Cadmium Exposure Research Articles

The Protective Impact of Aronia melanocarpa L. Berries Extract against Prooxidative Cadmium Action in the Brain-A Study in an In Vivo Model of Current Environmental Human Exposure to This Harmful Element.

Cadmium (Cd) is a prooxidant that adversely affects human health, including the nervous system. As exposure of the general population to this heavy metal is inevitable, it is crucial to look for agents that can prevent the effects of its toxic action. An experimental model on female rats of current lifetime human exposure to cadmium (3-24-months' treatment with 1 or 5 mg Cd/kg diet) was used to test whether low-level and moderate intoxication can exert a prooxidative impact in the brain and whether supplementation with a 0.1% extract from the berries of Aronia melanocarpa L. (Michx.) Elliott (AE; chokeberry extract) can protect against this action. Numerous parameters of the non-enzymatic and enzymatic antioxidative barrier, as well as total antioxidative and oxidative status (TAS and TOS, respectively), were determined and the index of oxidative stress (OSI) was calculated. Moreover, chosen prooxidants (myeloperoxidase, xanthine oxidase, and hydrogen peroxide) and biomarkers of oxidative modifications of lipids, proteins, and deoxyribonucleic acid were assayed. Cadmium dysregulated the balance between oxidants and antioxidants in the brain and led to oxidative stress and oxidative injury of the cellular macromolecules, whereas the co-administration of AE alleviated these effects. To summarize, long-term, even low-level, cadmium exposure can pose a risk of failure of the nervous system by the induction of oxidative stress in the brain, whereas supplementation with products based on aronia berries seems to be an effective protective strategy.

Cadmium Toxicity in the Seminal Vesicles and Lipid Profile of Wistar Rats: Can Uvaria chamae Ameliorate the Effect?

This research investigated the capacity of Uvaria chamae in alleviating cadmium-induced toxicity in the seminal vesicles and lipid profile of Wistar rats, addressing a critical gap in current knowledge. Cadmium, a hazardous heavy metal, poses substantial risks to male reproductive health. Conducted with 25 Wistar rats under controlled conditions, the study involved local sourcing of Uvaria chamae, extracting its bioative ingredients through alcohol maceration. Dosages for cadmium and the extract were meticulously determined for five experimental groups including the control group, with rats acclimatized for two weeks before a 28-day experiment. Seminal vesicle underwent detailed processing, and histological analysis, including dehydration, clearing, infiltration, embedding, sectioning, staining using hematoxylin/eosin and microscopic examination. Statistical analysis employed one-way ANOVA through GraphPad Prism (version 8.0.2), ensuring a concise and accurate data interpretation approach. Histological examinations revealed cadmium-induced damage, including epithelial degeneration and altered luminal structures etc. These structural changes were mitigated by Uvaria chamae in a dose-dependent manner. The study also assessed the impact of cadmium on lipid profiles, showing adverse changes, but counteracted by Uvaria chamae, signifying its role in preserving lipid homoeostasis. The findings underscore reproductive health risks from cadmium exposure and highlight Uvaria chamae's therapeutic potential, which is attributed to its antioxidant and anti-inflammatory properties. This research offers valuable scientific insights on the plant and thereby urging further investigations into molecular mechanisms, clinical trials, public awareness, environmental regulations, and nutritional guidance for enhanced reproductive health amid cadmium exposure.

Long-term cadmium exposure induces epithelial-mesenchymal transition in breast cancer cells by activating CYP1B1-mediated glutamine metabolic reprogramming in BT474 cells and MMTV-Erbb2 mice

Cadmium (Cd) exposure is known to enhance breast cancer (BC) progression. Cd promotes epithelial–mesenchymal transition (EMT) in BC cells, facilitating BC cell aggressiveness and invasion, but the underlying molecular mechanisms are unclear. Hence, transgenic MMTV-Erbb2 mice (6 weeks) were orally administered Cd (3.6 mg/L, approximately equal to 19.64 μΜ) for 23 weeks, and BC cells (BT474 cells) were exposed to Cd (0, 0.1, 1 or 10 μΜ) for 72 h to investigate the effect of Cd exposure on EMT in BC cells. Chronic Cd exposure dramatically expedited tumor metastasis to multiple organs; decreased E-cadherin density; and increased Vimentin, N-cadherin, ZEB1, and Twist density in the tumor tissues of MMTV-Erbb2 mice. Notably, transcriptomic analysis of BC tumors revealed cytochrome P450 1B1 (CYP1B1) as a key factor that regulates EMT progression in Cd-treated MMTV-Erbb2 mice. Moreover, Cd increased CYP1B1 expression in MMTV-Erbb2 mouse BC tumors and in BT474 cells, and CYP1B1 inhibition decreased Cd-induced BC cell malignancy and EMT in BT474 cells. Importantly, the promotion of EMT by CYP1B1 in Cd-treated BC cells was presumably controlled by glutamine metabolism. This study offers novel perspectives into the effect of environmental Cd exposure on driving BC progression and metastasis, and this study provides important guidance for comprehensively assessing the ecological and health risks of Cd.

Mechanisms of Gills Response to Cadmium Exposure in Greenfin Horse-Faced Filefish (Thamnaconus septentrionalis): Oxidative Stress, Immune Response, and Energy Metabolism.

Cadmium (Cd) pollution has become a global issue due to industrial and agricultural developments. However, the molecular mechanism of Cd-induced detrimental effects and relevant signal transduction/metabolic networks are largely unknown in marine fishes. Here, greenfin horse-faced filefish (Thamnaconus septentrionalis) were exposed to 5.0 mg/L Cd up to 7 days. We applied both biochemical methods and multi-omics techniques to investigate how the gills respond to Cd exposure. Our findings revealed that Cd exposure caused the formation of reactive oxygen species (ROS), which in turn activated the MAPK and apoptotic pathways to alleviate oxidative stress and cell damage. Glycolysis, protein degradation, as well as fatty acid metabolism might assist to meet the requirements of nutrition and energy under Cd stress. We also found that long-term (7 days, "long-term" means compared to 12 and 48 h) Cd exposure caused the accumulation of succinate, which would in turn trigger an inflammatory response and start an immunological process. Moreover, ferroptosis might induce inflammation. Overall, Cd exposure caused oxidative stress, energy metabolism disturbance, and immune response in greenfin horse-faced filefish. Our conclusions can be used as references for safety risk assessment of Cd to marine economic fishes.

Association between drinking water quality and mental health and the modifying role of diet: a prospective cohort study

BackgroundEnvironmental factors play an important role in developing mental disorders. This study aimed to investigate the associations of metal and nonmetal elements in drinking water with the risk of depression and anxiety and to assess whether diets modulate these associations.MethodsWe conducted a prospective cohort study including 24,285 participants free from depression and anxiety from the Yinzhou Cohort study in the 2016–2021 period. The exposures were measured by multiplying metal and nonmetal element concentrations in local pipeline terminal tap water samples and total daily drinking water intakes. Cox regression models adjusted for multi-level covariates were used to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (95%CIs).ResultsDuring an average follow-up period of 4.72 and 4.68 years, 773 and 1334 cases of depression and anxiety were identified, respectively. A 1 standard deviation (SD) increase in manganese exposure reduced the incidence of depression by 8% (HR 0.92, 95%CI 0.88 to 0.97). In contrast, with a 1 SD increase in copper and cadmium exposure, the incidence of depression increased by 6% (HR 1.06, 95%CI 1.01 to 1.11) and 8% (HR 1.08, 95%CI 1.00 to 1.17), respectively. The incidence of anxiety increased by 39% (HR 1.39, 95%CI 1.20 to 1.62), 33% (HR 1.33, 95%CI 1.03 to 1.71), and 14% (HR 1.14, 95%CI 1.03 to 1.25) respectively for a 1 SD increase in manganese, iron, and selenium exposure. Diets have a moderating effect on the associations of metal and nonmetal elements with the risk of anxiety. Stronger associations were observed in older, low-income groups and low-education groups.ConclusionsWe found significant associations between exposure to metal and nonmetal elements and depression and anxiety. Diets regulated the associations to some extent.

Integrated morphological, physiological and transcriptomic analyses reveal response mechanisms of rice under different cadmium exposure routes

Rice (Oryza sativa) is one of the major cereal crops and takes up cadmium (Cd) more readily than other crops. Understanding the mechanism of Cd uptake and defense in rice can help us avoid Cd in the food chain. However, studies comparing Cd uptake, toxicity, and detoxification mechanisms of leaf and root Cd exposure at the morphological, physiological, and transcriptional levels are still lacking. Therefore, experiments were conducted in this study and found that root Cd exposure resulted in more severe oxidative and photosynthetic damage, lower plant biomass, higher Cd accumulation, and transcriptional changes in rice than leaf Cd exposure. The activation of phenylpropanoids biosynthesis in both root and leaf tissues under different Cd exposure routes suggests that increased lignin is the response mechanism of rice under Cd stress. Moreover, the roots of rice are more sensitive to Cd stress and their adaptation responses are more pronounced than those of leaves. Quantitative PCR revealed that OsPOX, OsCAD, OsPAL and OsCCR play important roles in the response to Cd stress, which further emphasize the importance of lignin. Therefore, this study provides theoretical evidence for future chemical and genetic regulation of lignin biosynthesis in crop plants to reduce Cd accumulation.

Establishment of human cerebral organoid systems to model early neural development and assess the central neurotoxicity of environmental toxins.

JOURNAL/nrgr/04.03/01300535-202501000-00032/figure1/v/2024-05-14T021156Z/r/image-tiff Human brain development is a complex process, and animal models often have significant limitations. To address this, researchers have developed pluripotent stem cell-derived three-dimensional structures, known as brain-like organoids, to more accurately model early human brain development and disease. To enable more consistent and intuitive reproduction of early brain development, in this study, we incorporated forebrain organoid culture technology into the traditional unguided method of brain organoid culture. This involved embedding organoids in matrigel for only 7 days during the rapid expansion phase of the neural epithelium and then removing them from the matrigel for further cultivation, resulting in a new type of human brain organoid system. This cerebral organoid system replicated the temporospatial characteristics of early human brain development, including neuroepithelium derivation, neural progenitor cell production and maintenance, neuron differentiation and migration, and cortical layer patterning and formation, providing more consistent and reproducible organoids for developmental modeling and toxicology testing. As a proof of concept, we applied the heavy metal cadmium to this newly improved organoid system to test whether it could be used to evaluate the neurotoxicity of environmental toxins. Brain organoids exposed to cadmium for 7 or 14 days manifested severe damage and abnormalities in their neurodevelopmental patterns, including bursts of cortical cell death and premature differentiation. Cadmium exposure caused progressive depletion of neural progenitor cells and loss of organoid integrity, accompanied by compensatory cell proliferation at ectopic locations. The convenience, flexibility, and controllability of this newly developed organoid platform make it a powerful and affordable alternative to animal models for use in neurodevelopmental, neurological, and neurotoxicological studies.

Differentially expressed long non-coding RNAs and mRNAs of cadmium exposure on learning disability of offspring rats

BackgroundCadmium (Cd) exposure has been found to have detrimental effects on the development of the central nervous system and cognitive ability in children. However, there is ongoing debate regarding the impact of maternal Cd exposure on the cognitive ability of offspring. In this study, we aimed to investigate the mechanisms underlying the influence of maternal Cd exposure on the cognitive ability of offspring rats.MethodsHere, we constructed a model of cadmium poisoning in first-generation rats through gavage. The cognitive and memory abilities of its offspring were evaluated by water maze experiment. Then, we used the gene chip to find out the key genes, and we performed qRT-PCR detection of these genes. Subsequently, enrichment analysis was employed to identify pathways. Finally, we constructed a co-expression network consisting of LncRNAs and mRNAs to elucidate the biological functions and regulatory mechanisms of LncRNAs.ResultsThe results of the water maze trial demonstrated that the offspring of rats exposed to cadmium in the first generation had reduced cognitive and memory abilities. Through an analysis of gene expression in the hippocampus of the cadmium-treated rats' offspring and the control group, we identified a correlation between the islet secretion pathway and the cognitive impairment observed in the offspring. Utilizing various algorithms, we identified Cpa1 and Prss1 as potential key genes associated with the cognitive impairment caused by cadmium. The results of qRT-PCR demonstrated a decrease in the expression levels of these genes in the hippocampus of the cadmium-treated rats’ offspring. In addition, in the co-expression network, we observed that Cpa1 was co-expressed with 11 LncRNAs, while Prss1 was associated with 4 unexplored LncRNAs. Furthermore, we conducted an analysis to examine the relationship between Cpa1, Prss1-related transcription factors, and LncRNAs.ConclusionOverall, this study provides novel insights into the molecular effects of first generation Cd exposure on the cognitive ability of offspring. The target genes and signaling pathways investigated in this study could serve as potential targets for improving neurodevelopment and cognitive ability in children.

Cadmium Exposure Induces Apoptosis and Necrosis of Thyroid Cells via the Regulation of miR-494-3p/PTEN Axis.

Cadmium (Cd) exposure is a persistent pollution problem, necessitating caution in using cadmium-expelling complexing agents. Currently, there is no targeted therapy to treat Cd poisoning. The thyroid gland is a major endocrine organ that directly regulates thyroid hormones involved in various physiological processes and is a target organ for Cd accumulation. Herein, the effects of Cd exposure on swine thyroid glands were investigated. Six-week-old male pigs were randomly divided into the Cd and control groups. The control group was fed a normal diet containing 0mg Cd/kg, while the Cd group was fed a diet containing 20mg Cd/kg (CdCl2) for 40days. The regulation mechanism of phosphatase and tensin homolog (PTEN) microRNA-494-3p (miR-494-3p) was evaluated to determine the toxic effects of Cd exposure on free radicals' cleaner. Notably, heat shock proteins (HSPs) were triggered as defense agents against Cd. Cd exposure increased the enzyme activity of superoxide dismutase1(SOD1) and SOD2, catalase (CAT), and glutathione (GSH), and the endoplasmic reticulum stress in thyroid cells. Histopathological staining, RT-qPCR, and Western Blot assays were further employed to detect possible apoptosis and necroptosis of thyroid cells induced by Cd exposure. The assays revealed increased thyroid inflammatory injury, fibrosis, and apoptosis caused by Cd exposure. This study demonstrates the role of microRNAs in regulating Cd toxicity in pig thyroid tissue and provides evidence of Cd's negative effects. It further provides an assessment of the toxicological impact of Cd as an environmental endocrine disruptor (ED) that threatens public health and safety, which forms a basis for the development of Cd poisoning treatment therapies.

Chronic cadmium exposure impairs flight behavior by dampening flight muscle carbon metabolism in bumblebees

Cadmium pollution affects the global ecosystem because cadmium can be transferred up the food chain. The bumblebee, Bombus terrestris, is an important insect pollinator. Their foraging activity on flowers exposes them to harmful heavy metals, which damages their health and leads to massive population declines. However, the effects of chronic exposure to heavy metals on the flight performance of bumblebees have not yet been characterized. Here, we studied variation in the flight capacity of bumblebees induced by chronic cadmium exposure at field-realistic concentrations using behavioral, physiological, and molecular approaches. Chronic cadmium exposure caused a significant reduction in the duration, distance, and mean velocity of bumblebee flight. Transcriptome analysis showed that the impairment of carbon metabolism and mitochondrial dysfunction in the flight muscle were the primary causes. Physiological, biochemical, and metabolomic analyses validated disruptions in energy metabolism, and impairments in mitochondrial respiratory chain complexes activities. Histological analysis revealed muscle fiber damage and mitochondrial loss. Exogenous decanoic acid or citric acid partially restored sustained flight ability of bumblebees by mitigating muscle fiber damage and increasing energy generation. These findings provide insights into how long-term cadmium stress affects the flight ability of insects and will aid human muscle or exercise-related disease research.

Effects of cadmium exposure on haemocyte immune function of clam Ruditapes philippinarum at different temperatures

Haemocytes are crucial for the immune defence of mollusks. It is important to explore the immune performance of haemocytes of mollusks under the stress of heavy metals with global warming. In order to study the effects of cadmium (Cd) exposure and temperature stress on the haemocyte immune function of clam Ruditapes philippinarum, clams were exposed to different Cd concentrations (0.05, 0.10 and 0.25 mg/L) at 20 °C, 25 °C and 30 °C respectively. Haemocyte mortality, reactive oxygen species (ROS) and superoxide dismutase (SOD) activity were measured at day 1, day 3, day 5 and day 7. The results showed that the changes of the three indexes were not obvious when exposed to 0.05 mg/L of Cd at 20 °C, while significant differences were observed with the increase of temperature, Cd concentration and exposure time. Under a condition of relative high temperature coupling with high concentration of Cd, the clams were significantly influenced, showing an obvious synergistic effect. Selected indexes reflect the clam's response to the combined stress of temperature and Cd. Moreover, R. philippinarum might be an ideal biological index species to the Cd pollution.

Low-density polyethylene microplastics partially alleviate the ecotoxicological effects induced by cadmium exposure on the earthworm Eisenia fetida

Low-density polyethylene microplastics partially alleviate the ecotoxicological effects induced by cadmium exposure on the earthworm Eisenia fetida

Transcriptome analysis reveals cadmium exposure enhanced the isoquinoline alkaloid biosynthesis and disease resistance in Coptis chinensis

Coptis chinensis Franch is a perennial herb from the Ranunculaceae family with a long history of medicinal use. As the medicinal part, the rhizome of coptis often accumulates excessive cadmium (Cd) even at low concentrations in the soil, which not only compromises its medicinal safety but also raises concerns about adverse effects on human health. Therefore, effective strategies are needed to mitigate this accumulation and ensure its safe use in traditional medicine. This study utilized transcriptome profiling and physiological analysis to explore molecular mechanisms associated with ecological significance and the active accumulation of Cd in C. chinensis. The response to Cd in C. chinensis was assessed through RNA sequencing, Cd determination and isoquinoline alkaloid measurement using its roots, stems, and leaves. The transcriptome revealed, a total of 2667, 2998, or 2815 up-regulated deferentially expressed genes in roots, stems or leaves in response to Cd exposure. Furthermore, we identified phenylpropanoid and isoquinoline alkaloid biosynthesis as the key pathways response to Cd exposure, which suggests that C. chinensis may improve its tolerance to Cd through regulating the phenylpropanoid biosynthesis pathway. Under Cd exposure, plant-pathogen interaction in leaves was identified as the key pathway, which indicates that upregulation of genes involved in plant-pathogen interaction could enhance disease resistance in C. chinensis. WGCNA analysis identified WRKY8 (Cluster-55763.31419) and WRKY47 (Cluster-55763.221590) as potential regulators of secondary metabolic synthesis and plant-pathogen interaction pathway in C. chinensis triggered by Cd. The measurement of berberine, coptisine, palmatine, and epiberberine also demonstrated that Cd simulated the four isoquinoline alkaloids in roots. Therefore, our study not only presented a transcriptome expression profiles that revealed significant upregulation of genes involved in metal transport and detoxification pathways but also suggested a possible mechanism to cope with Cd accumulation. This knowledge provides a new insight into gene manipulation for controlling Cd accumulation, enhancing resistance and promoting synthesis of secondary metabolites with potential medicinal properties in other medicinal plant species.

Tim-3 deficiency aggravates cadmium nephrotoxicity via regulation of NF-κB signaling and mitochondrial damage

Kidney is the target organ of serious cadmium injury. Kidney damage caused by cadmium exposure is greatly influenced by the inflammatory response and mitochondrial damage. T cell immunoglobulin domain and mucin domain 3 (Tim-3) is an essential protein that functions as a negative immunological checkpoint to regulate inflammatory responses. Mice were given cadmium treatments at various dosages (0, 1.5, 3, 4.5 mg/kg) and times (0, 3, 5, 7 days) to assess the effects of cadmium on kidney damage. We found that the optimal way to induce kidney injury in mice was to inject 4.5 mg/kg of cadmium intraperitoneally for five days. It is interesting that giving mice 4.5 mg/kg of cadmium intravenously for seven days drastically lowered their survival rate. After cadmium exposure, Tim-3 knockout mice exhibited higher blood concentrations of urea nitrogen and creatinine compared to control mice. Tim-3 impacted the expression of oxidative stress-associated genes such as UDP glucuronosyltransferase family 1 member A9 (Ugt1a9), oxidative stress-induced growth inhibitor 2 (Osgin2), and S100 calcium binding protein A8 (S100a8), according to RNA-seq and real-time RT-PCR data. Tim-3 deficiency also resulted in activated nuclear factor-kappa B (NF-κB) signaling pathway. The NF-κB inhibitor 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1) significantly alleviated cell apoptosis, oxidative stress response, and renal tubule inflammation in Tim-3 knockout mice exposed to cadmium. Furthermore, cadmium caused obvious B-cell lymphoma protein 2 (Bcl-2)-associated X (Bax) translocation from cytoplasm to mitochondria, which can be inhibited by TPCA-1. In conclusion, Tim-3 prevented mitochondrial damage and NF-κB signaling activation, hence providing protection against cadmium nephrotoxicity.

Elevated CO2 and nitrogen addition enhance the symbiosis and functions of rhizosphere microorganisms under cadmium exposure

Soil microbes are fundamental to ecosystem health and productivity. How soil microbial communities are influenced by elevated atmospheric carbon dioxide (eCO2) concentration and nitrogen (N) deposition under heavy metal pollution remains uncertain, despite global exposure of terrestrial ecosystems to eCO2, high N deposition and heavy metal stress. Here, we conducted a four year's open-top chamber experiment to assess the effects of soil cadmium (Cd) treatment (10 kg hm−2 year−1) alone and combined treatments of Cd with eCO2 concentration (700 ppm) and/or N addition (100 kg hm−2 year−1) on tree growth and rhizosphere microbial community. Relative to Cd treatment alone, eCO2 concentration in Cd contaminated soil increased the complexity of microbial networks, including the number links, average degree and positive/negative ratios. The combined effect of eCO2 and N addition in Cd contaminated soil not only increased the complexity of microbial networks, but also enhanced the abundance of microbial urealysis related UreC and nitrifying related amoA1 and amoA2, and the richness of arbuscular mycorrhiza fungi (AMF), thereby improving the symbiotic functions between microorganisms and plants. Results from correlation analysis and structural equation model (SEM) further demonstrated that eCO2 concentration and N addition acted on functions and networks differently. Elevated CO2 positively regulated microbial networks and functions through phosphorus (P) and Cd concentration in roots, while N addition affected microbial functions through soil available N and soil organic carbon (SOC) concentration and microbial network through soil Cd concentration. Overall, our findings highlight that eCO2 concentration and N addition make microbial communities towards ecosystem health that may mitigate Cd stress, and provide new insights into the microbiology supporting phytoremediation for Cd contaminated sites in current and future global change scenarios.

Blood Pb levels are associated with prostate cancer prevalence among general adult males: Linking National Cancer Registry (2002–2017) and KNHANES (2008–2017) databases of Korea

BackgroundExposure to heavy metals may increase the risk of developing prostate cancer. However, these observations are often inconsistent and not based on clinically diagnosed cases. ObjectiveTo investigate the association of lead (Pb), cadmium (Cd), and mercury (Hg) exposure with clinically determined prostate cancer cases among adult males in South Korea. MethodsMetal biomonitoring data and cancer information from the general Korean population were extracted by linking National Cancer Center (NCC) cancer registration data (2002–2017) with Korea National Health and Nutrition Examination Survey (KNHANES) data (2008–2017). Among them, 46 prostate cancer cases (designated as ‘all-prostate’), including 25 diagnosed after heavy metal measurement (designated as ‘post-prostate’), and 93 matching controls were chosen. Logistic regression analysis was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) between the heavy metal levels and prostate cancer. ResultsPost-prostate patients exhibited higher blood Pb levels than controls (median 3.1 μg/dL vs. 2.38 μg/dL, p = 0.01). For all-prostate cancer, the OR of prostate cancer increased by 2.04-fold for every doubling of Pb levels (95% CI = 1.08–3.87, p = 0.03). The OR was also significantly elevated when comparing the third quartile (Q3) to the lowest quartile (Q1), with ORs ranging from 3.38 to 7.95, depending on model (p < 0.05). Blood Pb levels maintained a positive association with inconsistent significance for post-prostate cancer patients. For Cd and Hg, no statistically significant association was established. SignificanceBy linking two national health databases for the first time, we constructed an unbiased database of prostate cancer cases and matching controls. We found that blood Pb concentrations were associated with the risk of prostate cancer in Korean men at the current level of exposure.

Low dose cadmium exposure regulates miR-381–ANO1 interaction in airway epithelial cells

Chronic obstructive pulmonary disease (COPD) is the 3rd leading cause of death worldwide. Cigarette smoke which has approximately 2–3 µg of Cadmium (Cd) per cigarette contributes to the environmental exposure and development and severity of COPD. With the lack of a cadmium elimination mechanism in humans, the contribution of cadmium induced stress to lung epithelial cells remains unclear. Studies on cadmium responsive miRNAs suggest regulation of target genes with an emphasis on the critical role of miRNA–mRNA interaction for cellular homeostasis. Mir-381, the target miRNA in this study is negatively regulated by cadmium in airway epithelial cells. miR-381 is reported to also regulate ANO1 (Anoctamin 1) expression negatively and in this study low dose cadmium exposure to airway epithelial cells was observed to upregulate ANO1 mRNA expression via mir-381 inhibition. ANO1 which is a Ca2+-activated chloride channel has multiple effects on cellular functions such as proliferation, mucus hypersecretion and fibroblast differentiation in inflamed airways in chronic respiratory diseases. In vitro studies with cadmium at a high concentration range of 100–500 µM is reported to activate chloride channel, ANO1. The secretory epithelial cells are regulated by chloride channels like CFTR, ANO1 and SLC26A9. We examined “ever” smokers with COPD (n = 13) lung tissue sections compared to “never” smoker without COPD (n = 9). We found that “ever” smokers with COPD had higher ANO1 expression. Using mir-381 mimic to inhibit ANO1, we demonstrate here that ANO1 expression is significantly (p < 0.001) downregulated in COPD derived airway epithelial cells exposed to cadmium. Exposure to environmental cadmium contributes significantly to ANO1 expression.

The association of cadmium heavy metal with growth failure in children: A systematic review and meta-analysis.

Introduction: early exposure to cadmium toxic metal has been suggested to be associated with reduced infants/children growth; nevertheless, the available evidence is contradictory. Objective: this meta-analysis aimed to examine the association of cadmium exposure through biological samples to growth measurements of infants/children, including body weight, height, body mass index (BMI), BMI-for-age (BMI Z-score), weight-for-age (WAZ), height-for-age (HAZ), and weight-for-height (WHZ) z-scores. Methods: a systematic search in PubMed and Scopus was implemented to obtain the related studies. The standardized beta coefficients (β) and 95 % confidence intervals (95 % CI) were used as effect sizes to test the associations using the random effects analysis. Results: a total of 15 studies with 6,181 participants were included in the meta-analysis. In the overall analysis, pooled analysis of available data revealed that cadmium exposure was inversely linked to height (β = -0.06, 95 % CI = -0.12 to -0.01) and WAZ (β = -0.01, 95 % CI = -0.02 to -0.003). These relationships were also supported by prospective cohort studies and urinary cadmium exposure. In the stratified analysis, cadmium exposure was negatively linked to the weight of children in prospective cohort studies, in studies that assessed urinary cadmium exposure. No significant association was detected between cadmium exposure and BMI, BMI Z-score, WHZ, and HAZ in the overall and subgroup analyses. Conclusions: this meta-analysis emphasized the importance of cadmium exposure as a risk factor for growth failure in infants/children.

Cadmium Exposure and Health Effects

Cadmium Exposure and Health Effects

The effects of dietary cadmium on growth, antioxidant defence system and feed evaluation performance of rainbow trout (Oncorhynchus mykiss)

The present study was carried out to determine the effect of dietary cadmium exposure on growth performance, changes in manganese, zinc, copper, calcium, magnesium, iron, selenium, and cadmium metals in liver and muscle tissue, liver antioxidant enzymes, and the histology of the fish. Rainbow trout (Oncorhynchus mykiss) with weights of 39.45 ±1.13 g was used in the experiment conducted in 2 groups and three replicates. The Control group was fed a cadmium-free diet, and the Cadmium group was fed a diet containing 5.03 µg/kg of cadmium twice a day until satiation. It was determined that cadmium intake through the diet affected growth rate and the feed evaluation performance negatively. In fish exposed to cadmium, manganese, zinc, copper, calcium, magnesium, iron, selenium, superoxide dismutase, catalase and glutathione peroxidase values in both muscle and liver tissues were significantly (p&lt;0.05) decreased, whereas cadmium levels in muscle and liver and malondialdehyde levels in liver were significantly (p&lt;0.05) increased. The histopathological examination of the liver revealed that cadmium caused liver damage. These results showed that rainbow trout exposed to dietary cadmium were highly sensitive to the metal, and the decreased levels of metals such as copper, zinc, manganese, and selenium in the liver tissue, which are involved in the antioxidant defence system, can be considered an indicator of the weakening of the antioxidant defence system.