High Doses Of Cd Research Articles

Cadmium Through Disturbing MTF1-Mediated Metal Response Induced Cerebellar Injury.

Cadmium (Cd) is a toxic environmental contaminant, which bio-accumulate in animals through the food chain. Cerebellum is one of the primary target organs for Cd exposure. In this study, we established a chronic Cd exposure model; 60 chickens were treated with Cd (0 mg/kg, 35 mg/kg, 70 mg/kg) for 90 days. Clinical manifestations indicated that the chicken was depressed and has unstable gait under Cd exposure. Histopathological results indicated that Cd induced neuronal shrunken and indistinct nucleoli, and the number of Purkinje cells decreased significantly. Cerebellar metal contents were analyzed by ICP-MS. We found that Cd caused Cd and Cu accumulation and decreased the content of Se, Fe, and Zn, suggesting that Cd disturbed metal homeostasis. Besides, Cd treatment group also showed high levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) content and inhibited selenoprotein transcriptome, suggesting that Cd exposure resulted in oxidative stress. Notably, low-dose Cd exposure activated MTF1 mRNA and protein expression and its target metal-responsive genes, including MT1, MT2, DMT1, ZIP8, ZIP10, TF, and ATP7B which indicate cellular adaptive response against Cd-induced damage. On the other hand, 70 mg/kg Cd downregulated MTF1-mediated metal response, which was involved in Cd-induced cerebellar injury in chicken. In conclusion, our data demonstrated that molecular mechanisms are associated with Cd-induced cerebellar injury due to disturbing MTF1-mediated metal response.Graphical abstractThis study indicated that the cerebellum is one of the target organs of Cd-induced toxicity. Additionally, Cd exposure induced metal dyshomeostasis in chicken’s cerebellum, whereas this study found that lower level of Cd dose triggered the activation of the cytoprotective mechanism through activating the expression of MTF1 which regulate MT1, MT2, DMT1, ZIP8, ZIP10, TF, and ATP7B expressions in cerebellum. However, MTF1-mediated metal response was inhibited under the exposure of high dose of Cd, which ultimately caused cerebellar injury. The present study provides a new insight that Cd through disturbed MTF1-mediated metal response disrupts metal homeostasis that induced cerebellar injury. Supplementary InformationThe online version contains supplementary material available at 10.1007/s12640-022-00474-x.

Effects of Cd addition on soil phosphorus mineralization in reclaimed coastal wetlands along a 100-year reclamation chronosequence in the Pearl River Estuary (China)

The relationship between Cd and soil phosphatase activity has been given some concerns due to serious soil Cd contamination. However, the effects of high-risk Cd pollution on the soil phosphorus mineralization process are still kept unclear in reclaimed coastal wetlands. Here, we investigated the impacts of Cd additions at three levels on phosphorus mineralization and phosphatase activities in reclaimed coastal wetland soils with different reclamation ages (e.g., 100-year, 40-year, and 10-year) in the Pearl River Estuary by a 40-day laboratory incubation experiment. The results showed that lower soil phosphatase activity was observed in the reclaimed wetlands with longer reclamation age, which led to the lower increase in cumulative net phosphorus mineralization and Occluded P. High Cd exposure facilitated the phosphatase activities and phosphorus mineralization through the promotion of Occluded P and Al/Fe-P contents in the 100-year and 10-year reclaimed wetland soils, respectively. The addition of the low-dose of Cd to the soil inhibited phosphorus mineralization in the middle of incubation in 40-year reclaimed wetland soils, while the high-dose Cd addition had little effect. The findings of this work indicate that the older reclaimed wetlands might have lower phosphorus mineralization potentials, while higher Cd pollution might lead to soil phosphorus loss by improving phosphorus mineralization in reclaimed coastal wetlands.

Cadmium exposure causes mitochondrial fission and fusion disorder in the pig hypothalamus via the PI3K/AKT pathway

Cadmium (Cd) is the main environmental pollutant causing endocrine and nervous system dysfunction in animals. High doses of Cd cause cytotoxicity, including programmed necrosis and apoptosis, which has aroused widespread concern. Mitochondrial dynamics plays a key role in programmed necrosis and apoptosis of endocrine organs. Nevertheless, there is a lack of information on the relationship between Cd-induced programmed necrosis/apoptosis of the hypothalamus and the mitochondrial fusion-fission balance. Therefore, a hypothalamic injury model of Cd exposure was established by adding 20 mg/kg CdCl2 to the basic pig diet for 40 days. Analysis of the Cd toxicity mechanism was conducted by inductively coupled plasma mass spectrometry, hematoxylin and eosin staining, the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and quantitative reverse transcription-polymerase chain reaction, as well as western blot analyses. The results suggested that exposure to Cd inhibited the expression of PI3K and AKT, interfered with the balance of mitochondrial fusion and division, downregulated the expression of Mfn2, Mfn1, and OPA1, and upregulated the expression of Drp1 and Mff, which led to cell apoptosis and programmed necrosis in the pig hypothalamus. This study finds that cadmium exposure leads to mitochondrial fission and fusion dysfunction in porcine hypothalamus via the PI3K/AKT pathway.

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.

Cadmium exposure modulates the gut-liver axis in an Alzheimer\u2019s disease mouse model

The human Apolipoprotein E4 (ApoE4) variant is the strongest known genetic risk factor for Alzheimer’s disease (AD). Cadmium (Cd) has been shown to impair learning and memory at a greater extent in humanized ApoE4 knock-in (ApoE4-KI) mice as compared to ApoE3 (common allele)-KI mice. Here, we determined how cadmium interacts with ApoE4 gene variants to modify the gut-liver axis. Large intestinal content bacterial 16S rDNA sequencing, serum lipid metabolomics, and hepatic transcriptomics were analyzed in ApoE3- and ApoE4-KI mice orally exposed to vehicle, a low dose, or a high dose of Cd in drinking water. ApoE4-KI males had the most prominent changes in their gut microbiota, as well as a predicted down-regulation of many essential microbial pathways involved in nutrient and energy homeostasis. In the host liver, cadmium-exposed ApoE4-KI males had the most differentially regulated pathways; specifically, there was enrichment in several pathways involved in platelet activation and drug metabolism. In conclusion, Cd exposure profoundly modified the gut-liver axis in the most susceptible mouse strain to neurological damage namely the ApoE4-KI males, evidenced by an increase in microbial AD biomarkers, reduction in energy supply-related pathways in gut and blood, and an increase in hepatic pathways involved in inflammation and xenobiotic biotransformation.

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.

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.

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.

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.

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.

MAPK, AKT/FoxO3a and mTOR pathways are involved in cadmium regulating the cell cycle, proliferation and apoptosis of chicken follicular granulosa cells

The occurrence of cadmium (Cd) in feed is a major problem in animal health and production. Studies have confirmed that Cd depresses egg production of laying hens, which is closely related to follicular atresia. This study aimed to assess the toxic impacts of Cd on the ovarian tissue, and to examine the mechanism of Cd-induced granulosa cell proliferation and apoptosis. Results from the nitric oxide (NO) and malondialdehyde (MDA) content, total superoxide dismutase (T-SOD), glutathione peroxide (GSH-Px), total nitric oxide synthase (T-NOS) and adenosine triphosphatase (ATPase) activities, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay, and hematoxylin-eosin (H & E) staining indicated that excess Cd induced oxidative stress, granulosa cell apoptosis and follicular atresia in the layer ovary. Low-dose Cd exposure (1 μM) induced the granulosa cell proliferation, upregulated the mRNA levels of RSK1 and RHEB, activated FoxO3a, AKT, ERK1/2, mTOR and p70S6K1 phosphorylation, and promoted cell cycle progression from phase G1 to S. However, high-dose Cd exposure (15 μM) induced reactive oxygen species (ROS) generation and cell apoptosis, upregulated the mRNA levels of the inflammatory factors, ASK1, JNK, p38 and TAK1, downregulated the expressions of RSK1 and RHEB genes, and inhibited the phosphorylation of ERK1/2, mTOR and p70S6K1 proteins, and the cell cycle progression. Rapamycin pre-treatment completely blocked the phosphorylation of mTOR and p70S6K1 proteins, and the cell cycle progression induced by 1 μM Cd, and accelerated 15 μM Cd-induced cell apoptosis and cell cycle arrest. The microRNA sequencing result showed that 15 μM Cd induced differential expression of microRNA genes, which may regulate AKT, ERK1/2 and mTOR signaling and cell cycle progression by regulating the activity of G proteins and cell cycle-related proteins. Conclusively, these results indicated that Cd can cause the ovarian damage and follicular atresia, and regulate cell cycle, cell proliferation or apoptosis of granulosa cells through MAPK, AKT/FoxO3a and mTOR pathways in laying hens.

Prepubertal exposure to high dose of cadmium induces hypothalamic injury through transcriptome profiling alteration and neuronal degeneration in female rats

Cadmium (Cd) is a toxic metal, which seems to be crucial during the prepubertal period. Cd can destroy the structural integrity of the blood-brain barrier (BBB) and enters into the brain. Although the brain is susceptible to neurotoxicity induced by Cd, the effects of Cd on the brain, particularly hypothalamic transcriptome, are still relatively poorly understood. Therefore, we investigated the molecular effects of Cd exposure on the hypothalamus by profiling the transcriptomic response of the hypothalamus to high dose of Cd (25 mg/kg bw/day cadmium chloride (CdCl2)) during the prepubertal period in Sprague-Dawley female rats. After sequencing and annotation, differential expression analysis revealed 1656 genes that were differentially expressed that 108 of them were classified into 37 transcription factor (TF) families. According to gene ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, these differentially expressed genes (DEGs) were involved in different biological processes and neurological disorders including Alzheimer's disease (AD), Huntington's disease (HD), and Parkinson's disease (PD), prolactin signaling pathway, PI3K/Akt signaling, and dopaminergic synapse. Five transcripts were selected for further analyses with Real-time quantitative PCR (RT-qPCR). The RT-qPCR results were mostly consistent with those from the high throughput RNA sequencing (RNA-seq). Cresyl violet staining clearly showed an increased neuronal degeneration in the dorsomedial hypothalamus (DMH) and arcuate (Arc) nuclei of the CdCl2 group. Overall, this study demonstrates that prepubertal exposure to high doses of Cd induces hypothalamic injury through transcriptome profiling alteration in female rats, which reveals the new mechanisms of pathogenesis of Cd in the hypothalamus.

Rescue effects of Se-enriched rice on physiological and biochemical characteristics in cadmium poisoning mice.

Cadmium (Cd) is an element injurious for human health and is possibly toxic to organisms at minor concentrations. While some of other trace metallic elements have antagonistic features to it. One of them is the interaction between selenium (Se) and Cd in plant different organs. Literature review disclosed that the intake of Se to some extent can reduce the accumulation of Cd in plants, while the research on of trace metallic elements (Cd) and Se-enriched food (rice) in the living body has rarely been reported. This study intended to explore whether there was a mitigating effect of Se-enriched rice on mice poisoned with Cd. A mouse model of low-dose and high-dose Cd poisoning was established (supplemented with cadmium chloride(CdCl2·2½H20)), followed by feeding two groups (1) Se-enriched rice and (2) setting an equal amount of inorganic Se group. After that, the impact of Se-enriched rice on the antioxidant activity was evaluated. The Se-enriched diet enhanced the total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and enzyme activities of GSH peroxidase (GSH-Px) in mice livers and kidney whereas significantly decreased the malondialdehyde (MDA) contents. Moreover, the degree of physiological damage in mice with low cadmium poisoning was significantly alleviated, and the expression of antioxidant genes (Nrf-2, GPX1, TrxR2, TNF-2) was increased. In conclusion, the Se-enriched diet has a positive effect on the biological effects in mice, and it can be used as a daily diet to resist damage to the body's low Cd state and support enzymatic antioxidant systems by eliminating oxidative injury.

Methanogenesis and aerobic methanotrophy in arable soils contaminated with cadmium

Soil is a non-renewable environment in which, depending on the prevailing O2 conditions, two opposite processes – methanogenesis and methanotrophy - may take place. The rates of the processes may result in soil acting as a sink or a source of methane (CH4). Due to agricultural practices, heavy metals may accumulate affecting soil microbial processes. We tested the effect of cadmium (Cd) contamination on CH4 emission and uptake in three mineral soils (Eutric Cambisol, Haplic Podzol, Mollic Gleysol). Additionally, in the methanotrophy study, different soil moisture levels (pF 0; 2.2; 3.2) were studied. Based on the European annual and maximum limits, soils were polluted with cadmium in four doses (per dry soil mass): 0.048 mg Cd kg−1 (and its five-fold higher value) and 3.00 mg Cd kg−1 (and its five-fold higher value). The results showed that all tested soils produced and consumed CH4. Methane production rates were not significantly changed by the presence of the cadmium (except annual five-fold Cd dose in Podzol). In methanotrophy study, soil moisture was stronger regulator of CH4 oxidation (p < 0.05) than Cd pollution which effect depended on the soil type, Cd dose and pF level. CH4 was completely consumed in Cambisol (only at pF 0 with the rate significantly different from the rates at pF 2.2 and 3.2) and in Gleysol (at pF 0; pF 2.2; the CH4 oxidation rates were significantly different among all tested moistures with annual Cd dose), but this process was delayed after the application of the higher Cd doses. Among the tested soils, only the Podzol oxidized the added CH4 under all tested moisture levels (with the rate significantly different at pF 2.2 wit annual Cd dose), while Cd addition delayed CH4 uptake as well. In the Podzol, CH4 consumption was inhibited only by the highest Cd dose at low moisture (pF 3.2).

Subchronic Exposure to Cadmium Causes Persistent Changes in the Reproductive System in Female Wistar Rats.

Cadmium (Cd) is an environmental toxicant and endocrine disruptor in humans and animals, and recent studies have illustrated that the uterus is exceedingly sensitive to Cd toxicity. The aim of the study was to investigate the influence of subchronic (90 days) oral Cd exposure in daily doses of 0.09-4.5 mg/kg b.w. on the balance of sex hormones by estimating estradiol (E2) and progesterone (P) concentrations in the uterus and plasma in comparison with the effects of 17β-E2. Additionally, the uterine weight, histopathological changes in the uterus and ovaries, the regularity of the estrous cycle, Cd bioaccumulation in uterine tissue, and selected biochemical parameters of oxidative stress were determined. A long period of observation (three and six months following the administration period) was used to assess whether the existing effects are reversible. The lowest dose of Cd caused effects similar to 17β-E2: an increase of E2 concentration in the uterus, endometrial epithelium thickness, and disturbed estrous cycle with estrus phase prolongation. The obtained results suggest that Cd causes nonlinear response. Higher doses of Cd caused a significant decrease in E2 concentration in the uterus and plasma, estrous cycle disturbances, endometrium atrophy, and structural damage in the ovaries. This dose additionally induces lipid peroxidation in the uterine tissues. It is noteworthy that a prolonged time of observation after terminating the exposure showed persistent changes in the concentration of E2 in uterine tissue, as well as alterations in estrous cycle phases, and an increase in lipid peroxidation in the uterus. Moreover, significant positive correlations between the plasma E2 concentration and endometrial epithelium thickness in all studied groups were found. In summary, subchronic oral Cd exposure of female rats may result in impaired fertility processes.

Dietary Cadmium Chloride Supplementation Impairs Renal Function and Bone Metabolism of Laying Hens

Simple SummaryIn this study, the effects of cadmium (Cd) on renal function and bone metabolism of laying hens were investigated. Results indicated that supplementation with Cd can damage renal function, induce oxidative stress in the kidney, disrupt the body’s calcium balance and hormone secretion, and negatively affect bone metabolism of laying hens. The results demonstrated that chronic exposure to Cd could induce renal dysfunction and bone damage in laying hens.This study was conducted to evaluate the toxic effects of cadmium (Cd) on the kidney function and bone development in laying hens. A total of 480 Hy-line laying hens aged 38 weeks were randomly allocated into five treatments, each of which included six replicates of 16 birds. The concentrations of Cd in the diets of the five groups were 0.47, 7.58, 15.56, 30.55, and 60.67 mg/kg. Results showed that serum calcium (Ca) levels decreased significantly in the 60.67 mg Cd/kg diet group (p < 0.05). The activities of serum alkaline phosphatase (ALP) and bone ALP (BALP) decreased significantly in the 15.56, 30.55 and 60.67 mg Cd/kg diet groups (p < 0.05). The levels of parathyroid hormone (PTH) increased significantly in the 30.55 and 60.67 mg Cd/kg diet groups, and the estradiol (E2), 1,25-(OH)2-D3 and calcitonin (CT) decreased significantly with the increase of dietary Cd supplementation (p < 0.05). Histological results presented enlargements of renal tubules and tubular fibrosis in the kidney and decreased trabecular bone in the tibia. Tartrate-resistant acidic phosphatase (TRAP) staining results of tibia showed that osteoclast was significantly increased at the relatively high dose of dietary Cd (p < 0.05). In addition, the renal function indicators of blood urea nitrogen (BUN), urea acid (UA), and creatinine were significantly increased in Cd supplemented groups compared with the control group (p < 0.05). Low dose Cd exposure induced antioxidant defenses accompanying the increase in activities of catalase (CAT), glutathione peroxidase (GSH-Px), and the levels of glutathione (GSH) in renal tissue. At the same time, with the increased Cd levels, the activities of CAT, GSH-Px decreased significantly, and the level of malondialdehyde (MDA) increased significantly (p < 0.05). The activities of Na+/K+-ATPase and Ca2+/Mg2+-ATPase decreased significantly in the relatively high levels of dietary Cd (p < 0.05). These results suggest that Cd can damage renal function and induce disorders in bone metabolism of laying hens.

Cadmium exposure affects growth performance, energy metabolism, and neuropeptide expression in Carassius auratus gibelio.

Cadmium (Cd) is the most abundant heavy metal in aquatic environments and is easily detected on a global scale. Carassius auratus gibelio is a common aquaculture species. The aim of this study was to explore the toxic effects of 1, 2, and 4 mg/L Cd on the energy metabolism, growth performance, and neurological responses of C. gibelio. After 30 days of exposure, Cd concentrations in the liver and brain were significantly increased in Cd-exposed groups. Low-level Cd exposure (1 mg/L) increased weight and length gains, as well as food intake, in the fish. Acetylcholinesterase activity decreased significantly in the Cd-exposed groups. Energy metabolism levels (as reflected by oxygen consumption, ammonia excretion rate, and swimming activity), as well as serum T3 and T4 levels, increased significantly in the fish exposed to 1 mg/L Cd. However, energy metabolism and serum T3/T4 levels decreased significantly in the 4-mg/L Cd group. Neuropeptide gene expression levels in brain were consistent with the observed changes in food intake. In the Cd-exposed groups, the expression levels of neuropeptide Y (NPY), apelin, and metallothionein (MT) increased significantly, while those of pro-opinmelanocortin (POMC), ghrelin, and corticotrophin-releasing factor (CRF) decreased significantly. Our data suggested that in fish, low doses of Cd might increase food intake, as well as weight and length gains, but high doses of Cd might have the opposite effect. These effects might be a result of neurohumoral regulation. Long-term exposure to low doses of Cd might cause weight gain and affect food intake.

Effects of sub-chronic, low-dose cadmium exposure on kidney damage and potential mechanisms.

The present study was to investigate the potential mechanisms underlying the sub-chronic low-dose cadmium (Cd) exposure induced renal injury in rats. Totally 40 male adult SD rats were randomly divided into four groups: control group, low-dose Cd group (1 mg/kg CdCl2), moderate-dose Cd group (2.5 mg/kg) and high-dose Cd group (5 mg/kg). From the 3rd week, the body weight of rats in moderate-dose and high-dose declined significantly as compared to the control group (P<0.05); the liver to body weight ratio increased, the volumes of 24-hour urine and drinking-water decreased markedly (P<0.05), the BUN, SCr and β2-MG increased significantly, but the Fe2+ concentration decreased markedly as compared to the control group (P<0.05); the serum MDA and SOD1 content contents increased, but the serum SOD2 and CAT contents decreased significantly in Cd-treated groups (P<0.05); Renal injury deteriorated with the increase in Cd dose; swelling glomeruli showed stenotic renal-tubules, and epithelial-cell-necrosis, shedding and accumulation in the lumen, massive infiltrated inflammatory cells and interstitial hyperaemia were observed; The mitochondria in renal-tubular-epithelial-cells displayed swelling, deformation and vacuolation; the renal ROS content increased in Cd-exposure-groups; the renal SOD1 expression increased but the expression of SOD2 and CAT decreased (P<0.05). The Bcl-2 expression decreased, but Bax expression and Bax/Bcl-2 ratio increased significantly in a Cd-dose dependent manner. Cd may cause renal injury in a dose dependent manner, which may be ascribed to the disordered Fe2+ absorption, redox imbalance and apoptosis in the kidney.

Effect of Cadmium Application on Antimicrobial, Antioxidant and Total Phenolic Content of Basil Genotypes

Abstract: Background: Exposure to heavy metals leads to increase in reactive oxygen species. Plants have many strategies to counteract the toxic effects of heavy metal stress by activating certain intermediary metabolic activities and making physiological adjustments. Objective: This study was designed to determine total phenolic contents and antimicrobial and antioxidant activities of eight Ocimum basilicum L. genotypes grown in a soil exposed to cadmium at different levels. Methods: Total phenolic contents were calculated as gallic acid equivalent. Antioxidant activity was studied based on DPPH free radical scavenging activity. Antimicrobial activity was determined by disc diffusion method against several microorganisms. Results: The highest antimicrobial activity was observed in the case of genotype 5 against Bacillus subtilus with the inhibition diameter value as 18.50 mm for basil grown at Cd free soil. This value just decreased to 17.57 mm at the conditions with 40 mg/kg Cd. Depending on increase at cadmium dose, the best grade increase in antimicrobial activity was also observed against B.subtilus for genotype 7. Total phenolic content and DPPH radical scavenging activity values were also increased with the Cd application at low doses. At very high doses of Cd a little decrease was observed for these values. Both of the phenolic content values and DPPH scavenging activities reached their maximum values for genotypes 1,7 and 8 grown at soil exposed to 20 mg/ kg Cd. Conclusion: Although cadmium is toxic, known beneficial properties of the basil samples have not deteriorated. These improved results are due to resistance of the basil plant to survive on adverse conditions. Key words: Cadmium toxicity, Free radical scavenging activities Ocimum basilicum L.