Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes

Chen, Chunyan; Zhang, Shaoli; Liu, Zhiyong; Tian, Yong; Sun, Qian

doi:10.1042/bsr20140170

Cited by 69 publications

(31 citation statements)

References 28 publications

(31 reference statements)

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“…In many of the 10 μM Cd-treated larvae that were arched, the pericardium and ventricle were also enlarged, but we did not see evidence of abnormal looping as was reported in the medaka study. Some studies have shown toxic effects of Cd on cultured cardiomyocytes and in whole animals (Chen et al 2015; Ferramola et al 2012). The increased cell death might lower pumping efficiency, and the resulting drop in peripheral blood pressure could induce a compensatory baroreflex in heart rate.…”

Section: Discussionmentioning

confidence: 99%

“…Cd affects redox balance and survival in cultured neurons (Lopez et al 2006) and has been linked to amyloid accumulation and progression of neurodegenerative disorders (Jomova et al 2010; Li et al 2012). Cd has also been linked to the progression of heart disease and to toxicity of cardiomyocytes in vivo and in vitro (Chen et al 2015; Ferramola et al 2012; Limaye & Shaikh 1999), further evidence of the broad impact of this metal.…”

Section: Introductionmentioning

confidence: 97%

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The longitudinal effects of early developmental cadmium exposure on conditioned place preference and cardiovascular physiology in zebrafish

et al. 2017

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Cadmium (Cd) is a naturally occurring trace metal that is widely considered to be highly toxic to aquatic organisms and a significant health hazard to humans (Amzal et al 2009; Bernhoft 2013; Burger 2008; Satarug et al 2009). The zebrafish (Danio rerio) has been used as a model organism for toxicological studies with Cd (Banni et al 2011; Blechinger et al 2007; Chow et al 2009; Chow et al 2008; Favorito et al 2011; Kusch et al 2007; Matz et al 2007; Wang & Gallagher 2013). We asked what the lasting longitudinal effects would be from short early developmental Cd exposure (between 24-96 hours post-fertilization) in a range that larvae might experience living atop typical Cd-containing surface sediments (0, 0.01, 0.1, 1.0 and 10 μM CdCl2: 1.124, 11.24, 112.4 and 1124 μg Cd/L). The goal of this exposure window was to specifically target secondary neurogenesis, monoaminergic differentiation and cardiovascular development, without affecting earlier patterning processes. Developmental abnormalities in body size and CNS morphology increased with concentration, but were statistically significant only at the highest concentration used (10 μM). Heart rate for Cd-treated larvae increased with concentration, and was significant even at the lowest concentration used (0.01 μM). Longitudinal survival was significantly lower for fish developmentally exposed to the highest concentration. Except for brain weight, overall morphology was not affected by developmental Cd exposure. However, developmental exposure to lower concentrations of Cd (0.01, 0.1, and 1.0 μM) progressively lowered cocaine-induced conditioned place preference (CPP), used to measure function of the reward pathways in the brain. Baseline heart rate was significantly lower in longitudinal fish developmentally exposed to 1.0 μM Cd. Cardiovascular response to isoproterenol, a potent β-adrenergic agonist, in longitudinal adults was also significantly affected by developmental exposure to Cd at low doses (0.01, 0.1 and 1.0 μM). Surviving longitudinal adult fish exposed to the highest concentration of Cd showed normal CPP and cardiovascular physiology. The data imply that even lower exposure concentrations can potentially result in fitness-affecting parameters without affecting survival in a laboratory setting.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

The longitudinal effects of early developmental cadmium exposure on conditioned place preference and cardiovascular physiology in zebrafish

et al. 2017

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“…Maternal exposure to cadmium during pregnancy perturbs cardiovascular development of rat offspring which in turn contributes to a long term increased risk of cardiovascular diseases [18]. Cadmium damages vascular tissues, induces endothelial dysfunction and promotes atherosclerosis by oxidative mechanisms [19,20]. In addition to its teratogenic effects, cadmium also causes reproductive toxicity by affecting both testis and oocyte development; increased cadmium concentrations in the ovary have been associated with failure of oocyte development and failure to ovulate [10].…”

Section: Introductionmentioning

confidence: 99%

Transcriptomics analysis of early embryonic stem cell differentiation under osteoblast culture conditions: Applications for detection of developmental toxicity

Chen

Han

Fisher

et al. 2017

Reproductive Toxicology

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The mouse embryonic stem cell test (mEST) is a promising in vitro assay for predicting developmental toxicity. In the current study, early differentiation of D3 mouse embryonic stem cells (mESCs) under osteoblast culture conditions and embryotoxicity of cadmium sulfate were examined. D3 mESCs were exposed to cadmium sulfate for 24, 48 or 72 h, and whole genome transcriptional profiles were determined. The results indicate a track of differentiation was identified as mESCs differentiate. Biological processes that were associated with differentiation related genes included embryonic development and, specifically, skeletal system development. Cadmium sulfate inhibited mESC differentiation at all three time points. Functional pathway analysis indicated biological pathways affected included those related to skeletal development, renal and reproductive function. In summary, our results suggest that transcriptional profiles are a sensitive indicator of early mESC differentiation. Transcriptomics may improve the predictivity of the mEST by suggesting possible modes of action for tested chemicals.

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“…It frequently alters the activity of biological molecules by binding to nitrogen, oxygen, or sulfur-containing groups, eventually disrupting normal cell function [9, 10]. Multiple lines of evidence indicate that apoptosis plays an important role in acute and chronic Cd 2+ intoxication.…”

Section: Introductionmentioning

confidence: 99%

Cadmium-induced apoptosis of Siberian tiger fibroblasts via disrupted intracellular homeostasis

et al. 2016

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BackgroundHeavy metals can cause great harm to Siberian tigers in the natural environment. Cadmium (Cd2+) is an environmental contaminant that affects multiple cellular processes, including cell proliferation, differentiation, and survival. It has been shown to induce apoptosis in a variety of cell types and tissues.ResultsWe investigated the apoptotic effects of Cd2+ on Siberian tiger fibroblasts in vitro. Our research revealed the typical signs of apoptosis after Cd2+ exposure. Apoptosis was dose- (0–4.8 μM) and duration-dependent (12–48 h), and proliferation was strongly inhibited. Cd2+ increased the activity of caspase-3, -8, and -9 and disrupted calcium homeostasis by causing oxidative stress and mitochondrial dysfunction. It also increased K+ efflux and altered the mRNA levels of Bax, Bcl-2, caspase-3, caspase-8, Fas, and p53.ConclusionsOur results suggest that Cd2+ triggers the apoptosis of Siberian tiger fibroblasts by disturbing intracellular homeostasis. These results will aid in our understanding of the effects of Cd2+ on Siberian tigers and in developing interventions to treat and prevent cadmium poisoning.

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Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes

Cited by 69 publications

References 28 publications

The longitudinal effects of early developmental cadmium exposure on conditioned place preference and cardiovascular physiology in zebrafish

The longitudinal effects of early developmental cadmium exposure on conditioned place preference and cardiovascular physiology in zebrafish

Transcriptomics analysis of early embryonic stem cell differentiation under osteoblast culture conditions: Applications for detection of developmental toxicity

Cadmium-induced apoptosis of Siberian tiger fibroblasts via disrupted intracellular homeostasis

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