Cd Chloride Research Articles

Anion-pairing effect in Cd(II) coordination with a tetrabenzotetraza-crown macrocyclic ligand

Three new complexes of a tetrabenzotetraza-crown ether macrocyclic ligand (L) with Cd(II) chloride (1), iodide (2), and acetate (3) salts were synthesized and characterized by FT-IR, 1H NMR spectroscopy, elemental microanalysis, and single crystal X-ray diffraction. Complex 1 has the formula [Cd(L)Cl]2 [CdCl4] with two square pyramidal [Cd(L)Cl]+ subunits interconnected through the CdCl42− counter anion. Meanwhile, the reaction with CdI2 produces the discrete complex [Cd(L)I]I (2) with an octahedral geometry about the Cd(II) center. A distorted six-coordinated asymmetric unit was observed for [Cd(L)OAc]2(OAc·H2O)2 (3), wherein two [Cd(L)OAc]+ subunits are held together by a flat (OAc·H2O)2 acetate-water cluster. Hirshfeld Surface calculations were applied to confirm the dominant interactions in 1–3, namely π–π, and X⋯H/H⋯X (X-H, C, O, and halogen) interactions as the main factors for their structural differences. At the same time, the structure of [Cd(L)L′]+ (L′ = Cl, I, and OAc) core remained almost unchanged. The Cd(II) coordination with L in the presence of different Cd(II) salts was followed by 1H NMR spectroscopy. All three Cd(II) salt displays 1:1 stoichiometry, with binding constants in the order CdCl2 < CdI2 < Cd(OAc)2.

Prenatal double-hit with aluminium and cadmium mediate testicular atrophy and hypothalamic hypoplasia: the role of oxido-nitrergic stress and endocrine perturbations.

There is limited experimental evidence on the biochemical consequences of aluminium (Al) and cadmium (Cd) co-exposures during pregnancy and postnatal life.This study investigated the impacts of perinatal Al chloride (AlCl3) and Cd chloride (CdCl2) co-exposures on neuroendocrine functions in mice offspring during postnatal life. The study comprised of four pregnant experimental groups. Group 1 received AlCl3 (10mg/kg), group 2 were administered CdCl2 (1.5mg/kg), while group 3 received both AlCl3 (10mg/kg) and CdCl2 (1.5mg/kg) (AlCl3+CdCl2), and group 4 received saline (10mL/kg) only and served as control group. All experimental animals were chemically exposed once daily from gestation days 7-20. Upon delivery, male pups were regrouped based on maternal chemical exposure on postnatal day 21 (PND 21) and allowed to grow to adulthood until PND 78, after which they were sacrificed for assessment of neuroendocrine markers and histological investigations. There was no statistical significance (p > 0.05) on follicle stimulating hormone, testosterone, estrogen and progesterone, thyroid stimulating hormone, thyroxine (T4) in all treatment groups relative to controls|. However, AlCl3 and AlCl3-CdCl2 significantly (p < 0.05) reduced triiodothyronine (T3) levels, with a profound increase in T3:T4 ratio by AlCl3, and AlCl3+CdCl2 compared to control. Furthermore, pups from pregnant mice treated with CdCl2 and AlCl3+CdCl2 demonstrated increased testicular malondialdehyde concentration with increased catalase activity relative to controls, suggesting oxidative imbalance. In addition, AlCl3, CdCl2, and AlCl3+CdCl2 exposures induced testicular and hypothalamic architectural disruption compared to controls, with marked architectural derangement in the AlCl3+CdCl2 group. Our findings suggest that prenatal co-exposures to Alcl3 and CdCl2 induce testicular and hypothalamic alterations in offspring via a testicular oxidative stress and thyrotoxicosis-dependent mechanisms.

Roles of Cyt-c/Caspase-9/Caspase-3/Bax/Bcl-2 pathway in Cd-induced testicular injury in rats and the protective effect of quercetin

Cadmium (Cd) exposure causes oxidative damage to mitochondria, which would adversely affect rat testicular tissue. Quercetin (Que) is a natural antioxidant with anti-inflammatory, antioxidant and anti-apoptotic effects. However, the mechanism by which Que inhibits Cd-induced apoptosis of testicular cells remains unclear. The purpose of this study was to investigate the role of mitochondrial apoptosis pathway (Cyt-c/Caspase-9/Caspase-3/Bax/Bcl-2 pathway) in inhibiting Cd-induced apoptosis of testicular cells by Que. We used SD rats to simulate Cd chloride exposure by treating all sides of the rats with CdCl2 and/or Que. The levels of GSH and MDA in rat testis were detected using reagent kits. The effects of CdCl2 and/or Que on tissue damage, apoptosis, and gene and protein expression of the Cyt-c/Caspase-9/Caspase-3/Bax/Bcl-2 pathway in rat testis were examined by HE, TUNEL, RNA extraction and reverse-transcriptase polymerase chain reaction (RT-PCR), and Western blot (Wb). The results show that Cd significantly increased the contents of GSH and MDA in rat testis (P < 0.01); conversely, Que significantly reduced the contents of GSH and MDA (P < 0.01). Cd inflicted damage to testicular tissue, and Que addition significantly reduced the damage. Cd increased the number of apoptosis of testicle cells, and Que inhibited testicle-cell apoptosis. In addition, the results of reverse transcription PCR and Wb assays confirmed that, as expected, Cd increased the expression levels of Cyt-c, Caspase-9, Caspase-3, and Bax mRNAs as well as proteins. And at the same time decreased the expression of the anti-apoptotic factor Bcl-2 in the cells. Surprisingly, these effects were reversed when Que was added. Therefore, Que can play an antioxidant and anti-apoptotic role in reducing the testicular tissue damage caused by Cd exposure. This provides a conceptual basis for the later development and utilization of Que as well as the prevention and treatment of tissue damage caused by Cd exposure.

Effects of cadmium on liver function in turtle Mauremys reevesii.

This research was designed to investigate the effects of cadmium (Cd) on liver function in turtle Mauremys reevesii. Turtles were divided into 4 groups at random. The turtles were injected intraperitoneally with Cd at 0, 7.5, 15, 30mgkg-1 Cd chloride separately. Liver index was calculated. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and the content of TP in liver were examined with biochemical methods. The results indicated that the liver index of turtles changed obviously only at higher dose and longer time. The activities of ALT and AST in liver increased with prolongation of exposure time in a dose-dependent manner. TP content in liver was lower than that in the control. In summary, Cd had an obvious toxic effect on liver tissues of freshwater turtle Mauremys reevesii, and it was dose dependent with the extension of exposure time. But the results also showed that the turtle had strong tolerance to Cd.

Individual and combined effects of cadmium and lead exposure in rats

ABSTRACT The exposure of humans and animals to environmental compounds is rarely restricted to a single chemical. Cadmium (Cd) and lead (Pb) are two heavy metals known to be the most toxic. Deleterious effects of each metal alone are well documented. Unfortunately, very few studies were conducted to determine their combined effect. Four groups of Wistar rats were treated intravenously for 15 days. The control group received physiological saline solution; groups 2 and 3 were treated with Cd chloride and lead acetate, respectively ; and the treatment group 4 received a combined treatment of Cd and Pb . A significant decrease was recorded for hematological parameters , with an increase in white blood cells and an inhibition in δ-ALAD level. Cell injury in the livers and kidneys was clearly shown by the significant elevation of the biochemical markers. Cd and Pb induced oxidative stress and had adverse health effects at lower exposure levels than previously thought.

An aqueous extract of Prunella vulgaris L. ameliorates cadmium-induced bone loss by promoting osteogenic differentiation in female rats.

Cadmium (Cd) causes bone loss, concerning inhibiting osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). Prunella vulgaris L. (PV) has the potential for promoting osteogenic differentiation, but its influence on Cd-induced bone loss is unclear. This study investigated the effect of PV aqueous extract (PVE) on Cd-induced bone loss and its underlying mechanisms. Eight-week-old female SD rats were randomly assigned into four groups and treated for 16 weeks: Control, Cd (50mg/L of Cd chloride), Cd+PV Low (125mg/kg bw of PVE), and Cd+PV High (250mg/kg bw of PVE). PV ameliorated femoral bone loss in Cd-treated rats manifested as increases in bone mineral density, bone volume, trabecular thickness, number, and area, and decreases in trabecular separation. Compared with Cd group, PV-treatment groups had higher serum levels of bone formation markers (ALP, BGP). Additionally, in PV-treatment groups, expressions of bone formation markers (Osterix, Runx2) and molecules involved in osteogenic differentiation signal pathway BMP/Smad (BMP4, Smad1/5/9) in the tibia of rats and isolated rat primary BMSCs were upregulated. These results suggest that PV alleviates Cd-induced bone loss by promoting osteogenic differentiation, which is likely associated with BMP/Smad pathway.

Cadmium influence on lipid metabolism in Sprague-Dawley rats through linoleic acid and glycerophospholipid metabolism pathways.

Cadmium (Cd) is widely distributed in the environment and easy adsorbed by living organisms with adverse effects. Exposure to Cd-contaminated food may disrupt lipid metabolism and increase human health risk. To study the perturbation effect of Cd on lipid metabolism in vivo, 24 male Sprague-Dawley (SD) rats were randomly assigned four groups and treated by Cd chloride solution (0, 1.375 mg/kg, 5.5 mg/kg, 22 mg/kg) for 14 days. The characteristic indexes of serum lipid metabolism were analyzed. Afterwards, untargeted metabolomics analysis was applied to explore the adverse effects of Cd on rats by liquid chromatography coupled with mass spectrometry (LC-MS). The results revealed that Cd exposure obviously decreased the average serum of triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) and caused an imbalance of endogenous compounds in the 22 mg/kg Cd-exposed group. Compared with the control group, 30 metabolites with significant differences were identified in the serum. Our results indicated that Cd caused lipid metabolic disorders in rats by disrupting linoleic acid and glycerophospholipid metabolism pathways. Furthermore, there were three kinds of remarkable differential metabolites-9Z,12Z-octadecadienoic acid, PC(20:4(8Z,11Z,14Z,17Z)/0:0), and PC(15:0/18:2(9Z,12Z)), which enriched the two significant metabolism pathways and could be the potential biomarkers.

Antitoxic Principles from Moringa oleifera (Mo11) and Musa sapientum (Ms06) Ameliorated Cadmium Chloride-Induced Renal Hyperplasia and Apoptosis through Ki67/P53-Mediated Pathway in Rats

Background: Cadmium (Cd) is an established carcinogen. Cd-induced renotoxicity resulted in oxidative stress, loss of excretory kidney functions, and apoptosis of murine kidney cells. Objectives: This study evaluated renoprotective potentials of MO11 (isolated from Moringa oleifera leaves) and MS06 (isolated from Musa sapientum suckers) against Cd chloride (CdCl2)-induced renotoxicity, renal hyperplasia, and apoptosis in rats. Materials and Methods: Twenty-four adult male Wistar rats (average weight of 155 g) were randomly divided into seven groups (n = 4). Group 1 received physiological saline. Groups 2–4 and 6 received single intraperitoneal (i.p) administration of 1.5 mg/kg body weight of CdCl2 (i.p) (Day 1). Groups 3–4 and 6 were posttreated with 15 mg/kg body weight of MO11, 15 mg/kg body weight of MO11 +7 mg/kg body weight of MS06, and 3.35 mg/kg body weight of doxorubicin, respectively (days: 1–17). Group 5 received only olive oil dose (vehicle), respectively (days: 1–17). Kidney histopathology (hematoxylin and eosin technique) and enzyme-linked immunosorbent assay concentrations of biomarkers of proliferation (Ki67) and apoptosis (p53) in kidney homogenates of rats of Groups 1–6 were evaluated. Results: Histopathological analyses showed normal kidney histology in the rats of Groups 1–6. Posttreatments of CdCl2-induced renotoxicity with MO11, MO11+MS06, and doxorubicin resulted in downregulations of Ki67 and p53 in Groups 3, 4, and 6 as compared with Group 2. Conclusion: MO11 and MS06 possess renoprotective, anti-proliferation, and anti-apoptosis potentials.

GPX4 utilization by selenium is required to alleviate cadmium-induced ferroptosis and pyroptosis in sheep kidney.

Cadmium (Cd), a persistent and harmful heavy metal in the environment, can accumulate in the kidneys and cause nephrotoxicity. Selenium (Se) is a beneficial natural element that alleviates the toxicity of Cd. To ascertain the relationship between the protective mechanism of Se against Cd nephrotoxicity and ferroptosis and pyroptosis, we randomly divided 48 sheep into four groups and treated them with Cd chloride and/or sodium selenite for 50 days. The data confirmed that Cd apparently resulted in impaired kidney histology and function, depletion of GSH and nicotinamide adenine dinucleotide phosphate contents and CAT and SOD activities, elevation of MDA level, as well as the reduction in selenoprotein mRNA (GPX1, GPX4, TXNRD1, SELP) levels and GPX4 protein level and immunofluorescence intensity. Meanwhile, Cd induced ferroptosis by causing iron overload, up-regulating PTGS2, NCOA4, TFR1, and LC3B mRNA levels and PTGS2 and LC3B-II/LC3B-I protein levels, reducing SLC7A11 and FTH1 mRNA and protein levels, and enhancing the immunofluorescence co-localization of FTH1/LC3B. Moreover, it was also found that Cd triggered pyroptosis, which was evidenced by the increase of NLRP3 immunohistochemical positive signal, GSDMD-N immunofluorescence intensity, IL-1β and IL-18 release and the levels of pyroptosis-related mRNA (NLRP3, ASC, Caspase-1, GSDMD, IL-1β and IL-18) and proteins (NLRP3, Caspase-1p20, GSDMD-N, IL-1β and IL-18). Notably, Se increased the expression level of GPX4 and the transcription factors TFAP2c and SP1, and ameliorated Cd-induced changes in aforementioned factors. In conclusion, GPX4 utilization by Se might be required to alleviate Cd-induced ferroptosis and pyroptosis in sheep kidney.

The traditional Chinese medicine Qiangjing tablet prevents blood-testis barrier injury induced by CdCl2 through the PI3K/Akt/Rictor signaling pathway.

Environmental contaminants such as cadmium (Cd) may have a deleterious impact on sperm and reduce male fertility by compromising the blood-testis barrier (BTB). Hence, the effects of the traditional Chinese medicine Qiangjing tablet (QJP) on sperm quality and BTB alterations induced by Cd in mouse testes were examined. Adult KM mice challenged with Cd chloride were examined, QJP was administered to mice as an oral drug by gavage, and the experiments lasted 2 weeks. Testicular and epididymal weights, sperm quality, anti-sperm antibodies (AsAb), hormone levels, and histology were evaluated. Changes in the levels of N-cadherin, occludin, ZO-1, claudin-11, F-actin, and β-tubulin and their mRNAs were evaluated. The effects of QJP on the PI3K/Akt/Rictor pathway were evaluated. CdCl2 decreased reproductive organ weight, sperm quality, and testosterone (T) levels; increased AsAb, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) levels; induced structural damage in testicles with BTB disruption; increased BTB permeability; and decreased N-cadherin, occludin, ZO-1, claudin-11, F-actin, and β-tubulin expression. After treatment, QJP blocked the effects of Cd on reproductive organ weight, sperm quality, and T; mitigated germinal epithelium compartment alterations; decreased AsAb, FSH, and LH levels; and preserved BTB ultrastructure and function. In addition, QJP induced increases in N-cadherin, occludin, ZO-1, claudin-11, F-actin, and β-tubulin levels and the expression of their mRNAs through the PI3K/Akt/Rictor pathway. After the application of JRAB2011, the levels of a specific mTORC2 suppressor, Rictor, and the BTB-protective effect of QJP were greatly reduced. We demonstrated the effect of QJP against Cd-induced damage to the BTB, and the results indicate that QJP may play a significant role in opposing the effects of Cd through the PI3K/Akt/Rictor pathway.

Evaluation of the Potential Protectivity of Both Allium sativum and Zingiber officinale on the Cadmium-Induced Testicular Damage in Rats.

Cadmium (Cd) is a widely spread environmental pollutant, listed among the unsafe metals due to known toxic effects on multiple organs, including the testes. In this study, we aim to evaluate the potential protectivity of garlic and ginger extracts on Cd-induced damage of the testis in rats. Fifty-six adult male albino rats were alienated into seven groups; control group, garlic-treated group, and ginger-treated group were given garlic and ginger extracts at doses of 250 mg and 120 mg/kg b.wt/day, Cd-treated group received 8.8 mg/Kg b.wt/day of Cd chloride, and the protected groups were given Cd and co-treated with garlic, ginger, or both extracts. The testes were subjected to different procedures to assess the oxidative status and histopathological changes. Cd-treated rats showed a significant reduction in the testis weight and morphometric measurements of the seminiferous tubules compared to the control group. Cd administration resulted in a marked drop in the testosterone level and activities of antioxidative enzymes. Moreover, Cd induced histopathological changes in the seminiferous tubules. Co-administration of garlic and ginger extracts with the Cd showed partial improvement in the investigated parameters toward the control figures and improvement in the morphological changes. Co-treating both extracts together and the Cd resulted in complete normalization of these adverse effects of Cd. These findings indicated that garlic and ginger extracts could ameliorate the harmful effects of Cd on the testis. This effect was more prominent when garlic and ginger extracts were co-administered together with Cd.

JAK2/STAT3 Signaling Pathway and Klotho Gene in Cadmium-induced Neurotoxicity In Vitro and In Vivo.

Cadmium (Cd), a common heavy metal in the environment, is associated with cognitive impairment. In the present study, we carried out a preliminary inquiry to explore whether Cd causes neurotoxicity by regulating the JAK2/STAT3 signaling pathway and affecting the expression of klotho genes in vivo and in vitro, providing clues for the mechanism of Cd-induced cognitive dysfunction. The rat samples were injected with Cd chloride solution for 14weeks, and the memory function of the rats was detected. Different concentrations of Cd and JAK2/STAT3 signaling pathway inhibitors were used to treat PC12 cells and thus detect the apoptosis rate. The protein expression levels of JAK2, p-JAK2, STAT3, p-STAT3, and klotho in rat and PC12 cell were detected by ELISA and Western blot, respectively. With the increase in exposure dose, the memory function of rats was severely impaired. The expression of p-JAK2 and p-STAT3 proteins was significantly up-regulated, whereas that of klotho was significantly down-regulated both in vivo and in vitro (p < 0.05). In comparison with the high-dose Cd exposure group, after adding tyrphostin AG490 (AG490), the apoptosis rate of PC12 cells increased, whereas the phosphorylation levels of JAK2 and STAT3 in the cells decreased significantly (p < 0.05). Cd exposure may cause neurotoxicity by regulating the JAK2/STAT3 signaling pathway and down-regulating klotho protein expression, leading to cognitive dysfunction.

Rapid Accumulation of Cadmium and Antioxidative Response in Tobacco Leaves

Background: Cadmium (Cd) is one of the most dangerous environmental pollutants. Plant damage caused by oxidative stress during long-term Cd accumulation is well documented, while the primary response to Cd uptake is poorly understood. Objective: We assess the short-term injury and the primary reaction of the antioxidant system to the rapid accumulation of Cd in tobacco leaves. Methods: Leaf rosettes of the 5-week-old plants without roots were exposed to 100, 500 and 5000 μM Cd chloride for 2 and 12 hours. Cd accumulation, oxidation levels of proteins and lipids, content of reduced (Asc) and oxidized (DHA) ascorbate and activity of CAT, APX and POD were determined. Results: An accumulation of Cd in high concentration, but only a relatively small increase in the oxidation of proteins and lipids was found in the leaves after 2 hours of treatment. These effects were transient and disappeared after 12 hours. No visible damage to plants was observed. After 12 hours, the total ascorbate content (Asc + DHA) decreased by 18%, remained unchanged or increased by 85% after the application of 100, 500 and 5000 µM Cd chloride. The increase in the ascorbate pool, which should be considered as a component of the protective response, was caused by the accumulation of DHA. The activity of APX and POD remained unchanged, while that of CAT decreased, indicating that antioxidant enzymes activation is not involved in the primary response to Cd. Conclusions: The primary generation of ROS induced by Cd does not appear to be a deleterious manifestation of Cd toxicity, but rather a component of stress signaling that causes activation of the protective response. Uptake of Cd caused severe damage to the plant after long-term, but not after short-term treatment, suggesting that the damage is the result of secondary effects of Cd toxicity.

Metabolomics analysis of the effects of quercetin on Cd-induced hepatotoxicityin rats

Cadmium (Cd) is known to cause damage to the liver. In this study, metabolomics technology was used to investigate the effect of quercetin (QE) on Cd-induced hepatotoxicity. A total of 60 male SD rats were randomly divided into the following six groups: control group (C), low and high-dose QE group (Q1: 10 mg/kg·bw, Q2: 50 mg/kg·bw), Cd group (D), low and high-dose QE and Cd combined intervention group (DQ1, DQ2). The rats were given Cd chloride (CdCl2) at a concentration of 40 mg/L through free drinking water. After 12 weeks of treatment, liver samples of rats were collected for metabonlomic analysis. A total of 12 metabolites were identified, the intensities of PC (18:0/14:1(9Z)) and arachidonate acid were decreased in the Cd-treated group (p < 0.01), whereas the intensities of chenodeoxyglycocholic acid, cholic acid, taurochenodesoxycholic acid, glycocholic acid, prostaglandin D2, 15-deoxy-d-12,14-PGJ2, oxidized glutathione, cholesterol, protoporphyrin IX, bilirubin were increased significantly in the Cd-treated group compared with group C (p < 0.01). When rats were given high doses of QE and Cd at the same time, the intensity of the above metabolites was significantly restored in group DQ2. Results suggest that the protective effect of QE on Cd-induced liver injury is associated with antioxidant activity of QE, as well as QE can regulates hepatic bile acid metabolism by affecting FXR and BSEP, and regulates AA metabolism by inhibiting Cd-induced activities of COX-2 and PLA2.

The protective effects of chitosan oligosaccharide (COS) on cadmium-induced neurotoxicity in Wistar rats

The aim of the study was to investigate the influence of chitosan oligosaccharide (COS) on some antioxidant and cytokine levels in the rat hippocampus as well as synaptophysin (SYP) immunoreactivity in the cerebral cortex of the cadmium (Cd) exposed rats. Thirty-two male albino Wistar rats were divided randomly into four equal groups as control (C; n = 8), Cd (n = 8), COS (n = 8), and Cd + COS (CdCOS; n = 8). The rats in the Cd and CdCOS groups received Cd chloride (CdCl2) (2 mg/kg/d) orally by gastric gavage three times a week for 4 weeks. Besides, COS (200 mg/kg/d) was administered to COS and CdCOS groups five times a week for 4 weeks. Then, they were decapitated and hippocampal/cerebral cortex tissue samples were taken for measurement of GSH levels, CAT and SOD activities, MDA values, TNF-α, IL-6, and IL-10 levels as well as SYP immunoreactivity. Although tissue GSH levels were determined the lowest in the Cd group, these values were attenuated with COS treatment in the CdCOS group (p < .01). In addition, TNF-α levels were alleviated by COS treatment in the CdCOS group when compared to Cd (p < .01). SYP-positive cells were investigated in the cerebral cortex and found mild in the CdCOS group. COS exhibits potential protective effects on Cd-induced neurotoxicity in rats.

Responses of Soil Cadmium Desorption under Different Saline Environments and Its Controlling Factors

Heavy metal pollution of soil restricts the sustainable use of land and poses risks to human health throughout the world. Changes in the physicochemical properties of soil may increase the mobility of heavy metals in the soil ecosystem and lead to groundwater pollution. In this study, the effects of different salt solutions (NaCl, CaCl2, NaNO3, MgCl2, Na2SO4, and mixed salts) on the release of Cd from soil were investigated by batch desorption tests and the Freundlich isothermal sorption model. Increased concentrations of the salts, except for NaNO3, significantly promoted Cd release (R2 &gt; 0.9, p &lt; 0.01). Under the salt stress, Cd release from the test soils was promoted more by CaCl2 and MgCl2 than by the other salts, and the average desorption rates of eight soil samples at 3.5% salt concentration were 11.15% and 10.80%, respectively, which were much higher than those of NaCl (4.05%), Na2SO4 (0.41%), and NaNO3 (0.33%). Ca2+ and Mg2+ showed better ion exchange capacity than Na+ to promote Cd release; for anions, Cl− formed hydrophilic Cd chloride complexes with Cd in soil. In addition, principal component analysis results revealed that Cd release was mainly influenced by soil texture, cation exchange capacity, and iron–manganese oxide content of the soil. The Cd release level for different soil samples was most closely related to the proportion of fine particles in the soil. The higher the clay content was, the higher the Cd desorption rate.

Cadmium exposure promotes activation of cerebrum and cerebellum ferroptosis and necrosis in swine

Cadmium(Cd) is a toxic and carcinogenic heavy metal pollutant leading to serious damage in various organs. Ferroptosis and necrosis as inflammation-related cell death are involved in several diseases of nervous system. In the present study, 10 weaning piglets with similar weight for 6 weeks were randomly divided into two groups. The daily grain containing 0 mg and 20 mg/kg of Cd chloride was fed in 20–26 ℃ environment, animals were sacrificed to collect cerebrum and cerebellum tissues after 40 days. Morphology and ultrastructure results were observed using HE and TEM. Moreover, molecular biological technologies western blot and qRT-PCR were used to detect the expression abundance of genes. Cerebrum and cerebellum injury was observed in Cd-exposed group, antioxidant capacity decreased significantly and oxidative stress increased; immunofluorescence, real-time quantification, and western blot results showed decreased necrosis genes and increased ferroptosis pathway genes abundance in cerebrum, whereas the results were reversed in cerebellum. These results indicated that Cd exposure can activated necrosis and ferroptosis pathways by increased oxidative stress, further resulting in cerebrum and cerebellum damage in pigs. These findings may provide a theoretical basis for early monitoring of Cd exposure in environment.

TRAF2/ASK1/JNK Signaling Pathway Is Involved in the Lung Apoptosis of Swine Induced by Cadmium Exposure.

Cadmium (Cd), a toxic heavy metal, exists widely in the environment, which can enter organisms through a variety of ways and cause damage to various organs and tissues. However, the mechanism of lung toxicity in swine after Cd exposure is still unclear. To explore the molecular mechanism of swine lung damage caused by Cd exposure, we established the model of Cd exposure, and Cd chloride (20mg/kg CdCl2) was added to the diet of swine for continuous exposure for 40days. TUNEL staining showed that the apoptosis of swine lung increased significantly after Cd exposure. Meanwhile, the results of qRT-PCR showed that Cd induced oxidative stress and inhibited the expression of antioxidant enzymes including CAT, GCLM, GST, SOD, and GSH-px in lung tissue. Cd exposure activated mitochondrial apoptosis pathway via the TRAF2/ASK1/JNK signaling pathway. In brief, we considered that Cd exposure causes oxidative stress in lung and induces lung cell apoptosis through the TRAF2/ASK1/JNK pathway and increases the expression of HSPs to resist the toxicity of Cd. Our research enriches the theoretical basis of Cd toxicity and provides reference for comparative medicine.

Cadmium exposure induces inflammation and necroptosis in porcine adrenal gland via activating NF-κB/MAPK pathway

Cadmium (Cd) is a heavy metal harmful to animals and humans. Cd exposure causes inflammation or necroptosis in many tissues, including adrenal tissue. However, the current researches on the effects of Cd2+ in adrenal tissues are not enough. Therefore, in our experiment Cd chloride (CdCl2) was added to the piglet's diet at a concentration of 20 mg/kg to study the effects of Cd2+ exposure on the porcine adrenal tissue. Our results showed that Cd2+ exposure could cause inflammation by activating the nuclear factor kappa-B (NF-κB) pathway, which in turn induced necroptosis in adrenal tissue with the activated mitogen-activated protein kinase (MAPK) pathway. The expression increase of inflammatory factors and necroptosis downstream genes, and the downregualtion of cysteinyl aspartate specific proteinase 8 (Caspase 8) proved that Cd2+ exposure caused inflammation and necroptosis in adrenal tissue. We conclude that this report provides more basic theoretical data for exploring the mechanism of adrenal injury.

Highly luminescent CdS nanoparticles synthesized using microwave irradiation of Dithiocarbazate ligand as a single molecular precursor source

In this paper, we have reported microwave-assisted synthesis of highly luminescent cadmium sulfide nanocrystals using dithiocarbazate Cd (II) chloride complex single-molecule precursor route. The precursors were heated using microwave irradiation to obtain CdS nanocrystals. The irradiation of precursor in DMSO environment played an important role in reducing reaction time, minimizing possibility of side reactions, and resulted in obtaining good quality particles. The obtained samples were analyzed using structural, morphological, and optical characterizations. X-ray diffraction studies confirm the hexagonal crystalline phase. High-resolution electron microscopy and transmission electron microscopy exhibit rod-shape structures with an average particle size of 80 nm. Sharp absorption edge at 320 nm indicates good quality of the particles. Strong luminescence peaks in the visible wavelength range 450–490 nm is observed in PL spectra. Another luminescence peak at 680 nm for excitation at 320 nm ensured the involvement of deep donor and acceptor levels in the crystals. The luminescence spectra show strong dependence on excitation wavelength which makes these particles suitable for various optoelectronic applications. The method reported here is a good candidate for obtaining large-scale high-quality CdS nanoparticles for optoelectronic applications.