Doses Of Cd Research Articles

Protecting Effects of N-acetyl Cysteine Supplementation Against Lead and Cadmium-Induced Brain Toxicity in Rat Models

We aimed to investigate mitigating effects of N-acetylcysteine (NAC) on the oxidative stress, apoptosis and Parkinson's disease (PD)-related genes in the brain tissue of male rats exposed to continuous doses of cadmium and lead. Rats were randomly divided into five groups, including G1 (control), G2 (continuous dose of Cd), G3 (continuous dose of Pb), G4 (continuous dose of Cd + NAC), and G5 (continuous dose of Pb + NAC). Biomarkers of oxidative stress, malondialdehyde (MDA), and total antioxidant capacity (TAC) were measured. Expression of PD- and apoptosis-related genes was considered using RT-PCR. Chronic exposure to these heavy metals was associated with accumulation of Pb and Cd in the brain and blood and caused severe morphological changes in the brain, as well as decreased body and brain weights. Continuous exposure to Cd and Pb significantly decreased TAC content and SOD expression but increased MDA level in the brain tissues (P < 0.001). A significant increase was observed in expression of PD-related genes, Parkin, Pink1, LRRK2, SNCA, and Caspase-3 in the brain tissues following exposure to Cd and Pb. Pb exhibited stronger toxicity on the brain tissue compared to Cd. NAC supplementation not only improved morphological changes, but also compensated antioxidant capacity and expression of apoptosis- and PD-related genes in the brain tissues when compared to rats exposed to Pb and Cd alone. Chronic exposure to Pb and Cd is strongly associated with accumulation of these heavy metals in the brain, morphological changes, antioxidants depletion, oxidative stress, and brain cells apoptosis. Changes in expression of PD-related genes indicate the higher risk of PD among individuals who are chronically exposed to these heavy metals. NAC can protect brain tissue against Pb and Cd toxicity by elevating antioxidants capacity, mitigating oxidative stress, apoptosis, and down-regulating of PD-related genes.

Cadmium-induced ultrastructural changes and apoptosis in the gill of freshwater mussel Anodonta woodiana.

This study investigated the acute toxicity of cadmium (Cd) to the freshwater mussel Anodonta woodiana. The freshwater mussels were exposed to five concentrations of Cd (0mg/L, 8.43mg/L, 16.86mg/L, 33.72mg/L, and 67.45mg/L) for up to 96h. The 24-h, 48-h, 72-h, and 96-h LC50 values for Cd were estimated as 562.3mg/L, 331.1mg/L, 182.0mg/L, and 134.9mg/L, respectively. Caspase-3, caspase-8, caspase-9, and Ca-ATPase activities; protein and H2O2 levels; DNA fragmentation; and ultrastructure of the gill were also investigated. The activities of caspase-3 and caspase-9 in mussels were increased by Cd in a dose-dependent manner, where higher doses of Cd (33.72mg/L and 67.45mg/L) significantly increased the enzyme activities compared to the controls (P < 0.05). The caspase-8 activity was significantly depressed by a low dose of Cd (8.43mg/L) but was clearly induced by higher doses of Cd (16.86mg/L, 33.72mg/L, and 67.45mg/L) (P < 0.05). The Ca-ATPase activity and H2O2 levels were elevated and reached maximum values under the medium dose of Cd (16.86mg/L). However, protein levels were decreased by Cd in an inverse dose-dependent manner. In the gills of the mussels, Cd treatment induced DNA fragmentation as demonstrated by DNA ladders observed via agarose gel electrophoresis. Moreover, ultrastructural alterations in gill cells of mussels treated with Cd (16.86mg/L and 67.45mg/L) for 96h were observed by electronic microscopy. The ultrastructure abnormalities were characterized by the following features: (1) a disordered arrangement and breaking off of microvilli of epithelial cells; (2) chromatin condensed near the nuclear membrane and the appearances of extremely irregular nuclei, some with a fingerlike shape and an unclear, swollen, invaginated, or ruptured nuclear membrane and apoptotic bodies; (3) swollen and vacuolating mitochondria, some with disintegrated or missing cristae; (4) a disintegrated rough endoplasmic reticulum containing different sizes of vesicles; and (5) shrinking and deformation of Golgi bodies with decreased vesicle numbers. Our results demonstrated that Cd could activate caspase-3, caspase-8, caspase-9, and Ca-ATPase; cause ultrastructural changes; and produce DNA fragmentation in the mussels investigated. Based on the information obtained through this study, it is reasonable to conclude that Cd can induce apoptosis in the gills of the mussels, eventually leading to tissue damage.

Effects of Cadmium Sulfate on the Brown Garden Snail Cornu aspersum: Implications for DNA Methylation.

An extensive literature exists regarding the cellular, physiological, and genetic effects of cadmium (Cd)—A highly toxic, but commonly used trace metal in modern industry. However, limited data are available on its epigenetic effects, especially for terrestrial sentinel invertebrates. We determined Cd retention, total DNA methylation, and the methylation status of 5′ end of the Cd-MT gene in the hepatopancreas of the brown garden snail, Cornu aspersum, fed Cd sulfate for four weeks. Bodyweight changes and survival were also measured. Hepatopancreas cadmium increased in a dose-dependent manner from the third-lowest dose onward, with very large amounts being found for the highest treatment group. However, no mortalities occurred, irrespective of dietary Cd dose. We identified significant genome-wide hypermethylation in specimens given the highest dose, which overlapped with a significant bodyweight decrease. The Cd-MT gene showed an unmethylated 5′ end of the Cd-MT gene and this status was not affected by cadmium exposure. Hepatopancreas DNA methylation is as sensitive as bodyweight to non-lethal concentrations of dietary Cd given as cadmium sulfate but less responsive than tissue accumulation. Such an exposure event, by contrast, does not affect the methylation status of the Cd-MT gene 5′ end.

Dual role of cadmium in rat liver: Inducing liver injury and inhibiting the progression of early liver cancer

The heavy metal cadmium (Cd) can induce damage in liver and liver cancer cells; however, the mechanism underlying its toxicity needs to be further verified in vivo. We daily administered CdCl2 to adult male rats at different dosages via gavage for 12 weeks and established rat liver injury model and liver cancer model to study the dual role of Cd in rat liver. Increased exposure to Cd resulted in abnormal liver function indicators, pathological degeneration, rat liver cell necrosis, and proliferation of collagen fibres. Using immunohistochemistry, we found that the area of GST-P-positive precancerous liver lesions decreased in a dose-dependent manner. Real-time quantitative polymerase chain reaction, western blot, immunohistochemistry, and transmission electron microscopy revealed that Cd induced mitophagy, as well as mitophagy blockade, as evidenced by the downregulation of TOMM20 and upregulation of LC3II and P62 with increasing Cd dose. Next, the expression of PINK1/Parkin, a classic signalling pathway protein that regulates mitophagy, was examined. Cd was found to promote PINK1/Parkin expression, which was proportional to the Cd dose. In conclusion, Cd activates PINK1/Parkin-mediated mitophagy in a dose-dependent manner. Mitophagy blockade likely aggravates Cd toxicity, leading to the dual role of inducing liver injury and inhibiting the progression of early liver cancer.

Potential role of L-glutamic acid in mitigating cadmium toxicity in lentil (Lens culinaris Medik.) through modulating the antioxidant defence system and nutrient homeostasis

Using phosphate fertilizers and wastewater as a source of irrigation and residuals from industries have considerably increased the level of cadmium (Cd) in soil which severely reduced the growth and yield of crop. L-glutamic acid (L-Glu), an amino acid, plays key roles in plant stress tolerance. Hence, the current study was conducted to determine the potential role of L-Glu pre-treatment in alleviating Cd-induced toxicity in lentil (Lens culinaris Medik.). Lentil seedlings were exposed to two doses of Cd (1 and 2 mM CdCl2) with or without 10 mM L-Glu pre-treatment. The results suggested that a high dose of Cd negatively affected the shoot dry weight, root dry weight, and photosynthetic pigments (chlorophylls and carotenoids). Furthermore, Cd stress induced severe oxidative damage, a reduction in catalase (CAT) activity and ascorbate (AsA) content, and accumulation of Cd in both the roots and shoots. Adding L-Glu protected the photosynthetic pigments of the lentil seedlings and thus improved the growth of the seedlings. In addition, L-Glu pre-treatment enhanced the ascorbate (AsA) content; increased the activity of enzymes such as catalase, ascorbate peroxidase, monodehydroascorbate reductase, and glutathione peroxidase. L-Glu was also reduced Cd uptake and translocation, which in turn alleviated the oxidative damage in the Cd-stressed seedlings indicated the potential role of this chemical. Results suggest that pre-treatment with L-Glu reduces Cd toxicity in lentil seedlings by inhibiting Cd accumulation and by reducing oxidative damage.

Enhanced removal of cadmium from water using bio-sorbents synthesized from branches and leaves of Capparis decidua and Ziziphus mauritiana

In this work, powdered adsorbents synthesized from branches and leaves of Capparis decidua (CDB) and Ziziphus mauritiana (ZML) are used for the remediation of potentially toxic cadmium (Cd(II)) ions from wastewater. The effects of various operating parameters such as adsorbent dosage, pH, temperature, contact time and initial concentration of cadmium on the adsorption process were evaluated. The maximum adsorption capacity of CDB and ZML was 248.62 mg/g and 235.65 mg/g, respectively, for Cd(II) ions at room temperature, when the optimum pH, adsorbent dosage, contact time and concentration of Cd(II) were 6.0, 0.1 g/100mL, 60 min and 249 mg/L, respectively. Kinetic studies revealed that the bio-sorption process follows a pseudo-second order model (R 2 = 0 . 999 ) for both employed sorbents. The equilibrium data were found to be in good agreement with Freundlich and Langmuir adsorption isotherm in the case of C. decidua and Z. mauritiana, respectively. Thermodynamic analysis revealed that Cd(II) adsorption onto both bio-sorbents was spontaneous and exothermic in nature. The prepared adsorbents also exhibited excellent regeneration potential with a minor loss in the adsorption capacities after six cycles. • Plant-based adsorbents were employed for the removal of Cd(II) ions from water. • The q m of CDB and ZML was 248.62 and 235.65 mg/g , respectively, for Cd(II) ions. • The adsorption process follows a pseudo-second order kinetic model (R 2 = 0.999). • The prepared adsorbents showed excellent regeneration potential up to six cycles.

N-Acetyl cysteine mitigates histopathological changes and inflammatory genes expressions in the liver of cadmium exposed rats.

This study aimed to consider the expression of Nrf2, NLRP3 and caspase 1 genes, as well as oxidative stress, and the protective role of N-acetyl cysteine (NAC) in the liver of rats treated with cadmium (Cd). Male rats were randomly divided into five groups including G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd + NAC), and G5 (continuous dose of Cd + NAC). Levels of malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured. Expression of Nrf2, NLRP3 and caspase 1 genes was considered using RT-PCR. NAC treatments significantly improved TAC, but decreased MDA values in rats that exposed to continuous dose of Cd (p<0.05). Exposure to continuous dose of Cd caused a significant decrease in Nrf2 expression by 2.46-fold (p<0.001), but enhanced expression of NLRP3 and Caspase 1 genes by 3.13-fold and 3.16-fold), respectively (p<0.001). Compared to rats that treated to continuous dose of Cd, NAC supplementation enhanced the expression of Nrf2 by 1.67-fold (p<0.001) and reduced the expression of NLRP3 and Caspase 1 genes by 1.39-fold (p<0.001) and 1.58-fold (p<0.001), respectively. Down-regulation of Nrf2 and overexpression of NLRP3 and caspase 1 seems to be one of the main mechanisms of Cd toxicity on liver tissue. NAC protects liver tissue against Cd-induced oxidative injuries via enhancement of Nrf2 expression and reduction of NLRP3 and caspase 1 genes.

Combined toxicity of zinc oxide nanoparticles and cadmium inducing root damage in Phytolacca americana L.

In recent years, nano-contamination in the soil environment has aroused concern. But it is still uncertain whether the interactions of nano- and metal-pollutants would have a combined toxic effect on plants. In this study, we investigated the effects of joint exposure to zinc oxide nanoparticles (ZnO NPs) and Cd on the root tissue of Phytolacca americana L. Spin-polarized density functional theory simulations assumed that the plant may undergo metal toxicity or acidosis upon joint exposure to ZnO NPs/Cd. Subsequently, experimental exposure of P. americana verified the combined toxic effects. The plant grew normally with a single treatment of ZnO NPs (500 mg/kg) or low doses of Cd (10 mg/kg). However, root growth was significantly inhibited with the combined treatments (up to 43% reduction); additionally, Cd ions were transported to the shoot, leading to shoot growth inhibition (translocation factor > 1). The antioxidant enzymes in the root (superoxide dismutase, peroxidase, and catalase) were highly activated to resist stress, accompanied by a greater than two-fold increase in thiobarbituric acid reactive substances. Corresponding to physiological indicators, biological transmission electron microscopy revealed severe damage to the root cells. Moreover, ZnO NPs/Cd accumulation was observed in the root cytoderm, which confirmed the toxicity of the combined effects. Our study provides insight into the potential combined toxicity of ZnO NPs and heavy metals in polluted environments, such as mining areas and electronic waste sites, and agricultural soils.

The role of microRNAs in regulating cadmium-induced apoptosis by targeting Bcl-2 in IEC-6 cells

Cadmium (Cd) is one of the most harmful environmental pollutants and has been found to have adverse effects on the gut. However, the toxic effects and potential mechanism of Cd on intestinal epithelial cells (IECs) are poorly understood. This study evaluated the effects of Cd exposure (0, 0.25, 0.5, 1, 2, and 4 μM) on IEC-6 cells in terms of cell viability and apoptosis, as well as apoptosis-associated gene expression. The results indicated that low doses (0.25– 1 μM) of Cd exhibited hormetic effects, while high doses of Cd (2 and 4 μM) reduced cell viability. The apoptotic effect increased in a dose-dependent pattern. Moreover, the mRNA levels of the Bcl-2, Bax and Caspase 3 genes were altered, which was in agreement with their protein expression. Based on sequencing analysis, the expression pattern of the microRNAs (miRNAs) changed significantly in the 2 μM Cd-treated group. QRT-PCR verified that 7 miRNAs, including miR-124-3p and miR-370-3p, were all upregulated with dose-effect relationship. Besides, transfection of miR-124-3p and miR-370-3p mimics /inhibitor and Bcl-2 siRNA into IEC-6 cells verified that these two miRNAs could regulate Cd-induced apoptosis by targeting Bcl-2. Finally, the direct targeting relationship between miR-370-3p and Bcl-2 gene was confirmed by luciferase reporter assay. Overall, the results demonstrated that Cd exposure could induce apoptosis in IEC-6 cells. The potential mechanism may be interference with the regulation of Bcl-2 gene expression by miR-370-3p and miR-124-3p

IMPACT OF CADMIUM TOXICITY ON LEAF AREA AND STOMATAL CHARACTERISTICS IN FABA BEAN

Although changes in stomatal response to elevated doses of cadmium has already been observed in several plants, few studies have focused on this phenomenon in more detail. The effects of different doses of cadmium Cd2+ (50 and 100 mg.kg-1 soil) on leaf area and stomatal characteristics (number of stomata, number of epidermal cells, stomatal index and size of stomata) of faba bean (Vicia faba L. cultivar Aštar) were studied after 15 days of heavy metal treatment. No visual changes on adaxial or abaxial side of leaves of the tested variety of faba bean were found. The leaf area was higher by 14.15 % at lower and by 12.23 % at the higher doses of Cd. The tested doses of Cd did not lead to a change in the number of stomata. The number of epidermal cells was increased on adaxial side by 4.98 % at dose Cd50. Stomatal index was decreased due to the effect of higher dose of cadmium by 11.38 % on adaxial side of leaves. In stomatal widths, decrease by 2.04 % (adaxial side) and 2.26 % (abaxial side) was observed at higher doses of Cd. In stomatal length decrease by 1.85 % was observed at higher dose of Cd on adaxial and decrease by 3.89 % (Cd50) and 4.63 % (Cd100) on abaxial side of leaves respectively. The variations of response could be signals of tolerance or adaptive mechanisms of the leaves of tested bean cultivar under the used concentrations of cadmium.

Down-regulation of lncRNA MEG3 promotes chronic low dose cadmium exposure-induced cell transformation and cancer stem cell-like property

Cadmium (Cd) is a toxic heavy metal and one of carcinogens that cause lung cancer. However, the exact mechanism of Cd carcinogenesis remains unclear. To investigate the mechanism of Cd carcinogenesis, we exposed human bronchial epithelial cells (BEAS-2B) to a low dose of Cd (2.5 μM, CdCl2) for 9 months, which caused cell malignant transformation and generated cancer stem cell (CSC)-like cells. The goal of this study is to investigate the underlying mechanism. The long non-coding RNA (lncRNA) microarray analysis showed that the expression level of a tumor suppressive lncRNA maternally expressed 3 (MEG3) is significantly down-regulated in Cd-transformed cells, which is confirmed by further q-PCR analysis. Mechanistically, it was found that chronic Cd exposure up-regulates the levels of DNA methyltransferases (DNMTs), which increases the methylation of the differentially methylated region (DMR) 1.5 kb upstream of MEG3 transcription start site to reduce MEG3 expression. Functional studies showed that stably overexpressing MEG3 in Cd-transformed cells significantly reduces their transformed phenotypes. Moreover, stably overexpressing MEG3 in parental non-transformed human bronchial epithelial cells significantly impaired the capability of chronic Cd exposure to induce cell transformation and CSC-like property. Further mechanistic studies revealed that the cell cycle inhibitor p21 level is reduced and retinoblastoma protein (Rb) phosphorylation is increased in Cd-transformed cells to promote cell cycle progression. In addition, Cd-transformed cells also expressed higher levels of Bcl-xL and displayed apoptosis resistance. In contrast, stably overexpressing MEG3 increased p21 levels and reduced Rb phosphorylation and Bcl-xL levels in Cd-exposed cells and reduced their cell cycle progression and apoptosis resistance. Together, these findings suggest that MEG3 down-regulation may play important roles in Cd-induced cell transformation and CSC-like property by promoting cell cycle progression and apoptosis resistance.

Cadmium-induced hormesis effect in medicinal herbs improves the efficiency of safe utilization for low cadmium-contaminated farmland soil

Compared to other soil remediation technologies, Cd-contaminated farmland soil with low cadmium accumulation (LCA) plant-based safe utilization is more catered to developing countries with food in high demand. Hormesis, which describes the fortification of plant growth performance by a low level of environmental stress, can be innovatively used to achieve increases in crop yield and plant functional components, thus amplifying the safe utilization efficiency of low Cd-contaminated soil by LCA plants. In the present study, the growth and physiological responses of Polygonatum sibiricum, a traditional Chinese medicinal herb, were investigated under laboratory conditions of gradient Cd dosage concentrations and times. As a result, the growth performance of P. sibiricum reached the peak of an inverse U-shaped curve of hormesis under e0 mg kg−1 and 9 months of Cd stress, with elevations in tuber biomass (medicinal part), plant height and polysaccharide content (medicinal components) of 143%, 25% and 90%, respectively. Meanwhile, trace Cd accumulation (0.41 mg kg−1) in the tuber guaranteed medicinal edible safety. In addition, Cd-induced hormesis in P. sibiricum was verified to be overcompensated by antioxidation systems. In conclusion, such ‘win-win’ results, including low Cd accumulation and enhancement of plant pharmaceutical value, provided medicinal herbs with a possibility for safe soil utilization.

Adverse effects of cadmium on poultry and role of selenium against it: An updated review

Cadmium (Cd) is a toxic heavy metal, discharged into environments naturally or anthropogenically, where industrial and agricultural revolutions have led to serious Cd pollution into the environment. Poultry feed may be contaminated by Cd due to its presence in concentrates and supplements, and also in the machinery and equipment used in feed production and processing. After absorption in the digestive system, Cd largely accumulates in kidneys, liver, bones and other organs and causes irreversible damage to these organs. Higher doses of Cd in the poultry diet reduced feed intake, body weight, bone mineral density, egg production and eggshell quality. Selenium (Se) is an essential micronutrient and important component of a variety of antioxidant enzymes, with the ability to antagonize metal toxicity including Cd. Hence, in the current review, we try to summarize recent information about the toxicological effects of Cd and provide updated information about the role of Se as an effective strategy in reducing Cd toxicity in poultry.

Availability of Trace Elements in Soil with Simulated Cadmium, Lead and Zinc Pollution

The research was based on a pot experiment in which the impact of increasing Cd, Zn and Pb doses on the content of available trace elements in soil was compared. Seven series of trials were designed: 1 (Cd), 2 (Pb), 3 (Zn), 4 (Cd + Pb), 5 (Cd + Zn), 6 (Pb + Zn), 7 (Cd + Pb + Zn). Aside from the control one (without the metals), three increasing levels of contamination were considered within each series. Mobile forms of trace elements (Cd, Pb, Zn, Fe, Mn, Cu, Ni, Co, and Cr) in soil were determined, in addition to which selected physicochemical soil properties—reaction (pH), salinity (EC), hydrolytic acidity (HAC), total exchange bases (TEB)—were identified while cation exchange capacity (CEC), base saturation (BS) and availability factor (AF) were calculated. The application of Cd and Pb to soil resulted in an increase in the share of potentially available forms of these metals in their total content. The availability factor (AF) in the pots polluted with these metals was higher than in the control, in the range 17.5–20.0% for Cd, and 62.8–71.5% for Pb. In turn, the share of Zn mobile forms was comparable in most experimental objects, oscillating around 30%. Moreover, addition to soil of Cd, Pb and Zn usually caused a significant decrease in the content of available forms of Fe, Mn and Cu, and resulted in significantly higher content of available forms of Cr in the soil.

Effects of chronic cadmium exposure on the structure and function of intestinal mucosal flora in mice

Cadmium (Cd) is a serious environmental pollutant to human health. Intestinal flora is associated with human health. This study probed into the effects of Cd on the small intestinal mucosal flora in mice by drinking water intake 5 ppm, 20 ppm and 100 ppm cadmium chloride for 50 days respectively. Results indicated that diversity, taxonomic composition and community structure of intestinal mucosal flora were influenced by Cd exposure. Sphingomonas, Microbacterium and Desulfovibrio, as the characteristic bacteria, played vital roles in the different dose groups of Cd. Meanwhile, Cd exposure adjusted the metabolic function of intestinal mucosal flora, mainly involved in the effects on carbohydrate, amino acid and lipid metabolism. Furthermore, different doses of Cd had different effects on the microbial activity of intestinal mucosal. Conclusively, Cd exposure affected the structure and function of intestinal mucosal flora. We screened the Sphingomonas, Microbacterium and Desulfovibrio as the biomarkers of intestinal mucosal flora after Cd exposure.

Effect of Cadmium Chloride and Cadmium Nitrate on Growth and Mineral Nutrient Content in the Root of Fava Bean (Vicia faba L.).

The present study aimed to analyze the differences in the tolerance of fava bean (Vicia faba cv. Aštar) roots to cadmium in nitrate—Cd(NO3)2—and chloride—CdCl2—solutions. The physiological and biochemical parameters were assessed. The tested doses of Cd (50, 100, 150 and 300 mg/L) did not influence the germination of seeds. However, considerable growth inhibition and dehydration were observed after 96 h incubation. The thickness of roots and rupture of cell membranes increased along with the increasing concentration of the metal in the solution. At a Cd dose of 300 mg/L, irrespective of the solution used, increased nitrogen concentration and no change in sodium content were observed. The content of magnesium increased due to the dose of 100 mg/L (cadmium nitrate) and the content of calcium increased due to the dose of 300 mg/L (in either nitrate or chloride). The correlation analyses pointed to a possible effect of nitrates in the applied solutions on the accumulation of Cd and some minerals in the roots of the given variety of fava bean. This may be important for both research and agricultural practice. The identification of crops with high tolerance to cadmium, as well as knowledge about the mechanisms of ion interactions at the soil solution–plant level, is important in terms of such crops’ use in the process of the remediation of cadmium-contaminated soils coupled with food production.

Improved Cd (II) ions removal performance from aqueous solution using cerium doped activated carbon

The present work deals with the removal of Cd (II) ions in aqueous solution using modified activated carbon based palm kernel shells. The activated carbon surface was modified by incorporating cerium atoms. The experiments were performed in batch mode by varying the initial pH solution, adsorbent dose, contact time and initial concentration of Cd (II) ions. The experimental results analysis revealed that the Cd (II) ions removal percentage increased with the increase of the contact time and reached adsorption equilibrium within 150 min with a removal percentage of 51.24%. The adsorbed quantities were strongly linked to the ionic radius and hydration energy of oxides with optimal pH values ranging between 5 and 7 for optimal adsorbent dose of 0.03 g. Six isotherms models were investigated to explain the adsorption equilibrium. The Freundlich and Hasley isotherms models gave the best fit according to their correlation coefficient values R2 > 0.9. Moreover, the value of (1/n) was less than unity indicating the heterogeneity of Ce-doped activated carbon surface. The surface heterogeneity and material porosity were confirmed by scanning electron microscopy. Four kinetics models were used to identify the mechanisms that governed the Cd (II) ions adsorption. The pseudo second order and intraparticle diffusion kinetics models fitted well the experimental data. Both chemisorption and physisorption mechanisms of Cd (II) ions removal were controlled by hydrated radius and the diffusion process into AC-Ce network. Thus, the Ce-doped activated carbon obtained by carbonization/activation of palm kernel shells is an alternative and low-cost adsorbent which can be useful for the remediation of heavy metal contamination resulting from the migration from phosphogypsum production sites to water resources.

Cadmium induces endoplasmic reticulum stress-mediated apoptosis in pig pancreas via the increase of Th1 cells

Cadmium (Cd), an environmental pollutant, causes several adverse reactions in animals. High dose of Cd has serious cytotoxicities, including the induction of programmed cell necrosis, autophagy and apoptosis, which has aroused wide public concern. The balance of cytokine network is affected by Th1/Th2 balance which is closely related to immune response and the occurrence, development, treatment and outcome of various diseases. Cd can induce severe apoptosis, but the relationship between Cd induced apoptosis and Th1/Th2 balance has not been clarified. In this study, we established a pig Cd poisoning model, exposing to CdCl2 for 40 days (20 mg Cd/kg diet). Firstly, deviation of Th1/Th2 balance was observed by fluorescence staining, and apoptosis was observed by TUNEL staining. Then, real-time fluorescence quantitative analysis and Western blot were used to detect the expression of related proteins. The results show that Cd can interfere with the balance of Th1/Th2 and shift the balance towards Th1. In addition, through the experiments, we found that Cd exposure can increase the expression of glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78), marker proteins of unfolded protein response (UPR). Cd exposure can increase the expression of pancreatic endoplasmic reticulum kinase (PERK), CCAAT-enhancer-binding protein homologous protein (CHOP), inositol-requiring enzyme 1 (IRE-1), activating transcription factor 6 (ATF-6), cysteinyl aspartate specific proteinase (Caspase12), indicating the three branches (ATF6, PERK and IRE-1) of endoplasmic reticulum stress (ER-stress) were activated. Moreover, we found that the expression of pro-apoptosis genes in the downstream pathway of ER-stress increased. In summary, our results indicated that Cd exposure upregulated the expression of pro-apoptosis related genes and caused apoptosis via the activation of the ER-stress signaling pathways in pancreas cells. And these negative effects were correlated with the equilibrium drift of Th1/Th2, increase in the expression and secretion of Th1 cytokines.

Metal Accumulation Profile of Catharanthus roseus (L.) G.Don and Celosia argentea L. with EDTA Co-Application

The problem of metal-induced toxicity is proliferating with an increase in industrialization and urbanization. The buildup of metals results in severe environmental deterioration and harmful impacts on plant growth. In this study, we investigated the potential of two ornamental plants, Catharanthus roseus (L.) G.Don and Celosia argentea L., to tolerate and accumulate Ni, Cr, Cd, Pb, and Cu. These ornamental plants were grown in Hoagland’s nutrient solution containing metal loads (50 µM and 100 µM) alone and in combination with a synthetic chelator, ethylenediaminetetraacetic acid (EDTA) (2.5 mM). Plant growth and metal tolerance varied in both plant species for Ni, Cr, Cd, Pb, and Cu. C. roseus growth was better in treatments without EDTA, particularly in Ni, Cr, and Pb treatments, and Pb content increased in all parts of the plant. In contrast, Cd content decreased with EDTA addition. In C. argentea, the addition of EDTA resulted in improved plant biomass at both doses of Cu. In contrast, plant biomass reduced significantly in the case of Ni. In C. argentea, without EDTA, root length in Cd and Cu treatments was significantly lower than the control and other treatments. However, the addition of EDTA resulted in improved growth at both doses for Pb and Cu. Metal accumulation in C. argentea enhanced significantly with EDTA addition at both doses of Cu and Cd. Hence, it can be concluded that EDTA addition resulted in improved growth and better metal uptake than treatments without EDTA. Metal accumulation increased with EDTA addition compared to treatments without EDTA, particularly for Pb in C. roseus and Cu and Cd in C. argentea. Based on the present results, C. roseus showed a better ability to phytostabilize Cu, Cd, and Ni, while C. argentea worked better for Ni, Cd, Cu, and Pb.

Effects of N-Acetyl Cysteine on Genes Expression of c-myc, and Ask-1, Histopathological, Oxidative Stress, Inflammation, and Apoptosis in the Liver of Male Rats Exposed to Cadmium.

This study aimed to consider the oxidative damage induced by cadmium (Cd) and apoptosis and the role of N-acetylcysteine (NAC) in preserving hepatic cells against Cd toxicity. Male rats were randomly divided into seven groups including G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd +continuous dose of NAC), and G5 (continuous dose of Cd +continuous dose of NAC). Hepatic cells apoptosis was measured using TUNEL assay method. Levels of malondialdehyde (MDA), TNF-α, IL-10, and total antioxidant capacity (TAC) were measured by specific kits. Expression of c-myc and Ask-1 genes was considered using RT-PCR. NAC treatments significantly improved TAC and IL-10, but decreased MDA and TNF-α values in rats that were exposed to a single and continuous dose of Cd (p < 0.05). Exposure to a single and continuous dose of Cd caused a significant increase in c-myc expression by 3.76-fold (p < 0.001) and 8.17-fold (p < 0.0001), respectively. Single and continuous dose treatment of Cd led to a significant increase in Ask1 expression by 4.38-fold (p < 0.001) and 13.52-fold (p < 0.001), respectively. NAC treatments significantly decreased the expression of c-myc, and Ask-1 in rats exposed to single or continuous Cd. Cd exposure is strongly associated with oxidative stress, inflammation, antioxidant depletion, and liver cells apoptosis. NAC can protect liver tissue against Cd by elevating antioxidants capacity, mitigating oxidative stress and inflammation, as well as down-regulating of apoptotic genes.