Mechanism Of Cadmium Research Articles

Sorption mechanisms of cadmium onto nano-hydroxyapatite: Comparative uptake studies and correlative solubility analysis

Hydroxyapatite (HAP) nanorod was synthesized by using ordered bicontinuous microemulsion, and was characterized by X-ray diffraction spectrum, scanning electron microscopy and high-resolution transmission electron microscopy. The solubility was investigated using ion chromatogram measurement, and was sensitively dependent on the value of pH. The capabilities to capture cadmium ions of HAP nanorods and micro-particles from aqueous salt solution were studied, and besides, X-ray diffractometry was used in order to characterize the mechanisms of cadmium uptake. As Cd2+ adsorption occurred, it has undergone the coprecipitation of Cd2P2O7 crystal to give multiple solids composed of HAP and Cd2P2O7 crystallites, which affected the dissolution of hydroxyapatite. During Cd2+ sorption process, solubility variations of the sediments showed a more complex pattern than previously reported. Contribution of surface mechanisms, in association with precipitation of cadmium phosphate phases, could explain this behavior.

The effects of cadmium on VEGF‐mediated angiogenesis in HUVECs

Cadmium (Cd) is a highly toxic element that causes morphologic alterations and dysfunction in blood vessels. The altered vascular function caused by cadmium has been implicated in a range of chronic diseases, including hypertension. The effects of cadmium are a multisystem phenomenon involving inflammation, hypertrophy, apoptosis, angiogenesis and important processes involved in vascular remodeling systems. Vascular endothelial growth factor (VEGF) plays a major role in cell growth and angiogenesis under pathologic conditions. VEGF secretion is related to anti-apoptosis protein expression and attenuates apoptosis in endothelial cells. This study examined the VEGF-dependent mechanisms of angiogenesis and apoptosis in cadmium-treated endothelial cells (HUVECs). The effects and mechanisms of cadmium in endothelial cells (HUVECs) were examined by exposing the cells to different doses of cadmium chloride (2.5-40 μ m). After the cadmium treatment, the angiogenesis and apoptosis mechanisms related to VEGF in cadmium-treated HUVECs were examined. As a result, the low concentration of cadmium increased the tube formation in HUVECs. In addition, cadmium at concentrations of 5 and 10 μ m increased VEGF secretion and VEGFR2 activity, which suggest that cadmium affects the growth of blood vessels. All three MAPK pathways, namely ERK, JNK and p38, were activated by cadmium in HUVECs. However, high concentrations of cadmium caused cell damage, disrupted tube formation and inhibited VEGF expression and the activities of VEGFR2 and MAPK in HUVECs. Cadmium has dual functions through VEGF-dependent mechanisms in a dose-dependent manner. In this study, the dual effects of cadmium might alter angiogenesis and induce apoptosis through VEGF pathways in HUVECs.

Chemisorption and Physical Adsorption Roles in Cadmium Biosorption byChlamydomonas Reinhardtii

Abstract The aim of this study was to investigate the mechanism of cadmium (Cd) adsorbed by microalgae Chlamydomonas reinhardtii (C.reinhardtii). The kinetic and adsorption isotherm of the process could be well described by mathematical models. Chemical modification experiments and Fourier transform infrared spectra indicated that carboxyl and amine groups were the important functional groups for adsorption of Cd. The maximum contribution of physical adsorption in the overall adsorption process was evaluated as 5.5%. These results indicated that chemisorption was the dominating mechanism of Cd biosorption by C.reinhardtii.

Effect and mechanism of cadmium on progesterone synthesis in ovaries granule cells

目的 研究镉对孕激素合成过程中类同醇激素合成急性调节蛋白(StAR)、细胞色素P450胆固醇侧链裂解酶(P450scc)基因表达的影响及其与环磷腺苷(cAMP)的关系,为研究镉对孕激素合成影响的分子机制提供科学依据.方法 未成年Wistar大鼠皮下注射孕马血清促性腺激(PMSG)100U,48 h后取出卵巢颗粒细胞体外培养,备用.(1)取备用细胞随机分成4组,染镉剂量分别为0、10、20、40μmol/L,孵化30 min后,放射免疫方法测黄体酮、cAMP含量,用反转录-聚合酶链反应(RT-PCR)方法 测P450scc、StAR的mRNA表达水平.(2)再取备用细胞随机分为3组,分别为空白对照组、40μmol/L CdCl_2、l mmol/L 8-Br-cAMP(cAMP类似物)+40 μmol/L,CdCl_2,培养2 h后,测黄体酮含量及P450scc、StAR的mRNA表达水平.结果 (1)不同剂量染镉组卵巢颗粒细胞孵育液中黄体酮含量明显下降,差异有统计学意义(P<0.01);随着染镉剂量的增加,cAMP含量逐渐减少;各染镉剂量组StARmRNA和P450scc mRNA表达强度均低于对照组,差异有统计学意义(P<0.01).(2)加入1 mmol/L 8-Br-cAMP共同培养后,黄体酮含量增加,高于染镉(40 μmol/L)组和对照组.差异均有统计学意义(P<0.01);StAR mRNA和P450scc mRNA表达强度均高于40μmol/L染镉组,低于对照组,差异有统计学意义(P<0.05).结论 镉可通过直接和(或)间接途径影响孕激素合成过程StAR和P450scc的表达,进而干扰孕激素的合成;镉对细胞内cAMP的影响可能是其干扰StAR和P450scc基因表达的机制之一。

Adsorption behavior and mechanism of cadmium on strong-acid cation exchange resin

The adsorption behavior of Cd 2+ on 001×7 strong-acid cation exchange resin was studied with the static adsorption method. The adsorption process was analyzed from thermodynamics and kinetics aspects. The influences of experimental parameters such as pH, temperature, initial concentration and adsorption rate were investigated. The experimental results show that in the studied concentration range, 001×7 resin has a good sorption ability for Cd 2+, and the equilibrium adsorption data fit to Freundlich isotherms. The adsorption is an exothermic process which runs spontaneously. Kinetic analysis shows that the adsorption rate is mainly governed by liquid film diffusion. The best adsorption condition is pH 4–5. The saturated resin can be regenerated by 3 mol/L nitric acid, and the desorption efficiency is over 98%. The maximal static saturated adsorption capacity is 355 mg/g (wet resin) at 293 K. The adsorption mechanism of Cd 2+ on 001×7 resin was discussed based on IR spectra.

Surviving global change in polluted environments: Physiological and molecular mechanisms of cadmium and temperature interactions in a marine ectotherm Crassostrea virginica

Surviving global change in polluted environments: Physiological and molecular mechanisms of cadmium and temperature interactions in a marine ectotherm Crassostrea virginica

Effect and mechanism of cadmium on the progesterone synthesis of ovaries

The paper presents results of the effect of cadmium on the progesterone synthesis of ovaries. In the current study, we investigated whether Cd also disrupts progesterone synthesis via steroidogenic acute regulatory protein (StAR) and P450 cholesterol side-chain cleavage (P450scc), which play important roles in progesterone synthesis. The Wistar rats were exposed to cadmium in vivo (at 2.5, 5, 7.5 mg/kg, as a single s.c. dose). We showed that the serum P 4 and granule cells P 4 of rats were significantly lower than control group. Ovaries granule cells were incubated in Dulbecco-modified Eagle medium +15% fetal bovine serum with 0, 10, 20, or 40 μM CdCl 2 in vitro, progesterone levels were declined in a dose-dependent manner. Our data showed that the expression of StAR and P450scc in vivo or in vitro were inhibited when treated with CdCl 2 ( p < 0.05). Coculture with 8-bromo-cAMP enhanced progesterone secretion in untreated cultures and reversed the decline in progesterone secretion induced by CdCl 2 treatment; the expression of StAR mRNA and P450scc mRNA in 8-Br-cAMP + 40 μM CdCl 2 were significantly higher than 40 μM CdCl 2, and were lower than control group. We concluded that StAR, which delivers cholesterol to the inner mitochondrial membrane, is one site at which Cd interferes with progesterone production in cultured rats ovarian granule cells; P450scc, which conveys cholesterol to pregnenolone, is anther site. The mechanisms were mainly controlled by the cAMP-dependent pathway.

Mechanisms of cadmium (Cd 2+ ) induced G2 phase cell cycle arrest in renal proximal tubule (PT) cells

Mechanisms of cadmium (Cd ²⁺ ) induced G2 phase cell cycle arrest in renal proximal tubule (PT) cells

Enhanced cadmium accumulation in maize roots—the impact of organic acids

Low molecular weight organic acids are important components of root exudates and therefore, knowledge regarding the mechanisms of cadmium (Cd) uptake and distribution within plants under the influence of organic acids, is necessary for a better understanding of Cd behavior in the plant–soil system. In this study, acetic and malic acids increased the uptake of Cd by maize (Zea mays L. cv. TY2) roots and enhanced Cd accumulation in shoots under hydroponic conditions. Concentration-dependent net Cd influx in the presence and absence of organic acids could be resolved into linear and saturable components. The saturable component followed Michaelis–Menten kinetics, which indicated that Cd uptake across the plasma membrane was transporter-mediated. While the K m values were similar, the V max values in the presence of acetic and malic acids were respectively 6.0 and 3.0 times that of the control. Zinc transporters were the most probable pathways for Cd accumulation. It was hypothesized that Cd(II)–organic acid complexes associated with the root zone, could decompose and liberate Cd2+ for subsequent absorption by maize roots; and that in the layer of the roots or within the root free space, depletion of Cd2+ was buffered by the presence of Cd(II)–organic acid complexes. Plant response to elevated Cd levels involved overproduction of organic acids in maize roots as a resistance mechanism to alleviate Cd toxicity.

COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

In order to get insight into the mechanism of cadmium (Cd)-induced brain injury, we investigated the effects of Cd on the induction of COX-2 and ICAM-1 in bEnd.3 mouse brain endothelial cells (EC). Cd stimulated PGE 2 release in a time and dose dependent manner, which was accompanied by increase of COX-2 expression. The thiol-reducing antioxidant N-acetylcyteine attenuated Cd-induced PGE 2 production and COX-2 expression. Cd increased phosphorylation of p38 MAPK, but not of JNK and ERK1/2. A blockade of p38 MAPK pathway abrogated Cd-induced COX-2 expression and PGE 2 production. Cd-induced ICAM-1 expression and leukocyte-EC adhesion were diminished by non-steroidal anti-inflammatory drugs such as indomethacin and NS-398, which was reversed by addition of PGE 2. Together, these data suggest that Cd induces COX-2 expression through the activation of p38 MAPK, an oxidative stress-sensitive cellular signaling molecule, and induction of COX-2 is associated with ICAM-1 expression in brain endothelial cells following Cd exposure.

A new method to detect cadmium uptake in protoplasts.

The mechanism for cadmium (Cd2+) uptake into the cytosol of protoplasts from 5- to 7-day-old wheat seedlings (Triticum aestivum L. cv. Kadett) was investigated by a new method, using fluorescence microscopy and the heavy metal-specific fluorescent dye, 5-nitrobenzothiazole coumarin, BTC-5N. Cadmium fluorescence gradually increased in the cytosol of shoot and root protoplasts upon repeated additions of CdCl2 to the external medium, reflecting an uptake of Cd2+. The uptake was inhibited by calcium and potassium chloride, as well as by Verapamil and tetraethylammonium (TEA), inhibitors of calcium and potassium channels, respectively. Calcium competitively inhibited the cadmium uptake. The metabolic inhibitors vanadate and dinitrophenol partly inhibited the uptake, suggesting it was dependent on membrane potential. The results indicate that cadmium is taken up by channels permeable to both calcium and potassium. The total uptake of cadmium into the protoplasts was also detected by unidirectional flux analyses using 109Cd2+, and showed approximately the same maximal concentration of Cd2+ as the fluorescence measurements. By combining the two methods it is possible to detect both uptake into the cytosol and into the vacuole.

Effects of cadmium(II) on (+/-)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide-induced DNA damage response in human fibroblasts and DNA repair: a possible mechanism of cadmium's cogenotoxicity.

Cadmium, a widespread environmental pollutant and a cigarette smoke constituent, enhances the genotoxicity of benzo[a]pyrene (BP). The mechanism(s) underlying the potentiation of BP-induced genotoxicity by Cd2+ is not clearly understood. Our studies of the effects of noncytotoxic concentrations of Cd2+ on the levels of p53 and p21 in (+/-)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE)-treated human fibroblasts showed that Cd2+ decreased BPDE-induced p21 levels in a dose-dependent manner whereas p53 accumulation is attenuated only at higher noncytotoxic concentrations of cadmium. These findings suggest that both the activity and the accumulation of p53 in response of BPDE treatment are inhibited by Cd2+ although the possibility of p53-independent p21 transactivation cannot be ruled out. Exposure of synchronized human fibroblast cells to 0.5 microM of BPDE caused 72% of the cells remaining in G1 phase as compared to 52% in the case of untreated cells. Treatment of the cells with CdCl2 prior to exposing them to BPDE caused a decrease in the G1 population (72 to 54%) in a dose-dependent manner. An in vitro repair assay of BPDE-damaged pUC18 plasmid DNA using untreated and cadmium-treated nucleotide excision repair (NER) proficient HeLa extract showed that cadmium impaired the ability of HeLa cell extract to repair BPDE-damaged pUC18 DNA. Our findings indicate that cadmium not only inhibits NER pathway-dependent repair of BPDE-damaged DNA but also impairs p53 and p21 responses and overrides BPDE-induced G1-S cell cycle arrest. The effect of cadmium on these processes may explain, at least partly, the potentiating effect of the metal on the genotoxicity of BP.

Influence of the Anion Nature and the Metal-to-Additive Ratio on the Effectiveness of ε-Caprolactam during Cadmium Electrodeposition

The rate and mechanism of cadmium(II) electroreduction from electrolytes containing ε-caprolactam were found to significantly depend on the metal-to-additive ratio. Whatever the anion nature, the process sharply accelerates in the presence of an excess of cadmium cations, which form activated surface complexes with adsorbed ε-caprolactam molecules as bridging ligands. With an excess of the additive, metal depolarization due to the Ψ"-effect still persists in perchlorate media; in iodide solutions, ε-caprolactam inhibits this process. The formation of a dense adsorbed film composed of ε-caprolactam molecules and I– anions at the electrode ensures a high throwing power of the electrolyte and makes it possible to obtain uniform elastic organocadmium plating.

The evaporation rates and mechanisms of cadmium from a bubble-stirred molten copper bath

Experiments to determine the evaporation rates and aerosol formation mechanism of cadmium in molten copper at atmospheric pressure have been carried out. A small amount of cadmium (∼1 wt pct) was added to molten copper at 1473 K and allowed to evaporate while bubbling 750 and 1500 cm3/min of argon through the melt. Melt samples were periodically taken and analyzed by inductively coupled plasma/mass spectroscopy (ICP/MS) to determine their impurity content. A theoretical model to predict the evaporation rates of solutes from molten metals was developed and compared to the experimental results. Excellent correlation between experiment and theory was found for the cadmiumcopper system. The model has been extended to other solutes and also to molten Fe-3 (wt pct) C at 1873 K as a solvent.

Cadmium-mediated oxidative stress in kidney proximal tubule cells induces degradation of Na+/K(+)-ATPase through proteasomal and endo-/lysosomal proteolytic pathways.

The mechanisms of cadmium (Cd)-dependent nephrotoxicity were studied in a rat proximal tubule (PT) cell line. CdCl(2) (5 microM) increased the production of reactive oxygen species (ROS), as determined by oxidation of dihydrorhodamine 123 to fluorescent rhodamine 123. The levels of ubiquitin-conjugated cellular proteins were increased by Cd in a time-dependent fashion (maximum at 24-48 h). This was prevented by coincubation with the thiol antioxidant N-acetylcysteine (NAC, 15 mM). Cd also increased apoptosis (controls: 2.4+/-1.6%; Cd: 8.1+/-1.9%), but not necrosis (controls: 0.5 +/- 0.3%; Cd: 1.4+/- 2.5%). Exposure of PT cells with Cd decreased protein levels of the catalytic subunit (alpha1) of Na+/K(+)-ATPase, a long-lived membrane protein (t(1/2)>48 h) that drives reabsorption of ions and nutrients through Na(+)-dependent transporters in PT. Incubation of PT cells for 48 h with Cd decreased Na+/K(+)-ATPase alpha1-subunit, as determined by immunoblotting, by approximately 50%, and NAC largely prevented this effect. Inhibitors of the proteasome such as MG-132 (20 microM) or lactacystin (10 microM), as well as lysosomotropic weak bases such as chloroquine (0.2 mM) or NH(4)Cl (30 mM), significantly reduced the decrease of Na(+)/K(+)-ATPase alpha1-subunit induced by Cd, and in combination abolished the effect of Cd on Na+/K(+)-ATPase. Immunofluorescence labeling of Na+/K(+)-ATPase showed a reduced expression of the protein in the plasma membrane of Cd-exposed cells. After addition of lactacystin and chloroquine to Cd-exposed PT cells, immunoreactive material accumulated into intracellular vesicles. The data indicate that micromolar concentrations of Cd can increase ROS production and exert a toxic effect on PT cells. Oxidative damage increases the degradation of Na+/K(+)-ATPase through both the proteasomal and endo-/lysosomal proteolytic pathways. Degradation of oxidatively damaged Na+/K(+)-ATPase may contribute to the 'Fanconi syndrome'-like Na(+)-dependent transport defects associated with Cd-nephrotoxicity.

Cadmium inhibits vacuolar H+-ATPase and endocytosis in rat kidney cortex

The mechanism of cadmium (Cd)-induced damage in the mammalian proximal tubule that is manifested by defects in reabsorption of various compounds, is poorly understood. A vacuolar H(+)-ATPase (V-ATPase) in proximal tubule (PT) brush border and intracellular vesicles may be affected by Cd, and this may influence intracellular vesicle trafficking and reabsorption of the filtered proteins. We studied the effects of Cd on V-ATPase and endocytosis in rat renal PT in vivo and on acidification mechanisms in isolated renal cortical organelles in vitro. The V-ATPase activity in brush border membrane (BBM) from Cd-intoxicated rats was 40% lower compared to that in control animals. Immunofluorescence studies in cortical tissue sections and Western blot studies in BBM from Cd-treated rats showed a strongly decreased abundance of the 31 kDa and 70 kDa V-ATPase subunits. Functional studies in vivo showed a dramatically diminished endocytosis of fluorescein-labeled dextran in PT cells from Cd-treated animals, whereas morphological studies revealed a loss of endocytic invaginations and subapical vesicles in the same cells. In studies in vitro, Cd inhibited V-ATPase activity in a concentration- and time-dependent manner in both BBM and endocytic vesicles, whereas in endocytic vesicles, Cd inhibited ATP-driven intravesicular acidification and accelerated the dissipation of transmembrane pH gradients. We conclude that Cd may impair acidification in cell organelles by (a) causing a loss of V-ATPase protein in their limiting membranes, (b) inhibiting the intrinsic V-ATPase activity, and (c) dissipating the transmembrane pH gradient. This may inhibit endocytosis of filtered proteins and impair vesicle-mediated recycling of some membrane transporters, thus contributing to the loss of reabsorptive capacity of the PT.

Cadmium-Detoxification in the EarthwormEnchytraeus:Specific Expression of a Putative Aldehyde Dehydrogenase

The ubiquitous earthwormEnchytraeus buchholziis provided with a very effective, but still unknown, mechanism of Cadmium (Cd)-detoxification, a central role in which has been ascribed to the Cd-induciblecrp-gene encoding a novel cysteine-rich, non-metallothionein 25 kDa protein. This study identifies another Cd-responsive gene by differential screening of a cDNA-library constructed from Cd-exposedE. buchholzi.The isolated cDNA-clone designated Ebaldh encodes a putative aldehyde dehydrogenase. Northern blot analysis shows that theEbaldh-expression is strongly enhanced by Cd, but remains unaffected by other stressors such as Zn, Hg, and H2O2. This Cd-specificity ofEbaldhsuggests that Cd-detoxification inE. buchholzirequires low intracellular concentrations of aldehydes which are known to target sulfhydryl groups thus inactivating the Cd-binding capacity of CRP.

Mechanisms of cadmium and zinc accumulation in the polychaete Neanthes arenaceodentata

Mechanisms of cadmium and zinc accumulation in the polychaete Neanthes arenaceodentata

Observations on the distribution and movement of cadmium in epithelial cells of rat small intestine by light- and electron-microscope radioautography.

The localization of cadmium in the absorptive cells of the small intestine has been studied by light- and electron-microscope radioautography at intervals in the first 27 h after intubation of radiocadmium into the stomach of rats. Light-microscope autoradiographic studies showed that cadmium was taken up very quickly by the absorptive cells, and radioactivity in the absorptive layer was disseminated over the entire area of the absorptive cells. Electron-microscope autoradiography showed that there was no concentration of radioactive cadmium in any particular site in the epithelial cells or in the lamina propria. It suggests that the transport mechanism of cadmium through the intestine may be nonspecific. Radioautographic investigation using radiocadmium may provide useful information for cadmium distribution and movement in rat small intestine.

Lung aryl hydrocarbon hydroxylase: Inhibition following cadmium chloride inhalation

Polycyclic hydrocarbon metabolism in male Spraque-Dawley rats following inhalation of aerosolized cadmium chloride (CdCl 2) was examined. Constitutive activity of microsomal aryl hydrocarbon hydroxylase (AHH) (benzo( a)pyrene substrate) was monitored in lung and liver homogenates up to 10 days after exposure. Lung AHH activity was reduced by 85% during the first 2 days following cadmium inhalation, and did not return to normal levels until 7 days after exposure. Enzyme activity in the livers of cadmium-treated animals was similarly depressed (by 65%) within 24 hr. Cadmium inhalation also inhibited (by 50%) 3-methylcholanthrene (MC) induction of lung AHH when compared with MC-treated controls. No significant effect on AHH inducibility by MC was noted in liver homogenates from cadmium-exposed animals. Nonspecific microsomal damage appeared not to occur since glucose-6-phosphatase activity in lung was unaffected by cadmium treatment. Although the mechanism of cadmium's action remains unclear, it appears not to involve a direct interaction of the metal with enzyme. The alteration of AHH activity by cadmium may result from injury to a specific cell type within the lung, which may be a major site of pulmonary AHH activity, or may result from modulation of synthesis and/or degradation of heme proteins in the lung. These results suggest that cadmium, under these conditions, markedly reduces the constitutive and inducible activity of AHH in the lung.