Zinc Toxicity Research Articles

Application of Callopian clay to improve the productivity of zinc-contaminated soils in lawn ecosystems

Pollution of lawn soils with heavy metals leads to the suppression of life and activity of living organisms inhabiting these ecosystems. The use of various means of soil detoxification will make it possible to neutralize the effect of technogenic pressure on the functional properties of urban ecosystems. The article presents data on the sorption-fertilizing properties of Callovian clay when used in zinc-contaminated soils of lawn ecosystems. The study used a small-plot field experiment, which simulated artificial contamination of agro-gray soil with zinc. The article discusses 2 methods of tillage and 4 doses of fertilizer-sorbent. It was found that the use of Callovian clay led to an increase in the production of raw and dry phytomass of lawn grasses by 3.7 - 33.2%, microbiological activity of soils by 0.9 - 132.5 times, as well as a decrease in zinc toxicity by 10 - 25%. The sorption-fertilizing effect and the optimal doses of the applied Callovian clay were determined by the time when the Callovian clay was introduced into the soil (autumn or spring).

A Novel Zinc Exporter CtpG Enhances Resistance to Zinc Toxicity and Survival in Mycobacterium bovis.

ABSTRACTZinc is a microelement essential for the growth of almost all organisms, but it is toxic at high concentrations and represents an antimicrobial strategy for macrophages. Mycobacterium tuberculosis and Mycobacterium bovis are two well-known intracellular pathogens with strong environmental adaptability, including zinc toxicity. However, the signaling pathway and molecular mechanisms on sensing and resistance to zinc toxicity remains unclear in mycobacteria. Here, we first report that P1B-type ATPase CtpG acts as a zinc efflux transporter and characterize a novel CmtR-CtpG-Zn2+ regulatory pathway that enhances mycobacterial resistance to zinc toxicity. We found that zinc upregulates ctpG expression via transcription factor CmtR and stimulates the ATPase activity of CtpG. The APC residues in TM6 is essential for CtpG to export zinc and enhance M. bovis BCG resistance to zinc toxicity. During infection, CtpG inhibits zinc accumulation in the mycobacteria, and aids bacterial survival in THP-1 macrophage and mice with elevated inflammatory responses. Our findings revealed the existence of a novel regulatory pathway on mycobacteria responding to and adapting to host-mediated zinc toxicity.IMPORTANCE Tuberculosis is caused by the bacillus Mycobacterium tuberculosis and is one of the major sources of mortality. M. tuberculosis has developed unique mechanisms to adapt to host environments, including zinc deficiency and toxicity, during infection. However, the molecular mechanism by which mycobacteria promote detoxification of zinc, and the associated signaling pathways remains largely unclear. In this study, we first report that P1B-type ATPase CtpG acts as a zinc efflux transporter and characterize a novel CmtR-CtpG-Zn2+ regulatory pathway that enhances mycobacterial resistance to zinc toxicity in M. bovis. Our findings reveal the existence of a novel excess zinc-triggered signaling circuit, provide new insights into mycobacterial adaptation to the host environment during infection, and might be useful targets for the treatment of tuberculosis.

Zinc oxide nanoparticles dissolution and toxicity enhancement by polystyrene microplastics under sunlight irradiation

Zinc oxide nanoparticles (ZnO NPs) dissolution is a critical process for the transformation and toxicity of ZnO NPs in aquatic environments. However, the effect of microplastics (MPs) on dissolution and toxicity of ZnO NPs under sunlight irradiation is still lacking. Herein, the dramatic increase in sunlight-induced ZnO NPs dissolution by polystyrene (PS) MPs was proven, which was attributed to the increase in h+-dependent and proton-dependent ZnO NPs dissolution by PS MPs, yielding 1O2 generation inhibition and acid release, respectively. The sizes, functional groups and aging status of PS MPs and pH were characteristic ZnO NPs dissolution through modifying 1O2, •OH and O2•− generation and acid release. Furthermore, the ZnO NPs dissolution affected by PS MPs also occurred in three realistic water samples, which were mainly governed by dissolved organic matter (DOM) and CO32−, rather than Cl− or SO42−. The PS MPs (1 μg/mL) dramatically altered the Zn2+:ZnO ratio in ZnO NPs suspension after 96 h of sunlight irradiation and presented vehicle effects on Zn2+, which in turn significantly increased the ion-related toxicity of ZnO NPs to Daphnia magna. Based on the PS MPs enhanced dissolution and toxicity of ZnO NPs, the effects of PS MPs on the environmental risk assessment of ZnO NPs should be seriously considered in freshwater environments under sunlight irradiation.

Influence of water hardness on zinc toxicity in Daphnia magna.

Zinc is an essential trace metal required for the maintenance of multiple physiological functions. Due to this, organisms can experience both zinc deficiency and toxicity. Hardness is recognized as one of the main modifying physiochemical factors regulating zinc bioavailability. Therefore, the present study analyzed the effect of hardness on zinc toxicity using Daphnia magna . Endpoint parameters were acute‐toxicity, development, reproduction, and expression data for genes involved in metal regulation and oxidative stress. In addition, the temporal expression profiles of genes during the initiation of reproduction and molting were investigated. Water hardness influenced the survival in response to exposures to zinc. A zinc concentration of 50 μg/l in soft water (50 mg CaCO3/L) caused 73% mortality after 96 h exposure, whereas the same zinc concentration in the hardest water did not cause any significant mortality. Moreover, increasing water hardness from 100 to 200 mg CaCO3/L resulted in a reduced number of offspring. Fecundity was higher at first brood for groups exposed to higher Zn concentrations. The survival data were used to assess the precision of the bioavailability models (Bio‐met) and the geochemical model (Visual MINTEQ). As the Bio‐met risk predictions overestimated the Zn toxicity, a competition‐based model to describe the effects of hardness on zinc toxicity is proposed. This approach can be used to minimize differences in setting environmental quality standards. Moreover, gene expression data showed that using the toxicogenomic approach was more sensitive than the physiological endpoints. Therefore, data presented in the study can be used to improve risk assessment for zinc toxicity.

Improvement of the physiological response of barley plants to both Zinc deficiency and toxicity by the application of calcium silicate

An adequate availability of Zinc (Zn) is crucial for plant growth and development given the essentiality of this element. Thus, both Zn deficiency and Zn toxicity can limit crop yields. In plants, the responses to Zn imbalances involve important physiological aspects such as reactive oxygen species (ROS) accumulation, phytohormone balance, tricarboxylic acid cycle (TCA) metabolism, and organic acids (OAs) accumulation. However, a way to improve tolerance to stresses such as those produced by nutritional imbalances is the application of beneficial elements such as silicon (Si). In this study, we grew barley plants in hydroponics under Zn deficiency and toxicity conditions, applying Si in the form of CaSiO3 in order to assess its effectiveness against Zn imbalances. Parameters related to plant growth, oxidative stress, TCA enzyme activities, phytohormones and OAs accumulation were analyzed. Both Zn deficiency and toxicity reduced leaf biomass, increased ROS accumulation, and affected phytohormone and OAs concentrations and TCA enzyme activities. CaSiO3 treatment was effective in counteracting these effects enhancing Zn accumulation under Zn deficient conditions and limiting its accumulation under toxic conditions. In addition, this treatment decreased ROS levels, and improved ascorbate/glutathione and phytohormonal responses, citrate synthase activity, and malate/oxalate ratio. Therefore, this study enhanced the notion of the efficacy of CaSiO3 in improving tolerance to Zn imbalances.

Long-distance mobile mRNA CAX3 modulates iron uptake and zinc compartmentalization.

Iron deficiency in plants can lead to excessive absorption of zinc; however, important details of this mechanism have yet to be elucidated. Here, we report that MdCAX3 mRNA is transported from the leaf to the root, and that MdCAX3 is then activated by MdCXIP1. Suppression of MdCAX3 expression leads to an increase in the root apoplastic pH, which is associated with the iron deficiency response. Notably, overexpression of MdCAX3 does not affect the apoplastic pH in a MdCXIP1 loss-of-function Malus baccata (Mb) mutant that has a deletion in the MdCXIP1 promoter. This deletion in Mb weakens MdCXIP1 expression. Co-expression of MdCAX3 and MdCXIP1 in Mb causes a decrease in the root apoplastic pH. Furthermore, suppressing MdCAX3 in Malus significantly reduces zinc vacuole compartmentalization. We also show that MdCAX3 activated by MdCXIP1 is not only involved in iron uptake, but also in regulating zinc detoxification by compartmentalizing zinc in vacuoles to avoid iron starvation-induced zinc toxicity. Thus, mobile MdCAX3 mRNA is involved in the regulation of iron and zinc homeostasis in response to iron starvation.

AtTIP2;2 facilitates resistance to zinc toxicity via promoting zinc immobilization in the root and limiting root-to-shoot zinc translocation in Arabidopsis thaliana

Zinc (Zn) is an essential micronutrient for plants. However, excess Zn is toxic to non-accumulating plants like Arabidopsis thaliana. To cope with Zn toxicity, non-accumulating plants need to keep excess Zn in the less sensitive root tissues and restrict its translocation to the vulnerable shoot tissues, a process referred to as Zn immobilization in the root. However, the mechanism underlying Zn immobilization is not fully understood. In Arabidopsis, sequestration of excess Zn to the vacuole of root cells is crucial for Zn immobilization, facilitated by distinct tonoplast-localized transporters. As some members of the aquaporin superfamily have been implicated in transporting metal ions besides polar but non-charged small molecules, we tested whether Arabidopsis thaliana tonoplast intrinsic proteins (AtTIPs) could be involved in Zn immobilization and resistance. We found that AtTIP2;2 is involved in retaining excess Zn in the root, limiting its translocation to the shoot, and facilitating its accumulation in the leaf trichome. Furthermore, when expressed in yeast, the tonoplast-localized AtTIP2;2 renders glutathione (GSH)-dependent Zn resistance to yeast cells, suggesting that AtTIP2;2 facilitates the across-tonoplast transport of GSH-Zn complexes. Our findings provide new insights into aquaporins' roles in heavy metal resistance and detoxification in plants.

Molecular mechanisms of zinc toxicity in the potworm Enchytraeus crypticus, analysed by high-throughput gene expression profiling

Zinc (Zn) is known to be relatively toxic to some soil-living invertebrates including the ecologically important enchytraeid worms. To reveal the molecular mechanisms of zinc toxicity we assessed the gene expression profile of Enchytraeus crypticus (Enchytraeidae), exposed to the reproduction effect concentrations EC10 and EC50, over 4 consecutive days, using a high-throughput microarray (species customized). Three main mechanisms of toxicity to Zn were observed: 1) Zn trafficking (upregulation of zinc transporters, a defence response to regulate the cellular zinc level), 2) oxidative stress (variety of defence mechanisms, triggered by Reactive Oxygen Species (ROS)), and 3) effects on the nervous system (possibly the primary lesion explaining the avoidance behaviour and also why enchytraeids are relatively susceptible to Zn). The adverse outcome at the organism level (reproduction EC50) could be predicted based on gene expression (male gonad development, oocyte maturation), with Zn at the EC50 affecting processes related to higher stress levels. The gene expression response was time-dependent and reflected the cascade of events taking place over-time. The 1 to 4 days of exposure design was a good strategy as it captured the time for sequence of events towards zinc adverse outcomes in E. crypticus.

The ZIP3 Zinc Transporter Is Localized to Mossy Fiber Terminals and Is Required for Kainate-Induced Degeneration of CA3 Neurons

Tight regulation of neuronal Zn2+ is critical for physiological function. Multiple Zn2+ transporters are expressed in the brain, yet their spatial distribution and distinct roles are largely unknown. Here, we show developmental regulation of the expression of Zn2+ transporters ZIP1 and ZIP3 in mouse hippocampal neurons, corresponding to previously described increase in neuronal vesicular Zn2+ during the first postnatal month. Rates of Zn2+ uptake in cultured mouse hippocampal neurons, monitored using FluoZin-3 fluorescence, were higher in mature neurons, which express higher levels of ZIP1 and ZIP3. Zn2+ uptake was attenuated by ∼50% following silencing of either ZIP1 or ZIP3. Expression of both ZIP1 and ZIP3 was ubiquitous on somas and most neuronal processes in the cultured neurons. In contrast, we observed distinct localization of the transporters in adult mouse hippocampal brain, with ZIP1 predominantly expressed in the CA3 stratum pyramidale, and ZIP3 primarily localized to the stratum lucidum. Consistent with their localization, silencing of ZIP1 expression in vivo reduced Zn2+ uptake in CA3 neurons while ZIP3 silencing reduced Zn2+ influx into dentate gyrus (DG) granule cells in acute hippocampal slices. Strikingly, in vivo silencing of ZIP3, but not ZIP1, protected CA3 neurons from neurodegeneration following kainate-induced seizures. Our results indicate that distinct Zn2+ transporters control Zn2+ accumulation and toxicity in different neuronal populations in the hippocampus and suggest that selective regulation of Zn2+ transporters can prevent seizure induced brain damage.SIGNIFICANCE STATEMENT Zinc plays a major role in neuronal function and its dysregulation is associated with neurodegeneration. Multiple zinc transporters are expressed in neurons, yet little is known on their distinct roles. Here, we show that the plasma membrane ZIP1 and ZIP3 zinc transporters are expressed on distinct neuronal populations in the CA3 region of the hippocampus. We show that ZIP1 mediates zinc influx into postsynaptic cells, while ZIP3 is responsible for zinc re-uptake from this synapse into dentate granule cells. We further show that silencing of ZIP3, but not ZIP1, can rescue the postsynaptic cells from kainate-induced neurodegeneration. This suggests that neuronal zinc toxicity and degeneration can be modulated by regulation of specific zinc transporters function.

Zinc sequestration by human calprotectin facilitates manganese binding to the bacterial solute-binding proteins PsaA and MntC.

Zinc is an essential transition metal nutrient for bacterial survival and growth but may become toxic when present at elevated levels. The Gram-positive bacterial pathogen Streptococcus pneumoniae is sensitive to zinc poisoning, which results in growth inhibition and lower resistance to oxidative stress. Streptococcus pneumoniae has a relatively high manganese requirement, and zinc toxicity in this pathogen has been attributed to the coordination of Zn(II) at the Mn(II) site of the solute-binding protein (SBP) PsaA, which prevents Mn(II) uptake by the PsaABC transport system. In this work, we investigate the Zn(II)-binding properties of pneumococcal PsaA and staphylococcal MntC, a related SBP expressed by another Gram-positive bacterial pathogen, Staphylococcus aureus, which contributes to Mn(II) uptake. X-ray absorption spectroscopic studies demonstrate that both SBPs harbor Zn(II) sites best described as five-coordinate, and metal-binding studies in solution show that both SBPs bind Zn(II) reversibly with sub-nanomolar affinities. Moreover, both SBPs exhibit a strong thermodynamic preference for Zn(II) ions, which readily displace bound Mn(II) ions from these proteins. We also evaluate the Zn(II) competition between these SBPs and the human S100 protein calprotectin (CP, S100A8/S100A9 oligomer), an abundant host-defense protein that is involved in the metal-withholding innate immune response. CP can sequester Zn(II) from PsaA and MntC, which facilitates Mn(II) binding to the SBPs. These results demonstrate that CP can inhibit Zn(II) poisoning of the SBPs and provide molecular insight into how S100 proteins may inadvertently benefit bacterial pathogens rather than the host.

Lead, zinc tolerance mechanism and phytoremediation potential of Alcea rosea (Linn.) Cavan. and Hydrangea macrophylla (Thunb.) Ser. and ethylenediaminetetraacetic acid effect.

In this study, we aimed to elucidate the defense mechanism of Alcea rosea (Linn.) Cavan. and Hydrangea macrophylla (Thunb.) Ser. against the single and compound toxicity of lead (Pb) and zinc (Zn) along with the synergistic effect of ethylenediaminetetraacetic acid (EDTA) in accumulation of metals in these two species. The two plant species were subjected to single metal treatment (Pb 1000mgkg-1, Zn 600mgkg-1) and compound metal treatment (Pb 1000mgkg-1 + Zn 600mgkg-1) in a greenhouse. Besides, different levels of EDTA were applied (2.5, 5.0, and 10.0mmolkg-1) with compound metal treatment. Several physiological and biochemical parameters, including plant photosynthetic parameters, enzymatic antioxidant system, accumulation concentration of metals, and subcellular distribution were estimated. The results showed that the antioxidative enzymes, proline, root morphological changes, and metal localization all played important roles in resisting Pb and Zn toxicity. A notable difference was that Zn was concentrated in the roots (58.5%) of H. macrophylla to reduce the damage but in the leaves (38.5%) of A. rosea to promote photosynthesis and resist the toxicity of metals. In addition, Zn reduced the toxicity of Pb to plants by regulating photosynthesis, Pb absorption and Pb distribution in subcells. The biological concentration factors (BCF) and translocation factors (TF) for Pb in two plants were less than 1, indicating that they could be considered as phytostabilizators in Pb-contaminated soils. Moreover, EDTA could enhance the enrichment and transport capacity of Pb and Zn to promote the phytoremediation effect. In summary, both plants have a certain application potential for repairing Pb-Zn-contaminated soil.

Zincum Metallicum, a homeopathic drug, alleviates Zn-induced toxic effects and promotes plant growth and antioxidant capacity in Lepidium sativum L.

In this study, we investigated the effect of the homeopathic drug Zincum Metallicum (ZM) on zinc (Zn) toxicity in the plant species Lepidium sativum L. We focused on growth parameters, Zn uptake and numerous biochemical parameters. Seedlings were hydroponically subjected during 7days to 0.05, 500, 1000, 1500 and 2000µM Zn2+, in the absence or presence of 15ch or 9ch ZM. In the absence of ZM, Zn induced negative effect on growth especially at the dose of 2mM. Zn induced also chlorosis, reduced total chlorophyll and/or carotenoid content and increased the level of malondialdehyde (MDA). Under Zn toxicity (500, 1000 and 1500µM), the superoxide dismutase (SOD), catalase (CAT), gaiacol peroxidase (GPX) and glutathione reductase (GR) activities were increased or not significantly affected, while at 2000µM Zn affected the activity of these enzymes. At the highest Zn level (2mM), proline and total polyphenol and flavonoid contents were markedly increased in leaves and roots of L. sativum. Additionally, ZM supply considerably ameliorated the plant growth, photosynthetic pigment contents and increased non-enzymatic antioxidant molecules and enzymatic activities against Zn-induced oxidative stress. Our data suggest that homeopathic properties of ZM may be efficiently involved in the restriction of Zn-induced oxidative damages, by lowering Zn accumulation and translocation in the leaves and roots of Lepidium sativum L.

The antimicrobial activity of zinc against group B Streptococcus is strain-dependent across diverse sequence types, capsular serotypes, and invasive versus colonizing isolates

BackgroundStreptococcus agalactiae or Group B Streptococcus (GBS) is an encapsulated gram-positive bacterial pathobiont that commonly colonizes the lower gastrointestinal tract and reproductive tract of human hosts. This bacterium can infect the gravid reproductive tract and cause invasive infections of pregnant patients and neonates. Upon colonizing the reproductive tract, the bacterial cell is presented with numerous nutritional challenges imposed by the host. One strategy employed by the host innate immune system is intoxication of bacterial invaders with certain transition metals such as zinc.MethodologyPrevious work has demonstrated that GBS must employ elegant strategies to circumnavigate zinc stress in order to survive in the vertebrate host. We assessed 30 strains of GBS from diverse isolation sources, capsular serotypes, and sequence types for susceptibility or resistance to zinc intoxication.ResultsInvasive strains, such as those isolated from early onset disease manifestations of GBS infection were significantly less susceptible to zinc toxicity than colonizing strains isolated from rectovaginal swabs of pregnant patients. Additionally, capsular type III (cpsIII) strains and the ST-17 and ST-19 strains exhibited the greatest resilience to zinc stress, whereas ST-1 and ST-12 strains as well as those possessing capsular type Ib (cpsIb) were more sensitive to zinc intoxication. Thus, this study demonstrates that the transition metal zinc possesses antimicrobial properties against a wide range of GBS strains, with isolation source, capsular serotype, and sequence type contributing to susceptibility or resistance to zinc stress.

The influence of hardness at varying pH on zinc toxicity and lability to a freshwater microalga, Chlorella sp.

Zinc is an essential element for aquatic organisms, however, activities such as mining and refining, as well as zinc's ubiquitous role in modern society can contribute to elevated environmental concentrations of zinc. Water hardness is widely accepted as an important toxicity modifying factor for metals in aquatic systems, though other factors such as pH are also important. This study investigated the influence of increasing water hardness, at three different pH values (6.7, 7.6 and 8.3), on the chronic toxicity of zinc to the growth rate of a microalgae, Chlorella sp. Zinc toxicity decreased with increasing hardness from 5 to 93 mg CaCO3 L-1 at all three pH values tested. The 72 h growth rate inhibition EC50 values ranged from 6.2 μg Zn L-1 (at 5 mg CaCO3 L-1, pH 8.3) to 184 μg Zn L-1 (at 92 mg CaCO3 L-1, pH 6.7). Increases in hardness from 93 to 402 mg CaCO3 L-1 generally resulted in no significant (p > 0.05) reduction in zinc toxicity. DGT-labile zinc measurements did not correspond with the observed changes in zinc toxicity as hardness was varied within a pH treatment. This suggests that cationic competition from increased hardness is decreasing zinc toxicity, rather than changes in metal lability. This study highlighted that current hardness algorithms used in water quality guidelines may not be sufficiently protective of sensitive species, such as Chlorella sp., in high hardness waters.

Bio-efficacy of iron and zinc fortified wheat flour along with bio-assessment of its hepatic and renal toxic potential.

Study was planned to assess the bio-efficiency along with toxicity of iron and zinc fortified whole wheat flour in Sprague dawley albino rats. Whole wheat flour was fortified with different dosage of sodium iron EDTA (NaFeEDTA), ferrous sulphate (FeSO4), zinc oxide (ZnO) and zinc sulphate (ZnSO4). The rats (n=3) in each group were fed on fortified wheat flour for 2 months. Liver biomarkers including alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate aminotransferase (AST) and bilirubin were recorded from serum samples. Increased concentration of ZnSO4 affected the liver biomarkers to be highest among all whereas, bilirubin levels were less than the rats fed on control diet. The above mentioned fortificants have negligible effect on renal biomarkers including creatinine and urea. Moreover, hematological parameters were also checked and reportedly, sodium iron EDTA fed rats presented highest amount of hemoglobin, iron and total iron binding capacity. Highest zinc level was observed in rats fed on whole wheat flour fortified with 60mg/Kg Zinc oxide. Microscopic observation of liver tissue depicted that rats fed on iron and zinc fortified wheat flour have more toxic effects whereas, histopathology presentation of kidney tissue has least toxic impact. It has been concluded that mandatory fortification of wheat flour with iron and zinc may cause increased serum biomarkers along with toxicity of vital organs like liver, hence fraction of wheat flour may be fortified to fulfill the requirements of deprived and vulnerable group.

Natural Organic Matter Source and Ph Influences the Toxicity of Zinc to a Freshwater Microalga

Natural Organic Matter Source and Ph Influences the Toxicity of Zinc to a Freshwater Microalga

Natural Organic Matter Source and Ph Influences the Toxicity of Zinc to a Freshwater Microalga

Natural Organic Matter Source and Ph Influences the Toxicity of Zinc to a Freshwater Microalga

Protection of Cholinergic Neurons against Zinc Toxicity by Glial Cells in Thiamine-Deficient Media

Brain pathologies evoked by thiamine deficiency can be aggravated by mild zinc excess. Cholinergic neurons are the most susceptible to such cytotoxic signals. Sub-toxic zinc excess aggravates the injury of neuronal SN56 cholinergic cells under mild thiamine deficiency. The excessive cell loss is caused by Zn interference with acetyl-CoA metabolism. The aim of this work was to investigate whether and how astroglial C6 cells alleviated the neurotoxicity of Zn to cultured SN56 cells in thiamine-deficient media. Low Zn concentrations did not affect astroglial C6 and primary glial cell viability in thiamine-deficient conditions. Additionally, parameters of energy metabolism were not significantly changed. Amprolium (a competitive inhibitor of thiamine uptake) augmented thiamine pyrophosphate deficits in cells, while co-treatment with Zn enhanced the toxic effect on acetyl-CoA metabolism. SN56 cholinergic neuronal cells were more susceptible to these combined insults than C6 and primary glial cells, which affected pyruvate dehydrogenase activity and the acetyl-CoA level. A co-culture of SN56 neurons with astroglial cells in thiamine-deficient medium eliminated Zn-evoked neuronal loss. These data indicate that astroglial cells protect neurons against Zn and thiamine deficiency neurotoxicity by preserving the acetyl-CoA level.

Molecular Characterization and Toxicity of Heavy Metal Quinary Mixtures on Enterobacter cloacae Isolate from Nworie River

The molecular characterization and toxicity of Cadmium (Cd), Lead (Pb), Zinc (Zn), Chromium (Cr) and Copper (Cu) quinary mixtures on Enterobacter cloacae isolate from Nworie River was investigated. Quinary mixtures of the heavy metals were compounded using fixed ratio (%); and inhibitory effect assessed using inhibition of total dehydrogenase as toxicity response. The mixtures consisted of five heavy metals in the ratios: Pb (20%) + Cr (20%) + Cd (20%) + Zn (20%) + Cu (20%), Pb (30%) + Cr (20%) + Cd (10%) + Zn (30%) + Cu (10%). Pb (10%) + Cr (10%) + Cd (30%) + Zn (40%) + Cu (10%), Pb (15%) + Cr (25%) + Cd (25%) + Zn (15%) + Cu (20%), Pb (40%) + Cr (15%) + Cd (5%) + Zn (20%) + Cu(20%). Result obtained showed that toxicity of the metals against the bacterium ranked in the order Cu > Cr >Zn > Pb > Cd. The quinary mixtures Pb (20%) + Cr (20%) + Cd (20%) + Zn (20%) + Cu (20%), Pb (30%) + Cr (20%) + Cd (10%) + Zn (30%) + Cu (10%) and 10%Pb + 10%Cr + 30%Cd + 40%Zn + 10%Cu showed synergistic interaction, while 15%Pb + 25%Cr + 25%Cd + 15%Zn + 20%Cu and 40%Pb + 15%Cr + 5%Cd + 20%Zn + 20%Cu mixtures were antagonistic and additive respectively. Threshold inhibitory concentration (IC50) of the quinary mixtures was 0.054 ± 0.005mM, 0.053 ± 0.002 mM, 0.038 ± 0.002 mM, 0.077 ± 0.007 mM and 0.058 ± 0.006 mM for the respective mixtures. The toxic index values evaluated for the mixtures exhibited antagonistic, synergistic and additive interaction in the various ratios. The 16S rRNA and ITSF1 sequences obtained of the isolate showed the phylogenetic placement of the 16S rRNA of the isolate was closely related to Enterobacter cloacae strain DL01 (MH168084). The heavy metals mixtures demonstrated diverse toxicity interaction on the isolate depending on their relative composition, thus poses a threat to aquatic microbial diversity.

Calcium silicate ameliorates zinc deficiency and toxicity symptoms in barley plants through improvements in nitrogen metabolism and photosynthesis

Zinc (Zn) deficiency causes serious issues to plant growth and development, negatively affecting crops in many world regions. On the other hand, Zn toxicity impairs plant growth, producing physiological alterations, and even cell death. In plants, two of the processes that most determine growth are nitrogen (N) metabolism and photosynthesis. In the last decades, several authors proved that silicon (Si) and calcium (Ca) mitigate the effects of various abiotic and biotic stresses in plants. The objective of this research is to study the effect of Si application to barley (Hordeum vulgare cv. Nure) plants grown under Zn deficiency and Zn toxicity. Hence, barley plants were grown in hydroponics and supplied with a low Zn dose (0.01 µM ZnSO4) and a high Zn dose (100 µM ZnSO4) and were supplied with CaSiO3. Parameters related to Zn accumulation, N metabolism, and photosynthesis were measured. Zn stress affected leaf Zn concentration and reduced biomass in barley plants. Both Zn toxicity and deficiency inhibited N metabolism and enhanced photorespiration, increasing stress symptoms. CaSiO3 mitigated Zn stress effects, probably regulating Zn levels in plant cells and enhancing N metabolism and photosynthesis. We conclude that CaSiO3 could be beneficial to grow barley plants in soils with high or low availability of Zn.