT1 activator SRT1720. The experiments demonstrated that NaF was toxic to BV2 cells, inhibited their proliferative ability, halted their cell cycle progression, triggered cellular apoptosis, promoted cellular oxidative stress (detected by ROS, SOD, MDA, GSH-Px, T-AOC) and associated protein NQO-1 and HO-1, and elevated inflammatory mediator associated protein IL-1and IL-6 expression). The fluoride-exposed groups had reduced SIRT1, BDNF, TrkB, PI3K, AKT, and MAPK protein expression levels, and increased FOXO1A protein expression. SRT1720 mitigated the harmful effects of NaF, stimulated cell proliferation and cell cycle progression, decreased apoptosis, reduced oxidative stress and inflammatory factors, elevated SIRT1, BDNF, TrkB, PI3K, AKT, and MAPK protein levels, and suppressed FOXO1A protein expression. The results indicate that NaF potentially harms glial cells by suppressing SIRT1 activation, and SIRT1 significantly mitigated the damage. Furthermore, the SIRT1 signaling pathway might regulate the nerve damage caused by fluoride poisoning and may be a protective factor in treating fluoride-induced brain injury.

The aim of this study was to explore the role of the ZnT9 protein in obesity-induced sperm maturation disorders in men. We generated a mouse model of obesity-induced weak spermatogenesis via a high-fat diet (HFD) for 10 weeks. In addition to the HFD, a 5-week intervention of salubrinal (SAL) (an inhibitor of endoplasmic reticulum stress) (1 mg/kg/day), ZnSO₄ (15 mg/kg/day), and their combination was started at week 6, after which sperm viability and epididymal tissue damage were assessed. To investigate the role of the ZnT9 protein in spermatogenesis, the expression levels of the ZnT9 protein, endoplasmic reticulum stress (ERS)-related protein, Wnt pathway protein, and apoptosis-related protein in epididymal tissue were measured. Compared with those in the normal (N) group, the mice in the HFD group presented decreased sperm motility, damaged epididymal tissue, epididymal tissue showed decreased expression of ZnT9, β-catenin, LEF protein and mRNA, and increased expression of total cholesterol (TC) and triglycerides (TG), GRP78, Caspase-3, BAX protein and mRNA, as well as increased apoptosis as shown by TUNEL staining. Compared with the HFD group, HFD + ZnSO₄ group, HFD + SAL group, and HFD + ZnSO₄ + SAL groups resulted in reduced epididymal damage, improved decreased total cholesterol (TC) and triglycerides (TG), sperm viability, increased expression of ZnT9, β-catenin, LEF protein and mRNA, and decreased expression of GRP78, Caspase-3, and BAX protein and mRNA, as well as decreased apoptosis as shown by TUNEL staining in epididymal tissues. According to this study, obesity leads to elevated ERS and affects ZnT9 protein synthesis. Inhibition of the Wnt pathway ultimately leads to cell death and damage in epididymal tissue and decreased sperm viability.

As teeth develop, their mineralised composition is a bio-recorder of diet, environment, and growth. High-resolution elemental mapping provides a tool to reveal records of life history within teeth. The relative concentrations of a range of trace elements change between in utero development, birth, and weaning in eutherian mammals. Marsupials, however, have a different mode of development: altricial birth and growth within the pouch facilitated by compositional transitions in milk. How these differences alter patterns of elemental mineralisation and become recorded in marsupial teeth is previously unknown. This study analyses the distribution of calcium (major element), zinc (actively incorporated trace element), and strontium (passively incorporated trace element) in the teeth of five species of diprotodontian marsupial using synchrotron X-ray fluorescence microscopy. We find that the diprotodontian lower incisor concatenates elemental variation from across the molariform dentition, preserving a prolonged record of life history in four of the five species. Patterns of elemental incorporation in enamel, dentine, and cementum are presented, with Ca, Zn, and Sr having differing distributions. Zn accretion indicates a role in mineralisation and/or prevention of tooth degradation. Zn also demarcates incremental cementum lines. Sr is shown to be passively incorporated into marsupial teeth, with increasing Sr concentration in milk recorded in dental tissues formed contemporaneously. Older individuals have oscillatory signals in Sr that appear linked to seasonality. These findings highlight some similarities between eutherian and marsupial trace element incorporation, particularly in the distribution of Zn. Sr signals in marsupial teeth record key aspects of life history.

Iron overload has been shown to have deleterious effects in the brain through the formation of reactive oxygen species, which ultimately may contribute to neurodegenerative disorders. Accordingly, rodent studies have indicated that systemic administration of iron produces excess iron in the brain and results in behavioral and cognitive deficits. To what extent cognitive abilities are affected and which neurobiological mechanisms underlie those deficits remain to be more fully characterized. In the present study, we looked at the effects of a 30 mg/kg iron sub-chronic treatment on cognitive abilities in two hippocampal-dependent spatial tasks (place navigation, spatial/non-spatial object recognition), in relation with iron content and oxidative stress biomarkers (MDA, SOD, CAT) in the cerebellum, hippocampus, prefrontal cortex and striatum, four brain areas known to be involved in the processing of spatial information. Iron-treated rats were impaired in acquisition and retention of the platform location in the navigation task and in the spatial/non-spatial object recognition task. Iron content and MDA were found to be increased in the four brain regions of interest, but activity of the antioxidant enzymes was not modified. The results indicate that the ability of rats to process spatial information whether in place navigation or spontaneous object spatial/non-spatial recognition is disrupted following a 30 mg/kg sub-chronic treatment. The deficits are hypothesized to result from iron excess-induced oxidative stress in the network of brain areas involved in the processing of spatial information.