Association of urinary and seminal plasma vanadium concentrations with semen quality: A repeated-measures study of 1135 healthy men.

Although animal studies have shown the reproductive toxicity of vanadium, less is known about its effects on semen quality in humans. Among 1135 healthy men who were screened as potential semen donors, we investigated the relationships of semen quality with urinary and seminal plasma vanadium levels via inductively coupled plasma-mass spectrometry (ICP-MS). Spearman rank correlation tests and linear regression models were used to assess the correlations between average urinary and within-individual pooled seminal plasma vanadium concentrations (n = 1135). We utilized linear mixed-effects models to evaluate the associations of urinary and seminal plasma vanadium levels (n = 1135) with repeated sperm quality parameters (n = 5576). Seminal plasma vanadium concentrations were not significantly correlated with urinary vanadium concentrations (r = 0.03). After adjusting for possible confounders, we observed inverse relationships of within-individual pooled seminal plasma vanadium levels with total count, semen volume, and sperm concentration (all P values for trend < 0.05). Specifically, subjects in the highest (vs. lowest) tertile of seminal plasma vanadium concentrations had - 11.3% (-16.4%, -5.9%), - 11.1% (-19.1%, -2.4%), and - 20.9% (-29.0%, -11.8%) lower sperm volume, concentration, and total count, respectively; moreover, urinary vanadium levels appeared to be negatively associated with sperm motility. These relationships showed monotonically decreasing dose-response patterns in the restricted cubic spline analyses. Our results demonstrated a poor correlation between urinary and seminal plasma levels of vanadium, and elevated vanadium concentrations in urine and seminal plasma may be adversely related to male semen quality.

Manganese and Vanadium Co-Exposure Induces Severe Neurotoxicity in the Olfactory System: Relevance to Metal-Induced Parkinsonism.

Chronic environmental exposure to toxic heavy metals, which often occurs as a mixture through occupational and industrial sources, has been implicated in various neurological disorders, including Parkinsonism. Vanadium pentoxide (V2O5) typically presents along with manganese (Mn), especially in welding rods and high-capacity batteries, including electric vehicle batteries; however, the neurotoxic effects of vanadium (V) and Mn co-exposure are largely unknown. In this study, we investigated the neurotoxic impact of MnCl2, V2O5, and MnCl2-V2O5 co-exposure in an animal model. C57BL/6 mice were intranasally administered either de-ionized water (vehicle), MnCl2 (252 µg) alone, V2O5 (182 µg) alone, or a mixture of MnCl2 (252 µg) and V2O5 (182 µg) three times a week for up to one month. Following exposure, we performed behavioral, neurochemical, and histological studies. Our results revealed dramatic decreases in olfactory bulb (OB) weight and levels of tyrosine hydroxylase, dopamine, and 3,4-dihydroxyphenylacetic acid in the treatment groups compared to the control group, with the Mn/V co-treatment group producing the most significant changes. Interestingly, increased levels of α-synuclein expression were observed in the substantia nigra (SN) of treated animals. Additionally, treatment groups exhibited locomotor deficits and olfactory dysfunction, with the co-treatment group producing the most severe deficits. The treatment groups exhibited increased levels of the oxidative stress marker 4-hydroxynonenal in the striatum and SN, as well as the upregulation of the pro-apoptotic protein PKCδ and accumulation of glomerular astroglia in the OB. The co-exposure of animals to Mn/V resulted in higher levels of these metals compared to other treatment groups. Taken together, our results suggest that co-exposure to Mn/V can adversely affect the olfactory and nigral systems. These results highlight the possible role of environmental metal mixtures in the etiology of Parkinsonism.

Low-dose vanadium pentoxide perturbed lung metabolism associated with inflammation and fibrosis signaling in male animal and in vitro models.

Vanadium is available as a dietary supplement and also is known to be toxic if inhaled, yet little information is available concerning the effects of vanadium on mammalian metabolism when concentrations found in food and water. Vanadium pentoxide (V+5) is representative of the most common dietary and environmental exposures, and prior research shows that low-dose V+5 exposure causes oxidative stress measured by glutathione oxidation and protein S-glutathionylation. We examined the metabolic impact of V+5 at relevant dietary and environmental doses (0.01, 0.1, and 1 ppm for 24 h) in human lung fibroblasts (HLFs) and male C57BL/6J mice (0.02, 0.2, and 2 ppm in drinking water for 7 mo). Untargeted metabolomics using liquid chromatography-high-resolution mass spectrometry (LC-HRMS) showed that V+5 induced significant metabolic perturbations in both HLF cells and mouse lungs. We noted 30% of the significantly altered pathways in HLF cells, including pyrimidines and aminosugars, fatty acids, mitochondrial and redox pathways, showed similar dose-dependent patterns in mouse lung tissues. Alterations in lipid metabolism included leukotrienes and prostaglandins involved in inflammatory signaling, which have been associated with the pathogenesis of idiopathic pulmonary fibrosis (IPF) and other disease processes. Elevated hydroxyproline levels and excessive collagen deposition were also present in lungs from V+5-treated mice. Taken together, these results show that oxidative stress from environmental V+5, ingested at low levels, could alter metabolism to contribute to common human lung diseases.NEW & NOTEWORTHY We used relevant dietary and environmental doses of Vanadium pentoxide (V+5) to examine its metabolic impact in vitro and in vivo. Using liquid chromatography-high-resolution mass spectrometry (LC-HRMS), we found significant metabolic perturbations, with similar dose-dependent patterns observed in human lung fibroblasts and male mouse lungs. Alterations in lipid metabolism included inflammatory signaling, elevated hydroxyproline levels, and excessive collagen deposition were present in V+5-treated lungs. Our findings suggest that low levels of V+5 could trigger pulmonary fibrotic signaling.

Association of exposure to environmental vanadium and manganese with lung function among young children: A population-based study.

Exposure to environmental metals has been associated with health outcomes including respiratory health. Little is known about the impact of exposure to environmental metals on lung function among young children in general population. This study aimed to investigate the associations of exposure to metals with lung function among young children in a population-based cohort. A total of 1488 children aged 5-8 years attended a follow-up visit as part of the Longitudinal Investigation of Global Health in Taiwanese Schoolchildren (LIGHTS) cohort. We measured urinary samples of vanadium (median: 1.21 ng/mL; interquartile range (IQR): 0.73-1.98), manganese (median: 0.23 ng/mL; IQR: 0.13-0.47), arsenic (median: 40.51 ng/mL; IQR: 21.66-70.49), nickel (median: 1.09 ng/mL; IQR: 0.31-3.60), and cadmium (median: 0.26 ng/mL; IQR: 0.11-0.43) and performed lung function tests. Urinary vanadium concentrations were inversely associated with FVC (ß coefficient for the highest quartile versus the other quartiles: -33.40, p = 0.001), FEV1 (ß: -41.31, p < 0.001), FEV1/FVC ratio (ß: -1.00, p = 0.009), PEF (ß: -92.12, p = 0.004), and FEF25-75 (ß: -82.85, p < 0.001), after adjusting for relevant confounders. Urinary manganese concentrations were inversely associated with FVC (ß: -26.60, p = 0.007), FEV1 (ß: -31.62, p = 0.001), PEF (ß: -84.86, p = 0.009), and FEF25-75 (ß: -69.21, p = 0.002). Stratification analyses found inverse associations of urinary vanadium and manganese concentrations with lung function parameters predominantly among children exposed to environmental tobacco smoke. We did not find significant associations of urinary arsenic, nickel, and cadmium concentrations with lung function parameters. In conclusion, this study adds new evidence showing inverse associations of vanadium and manganese exposure with lung function among young children in the general population. Children with environmental tobacco smoke exposure are particularly vulnerable to adverse impact of vanadium and manganese exposure on lung function.

Biological Consequences of Vanadium Effects on Formation of Reactive Oxygen Species and Lipid Peroxidation.

Lipid peroxidation (LPO), a process that affects human health, can be induced by exposure to vanadium salts and compounds. LPO is often exacerbated by oxidation stress, with some forms of vanadium providing protective effects. The LPO reaction involves the oxidation of the alkene bonds, primarily in polyunsaturated fatty acids, in a chain reaction to form radical and reactive oxygen species (ROS). LPO reactions typically affect cellular membranes through direct effects on membrane structure and function as well as impacting other cellular functions due to increases in ROS. Although LPO effects on mitochondrial function have been studied in detail, other cellular components and organelles are affected. Because vanadium salts and complexes can induce ROS formation both directly and indirectly, the study of LPO arising from increased ROS should include investigations of both processes. This is made more challenging by the range of vanadium species that exist under physiological conditions and the diverse effects of these species. Thus, complex vanadium chemistry requires speciation studies of vanadium to evaluate the direct and indirect effects of the various species that are present during vanadium exposure. Undoubtedly, speciation is important in assessing how vanadium exerts effects in biological systems and is likely the underlying cause for some of the beneficial effects reported in cancerous, diabetic, neurodegenerative conditions and other diseased tissues impacted by LPO processes. Speciation of vanadium, together with investigations of ROS and LPO, should be considered in future biological studies evaluating vanadium effects on the formation of ROS and on LPO in cells, tissues, and organisms as discussed in this review.

CNS-Related Effects Caused by Vanadium at Realistic Exposure Levels in Humans: A Comprehensive Overview Supplemented with Selected Animal Studies.

Neurodegenerative disorders, which are currently incurable diseases of the nervous system, are a constantly growing social concern. They are progressive and lead to gradual degeneration and/or death of nerve cells, resulting in cognitive deterioration or impaired motor functions. New therapies that would ensure better treatment results and contribute to a significant slowdown in the progression of neurodegenerative syndromes are constantly being sought. Vanadium (V), which is an element with a wide range of impacts on the mammalian organism, is at the forefront among the different metals studied for their potential therapeutic use. On the other hand, it is a well-known environmental and occupational pollutant and can exert adverse effects on human health. As a strong pro-oxidant, it can generate oxidative stress involved in neurodegeneration. Although the detrimental effects of vanadium on the CNS are relatively well recognized, the role of this metal in the pathophysiology of various neurological disorders, at realistic exposure levels in humans, is not yet well characterized. Hence, the main goal of this review is to summarize data on the neurological side effects/neurobehavioral alterations in humans, in relation to vanadium exposure, with the focus on the levels of this metal in biological fluids/brain tissues of subjects with some neurodegenerative syndromes. Data collected in the present review indicate that vanadium cannot be excluded as a factor playing a pivotal role in the etiopathogenesis of neurodegenerative illnesses, and point to the need for additional extensive epidemiological studies that will provide more evidence supporting the relationship between vanadium exposure and neurodegeneration in humans. Simultaneously, the reviewed data, clearly showing the environmental impact of vanadium on health, suggest that more attention should be paid to chronic diseases related to vanadium and to the assessment of the dose-response relationship.

Attenuation of Vanadium-Induced Neurotoxicity in Rat Hippocampal Slices (In Vitro) and Mice (In Vivo) by ZA-II-05, a Novel NMDA-Receptor Antagonist.

Exposure to heavy metals, such as vanadium, poses an ongoing environmental and health threat, heightening the risk of neurodegenerative disorders. While several compounds have shown promise in mitigating vanadium toxicity, their efficacy is limited. Effective strategies involve targeting specific subunits of the NMDA receptor, a glutamate receptor linked to neurodegenerative conditions. The potential neuroprotective effects of ZA-II-05, an NMDA receptor antagonist, against vanadium-induced neurotoxicity were explored in this study. Organotypic rat hippocampal slices, and live mice, were used as models to comprehensively evaluate the compound's impact. Targeted in vivo fluorescence analyses of the hippocampal slices using propidium iodide as a marker for cell death was utilized. The in vivo study involved five dams, each with eight pups, which were randomly assigned to five experimental groups (n = 8 pups). After administering treatments intraperitoneally over six months, various brain regions were assessed for neuropathologies using different immunohistochemical markers. High fluorescence intensity was observed in the hippocampal slices treated with vanadium, signifying cell death. Vanadium-exposed mice exhibited demyelination, microgliosis, and neuronal cell loss. Significantly, treatment with ZA-II-05 resulted in reduced cellular death in the rat hippocampal slices and preserved cellular integrity and morphological architecture in different anatomical regions, suggesting its potential in countering vanadium-induced neurotoxicity.

Vanadium inhalation effects on the corneal ciliary neurotrophic factor (CNTF): study in a murine model.

PURPOSE: Air pollution is a public health problem caused by predatory human activities and the indiscriminate burning of fossil fuels that liberate particulate matter (PM) into the atmosphere. Vanadium (V) adheres to them and reaches the bloodstream and different organs such as the eye when inhaled. Another way to reach the eye is by direct contact, and the cornea is the first layer exposed. Ciliary neurotrophic factor (CNTF) is secreted by the corneal nerves and some of its functions include self-renewal maintenance and wound healing by the activation of STAT3. Previous reports from our group indicate the activation of STAT3 after the inhalation of V, adhered to PM. OBJECTIVE: To analyse the effect of V inhalation in the expression of CNTF. Method: CD-1 male mice were exposed for 4 and 8 weeks to V inhalation. The eyes were removed, and the corneas were processed for immunohistochemistry for CNTF and analysed by densitometry. The same slides were used to evaluate histological modifications and to measure the corneas' anterior epithelial and endothelial thickness. RESULTS: A decrease in CNTF expression in the anterior epithelium in the 8th week, as well as an increase in the endothelial and corneal thickness and disarray of all the layers of the anterior epithelium. CONCLUSION: V inhalation disturbs the architecture of the cornea and modifies the presence of CNTF which might modify the renewal of the corneas after exposure to PM air pollution.

High-throughput Sequencing Analysis of the Effects of Vanadium on Bacterial Community Structure in Purple Soil.

Vanadium (V) contamination in soil has received extensive attention due to its high toxicity. The change of mobility and bioavailability of soil V and the effects of V on the soil microbial community were studied under conditions of different V(V) spiking concentrations (0, 100, 250, and 500 mg kg-1) and aging time (1, 7, 14, 30, 45, and 60 d). The results showed that soil V mainly presented as V(IV) of all treatments throughout the aging process. At high levels of V(V) loading (250 and 500 mg kg-1), soil V(V) showed a downward trend, while bioavailable V did not change significantly within 60 d's aging. The analysis of soil bacterial community showed that Proteobacteria was the most abundant phylum in all soils, and the dominant genera Sphingomonas and Lysobacter can well adapt to high concentration V. These microorganisms exhibited great potential for bioremediation of V-contaminated soils.

Individual and joint associations of co-exposure to multiple plasma metals with telomere length among middle-aged and older Chinese in the Dongfeng-Tongji cohort.

Studies on associations of metals with leucocyte telomere length (LTL) were mainly limited to several most common toxic metals and single-metal effect, but the impact of other common metals and especially the overall joint associations and interactions of metal mixture with LTL are largely unknown. We included 15 plasma metals and LTL among 4906 participants from Dongfeng-Tongji cohort. Multivariable linear regression was used to estimate associations of individual metals with LTL. We also applied Bayesian kernel machine regression (BKMR) and quantile g-computation regression (Q-g) to evaluate the overall association and interactions, and identified the major contributors as well as the potential modifications by major characteristics. Multivariable linear regression found vanadium, copper, arsenic, aluminum and nickel were negatively associated with LTL, and a 2-fold change was related to 1.9%-5.1% shorter LTL; while manganese and zinc showed 3.7% and 4.0% longer LTL (all P < 0.05) in multiple-metal models. BKMR confirmed above metals and revealed a linearly inverse joint association between 15 metals and LTL. Q-g regression further indicated each quantile increase in mixture was associated with 5.2% shorter LTL (95% CI: -8.1%, -2.3%). Furthermore, manganese counteracted against aluminum and vanadium respectively (Pint<0.05). In addition, associations of vanadium, aluminum and metal mixture with LTL were more prominent in overweight participants. Our results are among the first to provide a new comprehensive view of metal mixture exposure on LTL attrition in the general population, including identifying the major components, metals interactions and the overall effects.

Vanadium(IV) oxide affects embryonic development in mice.

Vanadium(V) and vanadium(IV) are the predominant redox forms present in the environment, and epidemiological studies have reported that prenatal vanadium exposure is associated with restricted fetal growth and adverse birth outcomes. However, data about the toxic effects of vanadium(IV) oxide (V2 O4 ) on the development of mammals are still limited. Therefore, in this work, 4.7, 9.4, or 18.7 mg/kg body weight/injection/day V2 O4 was administered through an intraperitoneal (ip) injection to pregnant mice from gestational days 6 to 16. The results showed that V2 O4 produced maternal and embryo-fetal toxicity and external abnormalities in the offspring, such as malrotated and malpositioned hind limbs, hematomas and head injuries. Moreover, the skeletons of the fetuses presented reduced ossification of the cranial bones, including the frontal and parietal bones, corresponding to head injuries observed in the external assessment of the fetuses. These results demonstrate that administration of V2 O4 to pregnant females in the organogenesis period adversely affects embryonic development.

Toxicity of Vanadium during Development of Sea Urchin Embryos: Bioaccumulation, Calcium Depletion, ERK Modulation and Cell-Selective Apoptosis.

Vanadium toxicology is a topic of considerable importance as this metal is widely used in industrial and biomedical fields. However, it represents a potential emerging environmental pollutant because wastewater treatment plants do not adequately remove metal compounds that are subsequently released into the environment. Vanadium applications are limited due to its toxicity, so it is urgent to define this aspect. This metal is associated with sea urchin embryo toxicity as it perturbs embryogenesis and skeletogenesis, triggering several stress responses. Here we investigated its bioaccumulation and the correlation with cellular and molecular developmental pathways. We used cytotoxic concentrations of 1 mM and 500 µM to perform quantitative analyses, showing that vanadium accumulation interferes with calcium uptake during sea urchin development and provokes a disruption in the biomineralization process. At the end of the whole treatment, the accumulation of vanadium was about 14 and 8 µg for embryos treated respectively with 1 mM and 500 µM, showing a dose-dependent response. Then, we monitored the cell signaling perturbation, analyzing key molecular markers of cell survival/cell death mechanisms and the DNA fragmentation associated with apoptosis. This paper clarifies vanadium's trend to accumulate directly into embryonic cells, interfering with calcium uptake. In addition, our results indicate that vanadium can modulate the ERK pathway and activate a cell-selective apoptosis. These results endorse the sea urchin embryo as an adequate experimental model to study metal-related cellular/molecular responses.

Protective effect of indomethacin on vanadium-induced adrenocortical and testicular damages in rat.

Vanadium toxicity is a globally recognized threat to the reproductive health of man and animal. However the mechanism of vanadium-induced damage to the testicular and adrenocortical tissues is not fully characterized. It was hypothesized that prostaglandins may partially mediate the inflammatory response to vanadate damage. In this study prostaglandin (PG) mediated effects of vanadate on testicular and adrenocortical functions was substantiated by using indomethacin to block prostaglandin synthesis. Significant inhibition of spermatogenesis, decreased serum level of testosterone and gonadotropins in the vanadium-exposed group of rats indicated the damaging effects of vanadium-induced reactive oxygen species. This was also reflected in the appreciable increase in testicular lipid peroxidation (LPO) level and decline in the activities of steroidogenic and antioxidant enzymes. Histopathological studies revealed regressive and degenerative changes in testis. However, inhibition of cyclooxygenase activity by indomethacin increased steroid hormone production, gonadotropin level, elevated the specific activities of enzymes and decreased LPO level in rat testis exposed to vanadium. Vanadium also caused prostaglandin mediated adrenocortical hyperactivity, as inhibition of PG synthesis abolished these adrenal responses to vanadium. The studies showed that vanadium toxicity is directly linked to stimulation of prostaglandin synthesis. Therefore, indomethacin can be a good prospect to alleviate vanadium induced male infertility.

Application of boron reduces vanadium toxicity by altering the subcellular distribution of vanadium, enhancing boron uptake and enhancing the antioxidant defense system of watermelon.

Vanadium (V) is the fifth most abundant transition metal, elevated levels of V are hazardous to plants. Boron (B) is an essential micronutrient for plants and can mitigate heavy metal toxicity. However, the mechanism used by B to promote tolerance to vanadium is unknown. In this study, a combination of physiological and gene expression analysis was used to explain mechanism of B (75 µM) induced V (40 mg L-1) stress tolerance in watermelon. V stress severely reduced root and shoot growth and increased the accumulation of ROS. B application improved tolerance to V by enhancing the expression of B transporter genes (ClaNIP5;1-1, ClaNIP5;1-2, ClaBOR4) that facilitated B uptake and transport while restricting V transport in plant tissues. At cellular level, the higher V retention in leaves was achieved by cell wall chelation, whereas, the higher V exclusion in vacuole of root cell was driven by elevated vacuolar H+-ATPase, H+-PPase activities, and transcript level of ClaVHP1;1, ClaPDR12-1 and ClaPDR12-2 genes facilitated by B application. Moreover, B application reduced tissue ROS cascade by enhancing antioxidant enzymatic activity and expression of superoxide dismutase (ClaCSD1-1, ClaCSD1-2, ClaCSD3, ClaMSD1) and catalase (ClaCAT2-1, ClaCAT2-2) genes that enhanced the defense mechanism of the V treated plants, improved root and shoot growth and tolerance index of watermelon. In conclusion, we demonstrate that ameliorative effect of B in tolerance to V of watermelon was based on B homeostasis and improved antioxidant defense system. These findings might help to increase watermelon production in V polluted soils.

Growth responses, accumulation, translocation and distribution of vanadium in tobacco and its potential in phytoremediation.

The metal tolerance mechanism of plants is of great importance to explore the plant-based clean-up of environmental substrata contaminated by heavy metals. Indoor experiment of tobacco (Nicotiana tabacum L.) seedlings growing hydroponically in nutrient solution containing 0, 0.1, 0.5, 2.0, and 4.0 mg L-1 V was conducted. The results indicated that plant overall growth performance was significantly affected at ≥ 2.0 mg L-1 V. Oxidative stress degree as indicated by foliar O2-· and H2O2 content intensified markedly at ≥ 0.5 mg L-1 V treatments. In response, the plant activated its enzyme and non-enzyme protecting mechanism to cope with oxidative stress inflicted by vanadium. The activities of antioxidant enzymes, including SOD, POD, CAT, APX, and the concentration of non-enzyme antioxidants, e.g., AsA and GSH were all conspicuously (p < 0.5 or p < 0.1) enhanced at ≥ 0.5 mg L-1 V treatments. Vanadium accumulated in leaves, stems, and roots increased with increasing vanadium level. The majority of the absorbed vanadium retained in plant root, and minor portions were transferred to aerial parts. Vanadium concentration in plant tissues ordered as root ˃ stem ˃ leaf. Translocation factors (TF) in vanadium-treated tobaccos (TF « 1) were significantly lower than that of control (TF ˃ 1). In conclusion, although vanadium at ≥ 2.0 mg L-1 inhibited plant growth, tobacco exhibited a relatively good vanadium tolerance through self-adaptive regulation and has the potential as a phytostabilizer in decontaminating the environment contaminated by vanadium.

Mini review-vanadium-induced neurotoxicity and possible targets.

Vanadium, a transition metal, ubiquitous in nature is known to have therapeutic effect as well as toxic effect. It is known to possess antidiabetic, antitumor and antiparasitic activity. However, on long term exposure, it produces neurotoxicity which may result in memory impairment. The possible mechanism known to cause neurotoxicity suggested is oxidative stress and inflammation of neuronal cells. The present review has focused on discussing the role of protein P38 mitogen-activated protein kinase and oxidative stress as possible targets to treat vanadium-induced neurotoxicity.

Mechanism of vanadium(IV) resistance of the strains isolated from a vanadium titanomagnetite mining region.

Microbial treatment for vanadium contamination of soils is a favorable and environment-friendly method. However, information of the resistant mechanism of the strains in soils to vanadium, especially to tetravalent vanadium [vanadium(IV)], is still limited. Herein, potential of the vanadium(IV) biosorption and biotransformation of the strains (4K1, 4K2, 4K3 and 4K4) which were capable of tolerating vanadium(IV) was determined. For biosorption, the bioadsorption and the bioabsorption of vanadium(IV) occur on the bacterial cell wall and within the cell, respectively, were taken into consideration. Comparison of the vanadium(IV) adsorbed on the bacterial cell walls and remained in the cells after sorption indicated the major bacterial vanadium(IV) sorption role of the bioadsorption which was at least one order of magnitude higher than the bioabsorption amount. Isotherm study using various isotherm models revealed a monolayer and a multilayer vanadium(IV) biosorption by 4K2 and the others (4K1, 4K3 and 4K4), respectively. Higher biosorption was observed in acidic conditions than in alkaline conditions, and the maximum biosorption was 2.41, 9.35, 7.76 and 8.44 mg g-1 observed at pH 6 for 4K1, at pH 3 for 4K2, and at pH 4 for 4K3 and 4K4, respectively. At the present experimental range of the initial vanadium(IV) concentration, optimal biosorption capacity of the bacteria was observed at the vanadium(IV) level of 100-250 mg L-1. Different biotransformation level of vanadium(IV) in soils by the stains was observed during a 28-d pot incubation of the soils mixed with the strains, which can be attributed to the discrepancy of both soil properties and bacterial species. Present study can help to fill up the gaps of the insufficient knowledge of the vanadium(IV) resistant mechanism of the strains in soils.

Changes of root microbial populations of natively grown plants during natural attenuation of V-Ti magnetite tailings.

Mine tailings contain dangerously high levels of toxic metals which pose a constant threat to local ecosystems. Few naturally grown native plants can colonize tailings site and the existence of their root-associated microbial populations is poorly understood. The objective of this study was to give further insights into the interactions between native plants and their microbiota during natural attenuation of abandoned V-Ti magnetite mine tailings. In the present work, we first examined the native plants' potential for phytoremediation using plant/soil analytical methods and then investigated the root microbial communities and their inferred functions using 16 S rRNA-based metagenomics. It was found that in V-Ti magnetite mine tailings the two dominant plants Bothriochloa ischaemum and Typha angustifolia were able to increase available nitrogen in the rhizosphere soil by 23.3% and 53.7% respectively. The translocation factors (TF) for both plants indicated that B. ischaemum was able to accumulate Pb (TF = 1.212), while T. angustifolia was an accumulator of Mn (TF = 2.502). The microbial community structure was more complex in the soil associated with T. angustifolia than with B. ischaemum. The presence of both plants significantly reduced the population of Acinetobacter. Specifically, B. ischaemum enriched Massilia, Opitutus and Hydrogenophaga species while T. angustifolia significantly increased rhizobia species. Multivariate analyses revealed that among all tested soil variables Fe and total organic carbon (TOC) could be the key factors in shaping the microbial structure. The putative functional analysis indicated that soil sample of B. ischaemum was abundant with nitrate/nitrite reduction-related functions while that of T. angustifolia was rich in nitrogen fixing functions. The results indicate that these native plants host a diverse range of soil microbes, whose community structure can be shaped by plant types and soil variables. It is also possible that these plants can be used to improve soil nitrogen content and serve as bioaccumulators for Pb or Mn for phytoremediation purposes.

Changes in Ovarian and Uterine Morphology and Estrous Cycle in CD-1 Mice After Vanadium Inhalation.

Vanadium is a metal present in particulate matter and its reprotoxic effects have been demonstrated in males and pregnant females in animal models. However, the effects of this metal on the reproductive organs of nonpregnant females have not been sufficiently studied. In a vanadium inhalation model in nonpregnant female mice, we found anestrous and estrous cycle irregularity, as well as low serum concentrations of 17ß-estradiol and progesterone. A decrease in the diameter of secondary and preovulatory follicles, as well as a thickening of the myometrium and endometrial stroma, was observed in the vanadium-treated mice. There was no difference against the control group with respect to the presence of the estrogen receptor α in the uterus of the animals during the estrous stage. Our results indicate that when vanadium is administered by inhalation, effects are observed on the female reproductive organs and the production of female sex hormones.

The Pathopharmacological Interplay between Vanadium and Iron in Parkinson's Disease Models.

Parkinson's disease (PD) pathology is characterised by distinct types of cellular defects, notably associated with oxidative damage and mitochondria dysfunction, leading to the selective loss of dopaminergic neurons in the brain's substantia nigra pars compacta (SNpc). Exposure to some environmental toxicants and heavy metals has been associated with PD pathogenesis. Raised iron levels have also been consistently observed in the nigrostriatal pathway of PD cases. This study explored, for the first time, the effects of an exogenous environmental heavy metal (vanadium) and its interaction with iron, focusing on the subtoxic effects of these metals on PD-like oxidative stress phenotypes in Catecholaminergic a-differentiated (CAD) cells and PTEN-induced kinase 1 (PINK-1)B9Drosophila melanogaster models of PD. We found that undifferentiated CAD cells were more susceptible to vanadium exposure than differentiated cells, and this susceptibility was modulated by iron. In PINK-1 flies, the exposure to chronic low doses of vanadium exacerbated the existing motor deficits, reduced survival, and increased the production of reactive oxygen species (ROS). Both Aloysia citrodora Paláu, a natural iron chelator, and Deferoxamine Mesylate (DFO), a synthetic iron chelator, significantly protected against the PD-like phenotypes in both models. These results favour the case for iron-chelation therapy as a viable option for the symptomatic treatment of PD.