Ion Cadmium Research Articles

Cadmium Highlights Common and Specific Responses of Two Freshwater Sentinel Species, Dreissena polymorpha and Dreissena rostriformis bugensis.

Zebra mussel (ZM), Dreissena polymorpha, commonly used as a sentinel species in freshwater biomonitoring, is now in competition for habitat with quagga mussel (QM), Dreissena rostriformis bugensis. This raises the question of the quagga mussel's use in environmental survey. To better characterise QM response to stress compared with ZM, both species were exposed to cadmium (100 µg·L-1), a classic pollutant, for 7 days under controlled conditions. The gill proteomes were analysed using two-dimensional electrophoresis coupled with mass spectrometry. For ZM, 81 out of 88 proteoforms of variable abundance were identified using mass spectrometry, and for QM, 105 out of 134. Interestingly, the proteomic response amplitude varied drastically, with 5.6% of proteoforms of variable abundance (DAPs) in ZM versus 9.4% in QM. QM also exhibited greater cadmium accumulation. Only 12 common DAPs were observed. Several short proteoforms were detected, suggesting proteolysis. Functional analysis is consistent with the pleiotropic effects of the toxic metal ion cadmium, with alterations in sulphur and glutathione metabolisms, cellular calcium signalling, cytoskeletal dynamics, energy production, chaperone activation, and membrane events with numerous proteins involved in trafficking and endocytosis/exocytosis processes. Beyond common responses, the sister species display distinct reactions, with cellular response to stress being the main category involved in ZM as opposed to calcium and cytoskeleton alterations in QM. Moreover, QM exhibited greater evidence of proteolysis and cell death. Overall, these results suggest that QM has a weaker stress response capacity than ZM.

The least-square support vector regression model for the dyes and heavy metal ions removal prediction

Wastewater treatment plants are typically complex because they involve physical, chemical, and biological processes. Meanwhile, the efficiency of the removal of pollutants such as auramine (AO), methylene blue (MB), and ion Cadmium (Cd (II)) from the wastewater are difficult to be measured directly in real-time, as this measurement requires laboratory instruments that are time-consuming. The soft sensors could be the solution to perform the real-time prediction of the AO, MB, and Cd (II) removals’ capability. Hence, this study investigates the performances of a soft sensor, namely least-square support vector regression (LSSVR) to estimate the AO, MB, and Cd (II) removals’ ability. In this study, two wastewater-related case studies involving AO, MB, and Cd (II) removals were used to evaluate the predictive performance of the LSSVR. Additionally, its results were compared and analyzed with other soft sensors. For both case studies, notice that LSSVR gives the best results for AO, MB, and Cd (II) removals as compared to other soft sensor models where its root means square errors, mean absolute errors, and the approximate error, are lowered by 83% to 1,756%. Moreover, its coefficients of determination, denoted R 2 are the highest which are all more than or close to 0.9 for all the AO, MB, and Cd (II) removals even for the testing data for the case studies that were not used to develop the LSSVR model. In conclusion, LSSVR is more suitable for evaluating the effectiveness of the AO, MB, and Cd (II) removals at present.

L-Cysteine Functionalized Gold Nanoparticles as a Colorimetric Sensor for Ultrasensitive Detection of Toxic Metal Ion Cadmium

The toxic metal ion cadmium is known to be a widespread environmental contaminant and adversely affect human health. Exposure is largely via the respiratory or gastrointestinal tracts. Important non industrial sources of exposure are cigarette smoke and food (from contaminated soil and water). The kidney is the main organ affected by chronic Cd exposure and toxicity this has made us much more aware of the consequences of chronic environmental (or nonindustrial) exposure to heavy metal, and their impact on human health. Milk and dairy products can be contaminated in different ways. One of the most important and most challenging contaminations is due to heavy metals cadmium ions.. There are various ways to measure the amount of contamination in milk and dairy products. Therefore, reliable detection technique of metal ion levels in foods is essential for improving the public safety issues. In current investigation, we have developed l-cysteine modified gold nanoparticle (AuNPs) based colorimetric assays technique for detecting the toxic metal ion in food. It is a simple and low-cost alternative of spectroscopy based methods. Synthesized colloidal AuNPs possess intrinsically strong surface plasmon resonance (SPR) absorptions, with extremely high extinction coefficients, in the visible wavelength range. The extinction coefficient of the Au NPs and the wavelengths at which NPs absorb and scatter light depend on their shapes and sizes, the dielectric constant of their surrounding aqueous media, and their interactions with neighboring particles. We have synthesized small size L- cysteine AuNPs with dark red colour which has potent ability to aggregates with toxic metal ions and there is change in color. Red Au NPs change into deep blue. The aggregation of Au NPs was controlled by employing surface ligands that bind to target heavy metals ions in foods. When metal ions are introduced, it binds through the ligands of multiple Au NPs, which was caused due to uncontrolled aggregation and subsequent color change of the solution. The 24 nm spherical Au NPs were prepared by reduction of 1.0 mM HAuCl4.3H2O with sodium tri-citrate (38.8 mM). The average size of monodisperse AuNPs sizes (DLS and TEM) was 31 nm, which have given significant results

Bifunctional wood for electrocatalytic CO2 reduction to formate and electroanalytical detection of myricetin and cadmium (II)

In this work, we first discover the new bifunctional abilities of wood for highly selective electrocatalytic CO2 reduction to formate and highly sensitive electroanalytical detection of myricetin and cadmium (II). The highly developed microchannels in wood ensure most effective reactant and electrolyte transport, great facilitating the electrode reaction. The activated wood electrode displays excellent electrocatalytic CO2 reduction activity, attained the highest formate Faradaic Efficiency (FE) of 70.8% at −1.8 V with high current density of 53.8 mA cm−2 in aqueous solution, and displayed at least 24 h CO2 electrolysis durability. Furthermore, the wood is also first utilized as new electrode matrix for electroanalytical detection of drug (myricetin is as an example) and heavy metal ion (cadmium (II) is as an example). Compared with traditional glassy carbon electrode (GCE) and its derived modified electrodes, the wood electrode exhibits a wide linear detection range (0.01–50 μmol dm−3) and a low detection limit (0.002 μmol dm−3, S/N = 3) for myricetin, and displays a wide linear detection range (0.1–20 μg l−1) and a low detection limit (0.05 μg L−1, S/N = 3) for cadmium (II). These remarkable bifunctional performances of low cost wood electrode show great potential for large-scale using in CO2 electroreduction and electroanalytical detection.

Genes encoding hevein-like antimicrobial peptides WAMPs: Expression in response to phytohormones and environmental factors

We investigated the role of genes of hevein-like antimicrobial peptides of the WAMP family in the protection of wheat plants against biotic and abiotic stress. The semiquantitative RT-PCR method was used to examine the expression of wamp genes in wheat seedlings in response to infection by pathogens and exposure to phytohormones and ions of a heavy metal ion—cadmium. We discovered that wheat germ contamination by harmful fungi significantly increases expression of genes of the wamp family, and the primary transcript is wamp-2. We determined that salicylic acid, rather than methyl jasmonate, induces expression of genes of the wamp family. We showed that abiotic stress induced by cadmium ions inhibits expression of wamp genes in the roots with no effect on their expression in shoots. The results support the protective role of wamp genes in the response of wheat plants to infections by pathogens. In turn, the resistance to abiotic stress induced by cadmium ions does not appear to be associated with expression of genes of the wamp family.

Development of cadmium specific recombinant biosensor and its application in milk samples

A novel and highly specific recombinant biosensor has been investigated for detection of highly toxic metal ion cadmium (Cd(II)) based on Escherichia coli DH5α (pNV12). The working principle of biosensor is based on the expression of gfp gene under the control of cad promoter and the cadC gene of Staphylococcus aureus plasmid pI258. Escherichia coli DH5α (pNV12) was tested for its response in the presence of different combinations of Pb(II), Cd(II) and Zn(II) ions. The investigation resulted in the development of a cadmium specific recombinant whole cell biosensor with a response time as low as 15min. A good linear range for cadmium ion concentrations of 10–50μg/l with R2 0.9946 was obtained and the detection limit of 10μg/l. Further, we reduced the detection limit up to 5μg/l by increasing the incubation time from 15 to 30min. High throughput microarray techniques for testing of 48 samples simultaneously has also been developed with reaction volume miniaturized from 2000μl to 200μl. The developed biosensor was applied to detect cadmium ion concentration in milk samples collected from different areas of Punjab, India. Two samples collected from industrial areas, shown to have cadmium concentration above permissible limits (10μg/l).

Live and Let Die: Roles of Autophagy in Cadmium Nephrotoxicity.

The transition metal ion cadmium (Cd2+) is a significant environmental contaminant. With a biological half-life of ~20 years, Cd2+ accumulates in the kidney cortex, where it particularly damages proximal tubule (PT) cells and can result in renal fibrosis, failure, or cancer. Because death represents a powerful means by which cells avoid malignant transformation, it is crucial to clearly identify and understand the pathways that determine cell fate in chronic Cd2+ nephrotoxicity. When cells are subjected to stress, they make a decision to adapt and survive, or—depending on the magnitude and duration of stress—to die by several modes of death (programmed cell death), including autophagic cell death (ACD). Autophagy is part of a larger system of intracellular protein degradation and represents the channel by which organelles and long-lived proteins are delivered to the lysosome for degradation. Basal autophagy levels in all eukaryotic cells serve as a dynamic physiological recycling system, but they can also be induced by intra- or extracellular stress and pathological processes, such as endoplasmic reticulum (ER) stress. In a context-dependent manner, autophagy can either be protective and hence contribute to survival, or promote death by non-apoptotic or apoptotic pathways. So far, the role of autophagy in Cd2+-induced nephrotoxicity has remained unsettled due to contradictory results. In this review, we critically survey the current literature on autophagy in Cd2+-induced nephrotoxicity in light of our own ongoing studies. Data obtained in kidney cells illustrate a dual and complex function of autophagy in a stimulus- and time-dependent manner that possibly reflects distinct outcomes in vitro and in vivo. A better understanding of the context-specific regulation of cell fate by autophagy may ultimately contribute to the development of preventive and novel therapeutic strategies for acute and chronic Cd2+ nephrotoxicity.

Cadmium affects focal adhesion kinase (FAK) in mesangial cells: Involvement of CaMK‐II and the actin cytoskeleton

The toxic metal ion cadmium (Cd(2+)) induces pleiotropic effects on cell death and survival, in part through effects on cell signaling mechanisms and cytoskeletal dynamics. Linking these phenomena appears to be calmodulin-dependent activation of the Ca(2+)/calmodulin-dependent protein kinase II (CaMK-II). Here we show that interference with the dynamics of the filamentous actin cytoskeleton, either by stabilization or destabilization, results in disruption of focal adhesions at the ends of organized actin structures, and in particular the loss of vinculin and focal adhesion kinase (FAK) from the contacts is a result. Low-level exposure of renal mesangial cells to CdCl2 disrupts the actin cytoskeleton and recapitulates the effects of manipulation of cytoskeletal dynamics with biological agents. Specifically, Cd(2+) treatment causes loss of vinculin and FAK from focal contacts, concomitant with cytoskeletal disruption, and preservation of cytoskeletal integrity with either a calmodulin antagonist or a CaMK-II inhibitor abrogates these effects of Cd(2+). Notably, inhibition of CaMK-II decreases the migration of FAK-phosphoTyr925 to a membrane-associated compartment where it is otherwise sequestered from focal adhesions in a Cd(2+)-dependent manner. These results add further insight into the mechanism of the CaMK-II-dependent effects of Cd(2+) on cellular function.

Metal Ion Substrate Inhibition of Ferrochelatase

Ferrochelatase catalyzes the insertion of ferrous iron into protoporphyrin IX to form heme. Robust kinetic analyses of the reaction mechanism are complicated by the instability of ferrous iron in aqueous solution, particularly at alkaline pH values. At pH 7.00 the half-life for spontaneous oxidation of ferrous ion is approximately 2 min in the absence of metal complexing additives, which is sufficient for direct comparisons of alternative metal ion substrates with iron. These analyses reveal that purified recombinant ferrochelatase from both murine and yeast sources inserts not only ferrous iron but also divalent cobalt, zinc, nickel, and copper into protoporphyrin IX to form the corresponding metalloporphyrins but with considerable mechanistic variability. Ferrous iron is the preferred metal ion substrate in terms of apparent k(cat) and is also the only metal ion substrate not subject to severe substrate inhibition. Substrate inhibition occurs in the order Cu(2+) > Zn(2+) > Co(2+) > Ni(2+) and can be alleviated by the addition of metal complexing agents such as beta-mercaptoethanol or imidazole to the reaction buffer. These data indicate the presence of two catalytically significant metal ion binding sites that may coordinately regulate a selective processivity for the various potential metal ion substrates.

Synthesis, crystal structure and DNA cleavage activity of a novel Ni(II)–Cd(II) coordination polymer

A novel one-dimensional heterometallic complex, {Cd 2[NiL] 2(SCN) 4(H 2O)} n ( 1), has been synthesized and characterized by single-crystal X-ray analysis, where L is dianion of 2,3-dioxo-5,6,13,14-dibenzo-9,10-cyclohexyl-7,12-bis(ethoxycarbonyl)-1,4,8,11-tetraazacyclotetradeca-7,11-diene. The most striking feature of 1 is that in the structure there is one type of S–S bond (1.823(13) Å) formed by two thiocyanate groups which has not been reported to our knowledge. The DNA cleavage activity of 1 in the presence of H 2O 2 was compared with those of nickel(II) ion, cadmium(II) ion and corresponding mononuclear precursor NiL ( 2). The DNA cleavage kinetics was studied and the corresponding activation parameters of 1 were obtained.

The role of dihydropyridine-sensitive voltage-gated calcium channels in potassium-mediated neuronal survival

The survival of isolated neurons from chick embryo ciliary, sympathetic, and dorsal root ganglia is greatly enhanced by concentrations of extracellular potassium that significantly depolarize the neurons (ED 50 = 20–25mM). The survival-promoting effect of elevated potassium on each of these 3 types of neurons appears to be the result of the opening of voltage-gated calcium channels. The dihydropyridine, Bay K 8644, which increases calcium influx through L-type voltage-gated calcium channels in neurons, strongly potentiated the survival-promoting action of elevated potassium (ED 50 = 10.8 ± 7.0mM). In contrast, chemically closely related dihydropyridines, PN200-110 (ED 50 = 0.33 ± 0.15nM) and nitrendipine (ED 50 = 1.3 ± 0.3nM), which block calcium influx through the same voltage-gated channels, completely inhibited potassium-mediated neuronal survival. Chemically different agents that also block calcium influx through voltage-gated channels also inhibited potassium-mediated neuronal survival: the phenylalkylamine verapamil (ED 50 = 0.78 ± 0.38 μM), the benzothiazepine diltiazem (ED 50 = 1.7 μM), and the inorganic ion cadmium (ED 50 = 5.8 μM). These calcium-channel blockers are not simply toxic to neurons, since they did not inhibit neuronal survival mediated by the neurotrophic proteins, nerve growth factor, basic fibroblast growth factor, or ciliary neurotrophic factor, also suggesting that voltage-gated calcium channels are not involved in the action of these factors. These results suggest that neuronal survival in elevated potassium in ciliary, sympathetic, and dorsal root ganglion neurons is the result of calcium influx through dihydropyridine-sensitive, L-type voltage-gated calcium channels. These findings are discussed in relation to the neuronal toxicity of excitatory amino acids which is also thought to occur through increased calcium influx.