Due to anthropogenic activities, heavy metals still represent a threat for various trophic levels. If aquatic animals are exposed to heavy metals, we can obviously observe considerable toxicity. It is well known that organisms treated with heavy metals synthesize low molecular mass compounds rich in cysteine. In this work the effects of cadmium chloride (2.5, 5, 7.5, 10 and 12.5 mg/L) on common carp (Cyprinus carpio) was investigated. We determined cadmium content in tissue of muscle, liver and kidney by atomic absorption spectrometry with electrothermal atomization and content of metallothionein (MT) in the same tissues by the Brdicka reaction. Electrochemical methods can be considered as suitable and sensitive tools for MT determination in carp tissues. Results of our study showed a gradually enhancing of cadmium content in muscle with time and dose of cadmium chloride in water. MT levels in liver reached both high levels (above 130 ng/g) in fish exposed to 2.5, 5 and 7.5 mg/L and low level (to 50 ng/g) in fish exposed to 10 and 12.5 mg/L of cadmium chloride. This finding confirms that the synthesis of metallothioneins and binding capacity of these proteins is restricted.

Cadmium chloride has various industrial applications and considered an industrial and environmental pollutant. The aim of this study was to evaluate the effect of atorvastatin on Cadmium chloride-induced hepatotoxicity in male rats.

Osteosarcoma is a highly malignant disease and is associated with a poor patient prognosis and a high mortality rate. Disease prognosis significantly correlates with chemotherapeutic responses. Cadmium is a heavy metal with specific effects on bone, but its benefits for osteosarcoma treatment have not been characterized. In the present study, cadmium chloride was used to treat MG63 osteosarcoma cells, and their gene expression profiles were assessed by GeneChip technology. We found that forkhead box protein M1 (FOXM1) was downregulated by cadmium chloride, and lentiviral‑mediated silencing of FOXM1 confirmed a role for this factor in the cisplatin resistance of MG63 cells. In nude mice, cadmium chloride enhanced the sensitivity of osteosarcoma to cisplatin, an effect mediated by FOXM1. Collectively, these data indicate that cadmium chloride can alter the sensitivity of osteosarcoma cells to cisplatin through FOXM1, highlighting it as a potential therapeutic target and prognostic factor for osteosarcoma.

Cadmium is a potential environmental pollutant with worldwide health problems. Many Ficus species are reported to have an extensive diversity of traditional uses, among them the treatment of reproductive toxicity.

Pancreatic cancer (PC) is insidious with a high mortality rate due to the lack of symptomology prior to diagnosis. Mitochondrial involvement in PC development is becoming accepted, and exposure to cadmium (Cd) is suspected of being a risk factor for the development of PC; however, the mechanisms involved remain unclear. In this study, we examined the role of Cd as a mitochondrial toxicant and whether alterations in mitochondrial function may be an underlying cause for the development of PC. In this study, cadmium chloride (CdCl2)‑mediated toxicity in hTERT‑HPNE and AsPC‑1 pancreatic cell lines was determined by MTT assay. We also investigated the release of LDH and the generation of free radicals. Mitochondrial toxicity assays were performed in media containing glucose (25 mM) or galactose (10 mM) and following exposure to CdCl2 (0‑100 µM) followed by MTT assay. For the confirmation of mitochondrial toxicity, we measured the release of ATP following exposure to CdCl2. Initial experiments confirmed that exposure to CdCl2 did not reduce the viability of either cell line until a concentration of >10 µM was used. Non‑linear analysis of the response curves revealed lethal concentration 50% (LC50) values for CdCl2 in the HPNE cells of 77 µM compared to 42 µM in the AsPC‑1 cells (P<0.01). The CdCl2‑mediated mitochondrial toxic effects were greater in the HPNE cells, suggesting a heightened sensitivity to the effects of CdCl2, not due to elevated oxidative stress. Increased mitochondrial toxic sensitivity was indicated by a 73.4% reduction in IC50 values in the HPNE cells cultured in galactose compared to culture in glucose media, whereas the AsPC‑1 cells exhibited a 58.8% reduction in IC50 values. In addition, the higher concentration of CdCl2 elicited a significant cell‑dependent effect on ATP release in both cell lines, suggestive of CdCl2 being a mitochondrial toxicant. Cell survival was unaffected following exposure to low concentrations of CdCl2; however, exposure did alter mitochondrial function (control cells > tumor cells). Therefore, the findings of this study indicate that the mitochondria may be a site of action for cadmium in promoting tumor development.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal and aggressive malignancies with a 5-year survival rate less than 9%. Early detection is particularly difficult due to the lack of symptoms even in advanced stages. microRNAs (miRs/miRNAs) are small (~ 18-24 nucleotides), endogenous, non-coding RNAs, which are involved in the pathogenesis of several malignancies including PDAC. Alterations of miR expressions can lead to apoptosis, angiogenesis, and metastasis. The role of environmental pollutants such as cadmium (Cd) in PDAC has been suggested but not fully understood. This study underlines the role of miRs (miR-221, miR-155, miR-126) in response to cadmium chloride (CdCl2) in vitro. Lethal concentration (LC50) values for CdCl2 resulted in a toxicity series of AsPC-1 > HPNE > BxPC-3 > Panc-1 = Panc-10.5. Following the treatment with CdCl2, miR-221 and miR-155 were significantly overexpressed, whereas miR-126 was downregulated. An increase in epithelial-mesenchymal transition (EMT) via the dysregulation of mesenchymal markers such as Wnt-11, E-cadherin, Snail, and Zeb1 was also observed. Hence, this study has provided evidence to suggest that the environmental pollutant Cd can have a significant role in the development of PDAC, suggesting a significant correlation between miRs and Cd exposure during PDAC progression. Further studies are needed to investigate the precise role of miRs in PDAC progression as well as the role of Cd and other environmental pollutants.

Cadmium (Cd) is the most dangerous heavy metal that is becoming more widespread in nature as a result of industrial activities. One of the toxic effects of Cd on the body is its neurological effect. The mechanism of these effects has been attributed to the induction of oxidative stress. Ferulla plant has antioxidant properties. In the present study, the aim was to reduce the toxic effects of Cd on memory impairment in rats by through the consumption of Ferulla extract.

The ever-increasing human population with attendant industrialization poses serious global health challenge. Cadmium (Cd) with other heavy metals contribute greatly to environmental pollutions and humans are daily exposed to them, leading to diverse ailments. We explored whether Hesperidin (HSP) could protect against hepatic damage and dyslipidemia in Wistar rats exposed to Cd. Forty wistar rats were randomly assigned into five groups (n = 8). Group 1 received 2 mL/kg body weight of normal saline; Group 2 received 100 mg/kg body weight of HSP while Group 3 received 5 mg/kg body weight of Cadmium Chloride (CdCl2) for 28 days. Group 4 received 100 mg/kg body weight of HSP and after 90 min, CdCl2 (5 mg/kg) body weight was administered for 28 days. Group 5 received 50 mg/kg body weight of HSP and after 90 min, CdCl2 (5 mg/kg) body weight was administered for 28 days. The serum lipid profiles, hepatic dysfunction and oxidative stress markers were determined using standard methods. Cd toxicity in rats prominently elevated serum activities of AST, ALT, ALP and levels of total bilirubin, direct bilirubin, cholesterol, LDL-C and malondialdehyde with decreased levels of HDL-C, triglycerides, superoxide dismutase, catalase, glutathione and body weights. The pre-treatment of HSP before Cd intoxication prevented the dysregulated activities of liver enzymes and levels of lipid profiles, enzymatic and non-enzymatic antioxidants and other biomarkers investigated, thus suggesting anti-hyperlipidemic and hepato-protective potentials. HSP may have great potentials for development of therapeutics that could enhance the management of dyslipidemia and liver disorders associated with heavy metal exposure.

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.

Rhizotoxic ions in problem soils inhibit nutrient and water acquisition by roots, which in turn leads to reduced crop yields. Previous studies on the effects of rhizotoxic ions on root growth and physiological functions suggested that some mechanisms were common to all rhizotoxins, while others were more specific. To understand this complex system, we performed comparative transcriptomic analysis with various rhizotoxic ions, followed by bioinformatics analysis, in the model plant Arabidopsis thaliana.

Cadmium is a heavy metal that has been shown to cause its toxicity in humans and animals. Many documented studies have shown that cadmium produces various genotoxic effects such as DNA damage and chromosomal aberrations. Ailments such as bone disease, renal damage, and several forms of cancer are attributed to overexposure to cadmium. Although there have been numerous studies examining the effects of cadmium in animal models and a few case studies involving communities where cadmium contamination has occurred, its molecular mechanisms of action are not fully elucidated. In this research, we hypothesized that oxidative stress plays a key role in cadmium chloride-induced toxicity, DNA damage, and apoptosis of human liver carcinoma (HepG₂) cells. To test our hypothesis, cell viability was determined by MTT assay. Lipid hydroperoxide content stress was estimated by lipid peroxidation assay. Genotoxic damage was tested by the means of alkaline single cell gel electrophoresis (Comet) assay. Cell apoptosis was measured by flow cytometry assessment (Annexin-V/PI assay). The result of MTT assay indicated that cadmium chloride induces toxicity to HepG₂ cells in a concentration-dependent manner, showing a 48 hr-LD50 of 3.6 µg/mL. Data generated from lipid peroxidation assay resulted in a significant (p < 0.05) increase of hydroperoxide production, specifically at the highest concentration tested. Data obtained from the Comet assay indicated that cadmium chloride causes DNA damage in HepG₂ cells in a concentration-dependent manner. A strong concentration-response relationship (p < 0.05) was recorded between annexin V positive cells and cadmium chloride exposure. In summary, these in vitro studies provide clear evidence that cadmium chloride induces oxidative stress, DNA damage, and programmed cell death in human liver carcinoma (HepG₂) cells.

Cadmium is a known industrial pollutant which accumulates in the kidney and its exposure leads to the production of reactive oxygen species (ROS). The present study was carried out to evaluate the protective effects of Peucedanum grande against CdCl2 induced renal toxicity in Wistar rats. Wistar rats were subjected to oral pre-treatment of P. grande (60 and 120 mg/kg b.wt) against the renal toxicity induced by administration of CdCl2 (3mg/kg b.wt). Efficacy of P. grande against the renal toxicity was evaluated in terms of biochemical estimation of antioxidant enzyme activities and histopathological changes. P. grande pretreatment prevented deteriorative effects induced by CdCl2 through a protective mechanism that involved reduction of increased oxidative stress as well as by restoration of histopathological changes against CdCl2 administration.

Introduction: Testicular tissue is part of the reproductive system that some mineral compounds such as cadmium chloride (CdCl2) destroy. Green tea (Camellia sinensis) extract can reduce the tissue damage caused by toxins due to its antioxidant properties. The aim of this study was to evaluate the effect of green tea extract on sperm quality in cadmium chloride toxicity. Materials and Methods: In the present study, male Wistar rats were allotted randomly into four groups, namely control group (C), CdCl2 (1.5mg/kg), GT 1.5% (w/v) and in combinationCdCl2+GT groups. CdCl2 was injected intraperitoneally (1.5 mg /kg) whereas the green tea extract was administrated orally. At 13, 25 and 49 days after treatment, the rats were euthanized and the reproductive organs (testes, epididymis) were excised and used for sperm analysis and histo-morphometric examinations. Results: The mean of the diameter of seminiferous tubes, the number of spermatogonia, Sertoli, Leydig cells and thickness of the germinal layer in the testis were significantly increased (P<0.05) in all groups compared to the CdCl2 group (P<0.05). Sperm motility, sperm count and testosterone were significantly decreased in the CdCl2 group compared to all groups of treatment (p<0.05). The mean of MDA was significantly increased in the CdCl2 group compared to other groups (p<0.05). Conclusion: Green tea has an antioxidant effect that reduces the effects of free oxygen radicals produced from toxins such as cadmium chloride. In addition, it could decrease lipid peroxidation of the cell membrane and ultimately prevent the destruction of tissues in the long run.

The present study was designed to evaluate the antihypertensive activity and cardioprotective effects of magnesium taurate against cadmium chloride (CdCl2)-intoxicated albino rats. Sprague Dawley male albino rats (120-150 g) were divided into five groups having six animals in each group. Hypertension and cardiotoxicity were induced in animals by administration of CdCl2 (0.5 mg/kg/day, i.p.) for four weeks. Magnesium taurate (2 and 4 mg/kg/day) was administered orally after induction of hypertension (after two weeks) in their respective groups concurrently with CdCl2 for next two weeks. Amlodipine (3 mg/kg/day, p.o.) was used as a standard and administered after induction of hypertension. Blood pressure was monitored biweekly by using non-invasive blood pressure system and biochemical parameters and histopathology of the heart were evaluated after four weeks of the experimental protocol. During the four weeks of the experimental protocol, the toxic control group showed significant elevation of systolic and diastolic blood pressure concomitant with augmentation of cardiotoxicity as indicated by reduction in myocardial antioxidants including glutathione peroxidase, catalase, superoxide dismutase, reduced glutathione and increased malondialdehyde level in heart as compared to the normal group. The oral administrations of magnesium taurate significantly restored the blood pressure, myocardial antioxidants and malondialdehyde level as compared to toxic control group. In addition, histopathological examination showed that magnesium taurate treatments substantially reduced the myocardial damages against CdCl2 treatment. The results suggest that magnesium taurate has prominent antihypertensive and cardioprotective activity via its potent antioxidant activity and can be used as a nutrition supplement to improve the cardiovascular health.

In order to address the large percentage of unexplained male infertility in humans, more detailed investigations using sperm functional tests are needed to identify possible causes for compromised fertility. Since many environmental and lifestyle factors might be contributing to infertility, future studies aiming to elucidate the effect of such factors on male fertility will need the use of appropriate research models. The current study aimed to assess the effects of two heavy metals, namely copper sulphate, and cadmium chloride, on non-human primate (NHP) sperm function in order to establish the possibility of using these primate species as models for reproductive studies. Our combined results indicated that the functionality of NHP spermatozoa is inhibited by the two heavy metals investigated. After in vitro exposure, detrimental effects, and significant lowered values (p < 0.05) were obtained for sperm motility, viability and vitality, acrosome intactness, and hyperactivation. These metals, at the tested higher concentrations, therefore, have the ability to impair sperm quality thereby affecting sperm fertilizing capability in both humans and NHPs.

We report the evolution of electrical transport and grain size during the sintering of thin films spin-cast from soluble phosphine and amine-bound, chloride-terminated cadmium selenide nanocrystals. Sintering of the nanocrystals occurs in three distinct stages as the annealing temperature is increased: (1) reversible desorption of the organic ligands (≤150 °C), (2) irreversible particle fusion (200-300 °C), and (3) ripening of the grains to >5 nm domains (>200 °C). Grain growth occurs at 200 °C in films with 8 atom % Cl(-), while films with 3 atom % Cl(-) resist growth until 300 °C. Fused nanocrystalline thin films (grain size = 4.5-5.5 nm) on thermally grown silicon dioxide gate dielectrics produce field-effect transistors with electron mobilities as high as 25 cm(2)/(Vs) and on/off ratios of 10(5) with less than 0.5 V hysteresis in threshold voltage without the addition of indium.

To investigate the protective roles of pyracantha fortune fruit extract (PFE) on acute renal toxicity induced by cadmium chloride (CdCl2) in rats.

Cadmium (Cd) is a common environmental toxicant that has harmful effects on plants, animals, and humans. The present study evaluated the protective effects of Fragaria ananassa methanolic extract (SME) on cadmium chloride (CdCl2)-induced neuronal toxicity in rats. Male albino rats were intraperitoneally (i.p) injected with CdCl2 (6.5 mg/kg) for 5 days with or without the SME (250 mg/kg). We measured the levels of Cd, lipid peroxidation (LPO), nitric oxide, glutathione (GSH), and oxidative enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase, and glutathione reductase (GR) in the whole brain homogenate. Compared with the control group, the Cd-intoxicated group showed a marked increase in the brain levels of Cd, LPO, and nitric oxide and a decrease in the levels of GSH and all tested antioxidant enzymes. Compared with Cd-intoxicated rats, the rats pretreated with SME showed restoration of oxidative balance in the brain tissue. While the expression of brain SOD2, CAT, glutathione peroxidase 1, and GR was down-regulated in the Cd-treated group, the expression of these enzymes was up-regulated in rats pretreated with SME. In addition, administration of SME before CdCl2 increased the Bcl-2 expression, but significantly decreased the expression of Bax. Immunohistochemical analysis showed that compared with Cd-intoxicated rats, rats pretreated with SME showed a decrease in the protein expression of tumor necrosis factor α (TNF-α). Our findings indicate that SME protects the brain tissue from Cd-induced neuronal toxicity by improving the antioxidant system and increasing antiapoptotic and anti-inflammatory activities.

We examined the dose⁻response effect of MnCl₂ on the proliferative behavior of triple-negative breast cancer MDA-M231 cells vs. immortalized HB2 cells from breast epithelium taken as nontumoral counterparts. We also tested the effect of MnCl₂ on tumor cell invasiveness in vitro by evaluating the relative invasion indexes through Boyden chamber assays. Moreover, we checked whether cotreatment with both MnCl₂ and CdCl₂ could modify the observed biological response by MDA-MB231 cells. Our results show a promotional impact of MnCl₂ on cell proliferation, with 5 µM concentration inducing the more pronounced increase after 96-h exposure, which is not shared by HB2 cells. Exposure to 5 µM MnCl₂ induced also an elevation of the relative invasion index of cancer cells. The Mn-mediated stimulatory effects were counteracted by cotreatment with CdCl₂. These data support the concept that human exposure to high environmental concentrations of Mn may increase the risk of carcinogenesis and metastasis by prompting the expansion and dissemination of triple-negative breast cancer cells. On the other hand, the Mn-counteracting anticancer property of Cd looks promising and deserves a more detailed characterization of the involved intracellular targets aimed to the molecular modeling of specific antineoplastic agents against malignant breast cancer spreading.

Cadmium chloride which is potentially toxic is currently used in industry. The toxic effects of cadmium on testes have been reported to range from apoptosis to necrosis, with different effects on fertility. This research aimed to study the effect of different doses of cadmium on testicular tissues at acute stage by light and electron microscopy.