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[en] The National Research Council has outlined the need for non-mammalian toxicological models to test the potential health effects of a large number of chemicals while also reducing the use of traditional animal models. The nematode Caenorhabditis elegans is an attractive alternative model because of its well-characterized and evolutionarily conserved biology, low cost, and ability to be used in high-throughput screening. A high-throughput method is described for quantifying the reproductive capacity of C. elegans exposed to chemicals for 48 h from the last larval stage (L4) to adulthood using a COPAS Biosort. Initially, the effects of exposure conditions that could influence reproduction were defined. Concentrations of DMSO vehicle ≤ 1% did not affect reproduction. Previous studies indicated that C. elegans may be influenced by exposure to low pH conditions. At pHs greater than 4.5, C. elegans reproduction was not affected; however below this pH there was a significant decrease in the number of offspring. Cadmium chloride was chosen as a model toxicant to verify that automated measurements were comparable to those of traditional observational studies. EC50 values for cadmium for automated measurements (176-192 μM) were comparable to those previously reported for a 72-h exposure using manual counting (151 μM). The toxicity of seven test toxicants on C. elegans reproduction was highly correlative with rodent lethality suggesting that this assay may be useful in predicting the potential toxicity of chemicals in other organisms.
[en] Trace metal accumulation and thiol compounds synthesis as induced by cadmium exposure was studied in the seagrass Thalassia testudinum. Shoots were exposed for 24, 48, 96 and 144 h to several CdCl2 concentrations (0, 30, 50 and 70 μM). Levels of cadmium, cysteine, glutathione (GSH), γ-glutamylcysteine (γ-EC), and phytochelatin-like peptides were determined in green blades, live sheaths and root/rhizomes tissues. Metal accumulation was dependent on Cd concentration and type of tissue, with green blades showing the highest content followed by live sheaths and root/rhizomes. All tissues experienced an increase in thiol-containing compounds as a response to cadmium exposure. Live sheaths showed the highest levels of cysteine, GSH and γ-EC. This is the first report of induction of thiol peptides, presumably phytochelatins, by a trace metal in a sea grass species
[en] The original version of this article unfortunately contains errors in Abstract, Section 4.4 Vickers microhardness test and Section 5 Conclusion. In Abstract (7th line) the word “hard” should be changed to “soft”, in Section 4.4 Vickers microhardness test, 15th line the value 1.04 should be changed to 3.27 and in the same sentence the word “hard” should be changed to “soft”. In Section 5 Conclusion (18th line) the word “hard” should be changed to “soft”.
[en] ATF5 is a member of the CREB/ATF family of transcription factors. In the current study, using a transient transfection system to express FLAG epitope fusion proteins of ATF5, we have shown that CdCl2 or NaAsO3 increases the protein levels of ATF5 in cells, and that cadmium stabilizes the ATF5 protein. Proteasome inhibitors had a similar effect to cadmium on the cellular accumulation of ATF5. Proteasome inhibition led to an increase in ubiquitinated ATF5, while cadmium did not appear to reduce the extent of ATF5 ubiquitination. ATF5 contains a putative nuclear export signal within its N-terminus. We demonstrated that whereas deletion of N-terminal region resulted in a increase of ATF5 levels, this region does not appear to be involved in the ubiquitination of ATF5. These results indicate that ATF5 is targeted for degradation by the ubiquitin-proteasome pathway, and that cadmium slows the rate of ATF5 degradation via a post-ubiquitination mechanism.
[en] With increased industrial development, cadmium is an increasingly important environmental pollutant. Studies have identified various adverse effects of cadmium on human beings. However, the relationships between cadmium pollution and the pathogenesis of preeclampsia remain elusive. The objective of this study is to explore the effects of cadmium on immune system among preeclamptic patients and rats. The results showed that the cadmium levels in the peripheral blood of preeclamptic patients were significantly higher than those observed in normal pregnancy. Based on it, a novel rat model of preeclampsia was established by the intraperitoneal administration of cadmium chloride (CdCl2) (0.125 mg of Cd/kg body weight) on gestational days 9–14. Key features of preeclampsia, including hypertension, proteinuria, placental abnormalities and small foetal size, appeared in pregnant rats after the administration of low-dose of CdCl2. Cadmium increased immunoglobulin production, mainly angiotensin II type 1-receptor-agonistic autoantibodies (AT1-AA), by increasing the expression of activation-induced cytosine deaminase (AID) in B cells. AID is critical for the maturation of antibody and autoantibody responses. In addition, angiotensin II type 1-receptor-agonistic autoantibody, which emerged recently as a potential pathogenic contributor to PE, was responsible for the deposition of complement component 5 (C5) in kidneys of pregnant rats via angiotensin II type 1 receptor (AT1R) activation. C5a is a fragment of C5 that is released during C5 activation. Selectively interfering with C5a signalling by a complement C5a receptor-specific antagonist significantly attenuated hypertension and proteinuria in Cd-injected pregnant rats. Our results suggest that cadmium induces immune abnormalities that may be a key pathogenic contributor to preeclampsia and provide new insights into treatment strategies of preeclampsia. - Highlights: • The cadmium levels in the peripheral blood of preeclamptic patients were higher than those in normal pregnancy. • A novel rat model of preeclampsia by injection with low-dose CdCl2 during GD 9-14 was established. • Cadmium increased AT1-AA level by upregulating activation-induced cytosine deaminase in B cells. • AT1-AA-mediated AT1 receptor activation is responsible for C5 elevation. • Elevated C5a contributes to key features of PE seen in the CdCl2-injection model. - We established the preeclampsia model by injection with low-dose of cadmium chloride during GD 9–14. Cadmium-induced immune abnormality may be a key pathogenic event in preeclampsia.
[en] Highlights: ► Diffusion coefficients of cadmium chloride in aqueous solutions. ► Influence of the electrophoretic and thermodynamic effects on diffusion of cadmium chloride in the aqueous media. ► Estimation of the equivalent conductance of the cadmium (II) ion at infinitesimal concentration and at 310.15 K. - Abstract: Mutual diffusion coefficients (interdiffusion coefficients) of cadmium (II) chloride in water at T = 310.15 K at concentrations between 0.001 mol·dm−3 and 0.400 mol·dm−3 have been determined, using the Taylor technique. The results are discussed on the basis of Nernst, and Onsager and Fuoss’ theories, taking into account different phenomena such as electrophoretic and thermodynamic effects. Using such results, the equivalent conductance at infinitesimal concentration of the cadmium (II) ion in these solutions at T = 310.15 K has been estimated. These results permit us to have a better understanding of the structure of the cited systems and the thermodynamic behaviour of cadmium chloride in aqueous solutions.
[en] The solubility isotherms of the ternary systems CdX2-CS(NH2)2-CH3OH (X=Cl, Br, I) at 25 deg C have been investigated. The fields of equilibrium existence of the salts CdCl2·2CH3OH, CdCl2·2CS(NH2)2, CS(NH2)2, CdBr2·3CH3OH, CdBr2·CS(NH2)2, CdBr2·2CS(NH2)2, CdI2 and CdI2·2CS(NH2)2 were determined. The formation of CdS by thermal dissociation of double salts and saturated solutions is discussed. (author)