Cadmium-induced changes in genomic DNA-methylation status increase aneuploidy events in a pig Robertsonian translocation model

Inglot, Paulina; Lewińska, Anna; Potocki, Leszek; Oklejewicz, Bernadetta; Tabęcka-Łonczyńska, Anna; Koziorowski, Marek; Bugno‐Poniewierska, Monika; Bartosz, Grzegorz; Wnuk, Maciej

doi:10.1016/j.mrgentox.2012.05.007

Cited by 44 publications

(15 citation statements)

References 60 publications

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“…Cells derived from the pig hybrid were treated with different doses of cadmium sulfate (1 μM and 5μM) for 72 h. A cadmium-mediated increase in aneuploidy was observed along with a global increase in 5mC for both doses as detected by HPLC and immunostaining. Cadmium-induced aneuploidy may be mediated by global DNA hypermethylation and this may be one mechanism of cadmium-induced carcinogenesis (Inglot et al, 2012). …”

Section: Dna Methylation and Metal-induced Carcinogenesismentioning

confidence: 99%

Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis

Brocato

Costa

2013

Critical Reviews in Toxicology

124

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DNA methylation plays an intricate role in the regulation of gene expression and events that compromise the integrity of the methylome may potentially contribute to disease development. DNA methylation is a reversible and regulatory modification that elicits a cascade of events leading to chromatin condensation and gene silencing. In general, normal cells are characterized by gene-specific hypomethylation and global hypermethylation, while cancer cells portray a reverse profile to this norm. The unique methylome displayed in cancer cells is induced after exposure to carcinogenic metals such as nickel, arsenic, cadmium, and chromium (VI). These metals alter the DNA methylation profile by provoking both hyper- and hypomethylation events. The metal-stimulated deviations to the methylome are possible mechanisms for metal-induced carcinogenesis and may provide potential biomarkers for cancer detection. Development of therapies based on the cancer methylome requires further research including human studies that supply results with larger impact and higher human relevance.

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Section: Dna Methylation and Metal-induced Carcinogenesismentioning

confidence: 99%

Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis

Brocato

Costa

2013

Critical Reviews in Toxicology

124

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“…At the cellular level, excessive Cd concentrations can cause chromosomal aberrations and alteration of cell cycles and division (Inglot et al 2012;Filipič 2012) as well as enhanced production of reactive oxygen species (ROS) (Lin et al 2012;Gill et al 2013). Overproduction of ROS may cause cell death due to oxidative processes such as DNA and RNA damage, enzyme inhibition, protein oxidation and membrane lipid peroxidation (Tian et al 2011;Shahid et al 2013aShahid et al , 2014a.…”

Section: Introductionmentioning

confidence: 99%

Cadmium Bioavailability, Uptake, Toxicity and Detoxification in Soil-Plant System

Shahid

Dumat

Khalid

et al. 2016

Reviews of Environmental Contamination and Toxicology

225

175

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This review summarizes the findings of the most recent studies, published from 2000 to 2016, which focus on the biogeochemical behavior of Cd in soil-plant systems and its impact on the ecosystem. For animals and people not subjected to a Cd-contaminated environment, consumption of Cd contaminated food (vegetables, cereals, pulses and legumes) is the main source of Cd exposure. As Cd does not have any known biological function, and can further cause serious deleterious effects both in plants and mammalian consumers, cycling of Cd within the soil-plant system is of high global relevance.The main source of Cd in soil is that which originates as emissions from various industrial processes. Within soil, Cd occurs in various chemical forms which differ greatly with respect to their lability and phytoavailability. Cadmium has a high phytoaccumulation index because of its low adsorption coefficient and high soil-plant mobility and thereby may enter the food chain. Plant uptake of Cd is believed to occur mainly via roots by specific and non-specific transporters of essential nutrients, as no Cd-specific transporter has yet been identified. Within plants, Cd causes phytotoxicity by decreasing nutrient uptake, inhibiting photosynthesis, plant growth and respiration, inducing lipid peroxidation and altering the antioxidant system and functioning of membranes. Plants tackle Cd toxicity via different defense strategies such as decreased Cd uptake or sequestration into vacuoles. In addition, various antioxidants combat Cd-induced overproduction of ROS. Other mechanisms involve the induction of phytochelatins, glutathione and salicylic acid.

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“…In addition to the alterations of the mitotic spindle, to the weakness of mitotic checkpoints and to cytoskeletal defects, a growing body of evidence suggests that aneuploidy can be also induced by epigenetic mechanisms. 49,50 Chromatin condensation and reorganization, as well as global gene expression alterations, were observed in fibroblasts exposed to Au NPs, providing further insights into the molecular mechanisms underlying toxicity of Au NPs and their impact on epigenetic processes.…”

mentioning

confidence: 98%

Aneuploidogenic effects and DNA oxidation induced in vitro by differently sized gold nanoparticles

Bucchianico¹,

Fabbrizi²,

Cirillo³

et al. 2014

IJN

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Gold nanoparticles (Au NPs) are used in many fields, including biomedical applications; however, no conclusive information on their potential cytotoxicity and genotoxicity mechanisms is available. For this reason, experiments in human primary lymphocytes and murine macrophages (Raw264.7) were performed exposing cells to spherical citrate-capped Au NPs with two different nominal diameters (5 nm and 15 nm). The proliferative activity, mitotic, apoptotic, and necrotic markers, as well as chromosomal damage were assessed by the cytokinesis-block micronucleus cytome assay. Fluorescence in situ hybridization with human and murine pancentromeric probes was applied to distinguish between clastogenic and aneuploidogenic effects. Our results indicate that 5 nm and 15 nm Au NPs are able to inhibit cell proliferation by apoptosis and to induce chromosomal damage, in particular chromosome mis-segregation. DNA strand breaks were detected by comet assay, and the modified protocol using endonuclease-III and formamidopyrimidine-DNA glycosylase restriction enzymes showed that pyrimidines and purines were oxidatively damaged by Au NPs. Moreover, we show a size-independent correlation between the cytotoxicity of Au NPs and their tested mass concentration or absolute number, and genotoxic effects which were more severe for Au NP 15 nm compared to Au NP 5 nm. Results indicate that apoptosis, aneuploidy, and DNA oxidation play a pivotal role in the cytotoxicity and genotoxicity exerted by Au NPs in our cell models.

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Cadmium-induced changes in genomic DNA-methylation status increase aneuploidy events in a pig Robertsonian translocation model

Cited by 44 publications

References 60 publications

Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis

Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis

Cadmium Bioavailability, Uptake, Toxicity and Detoxification in Soil-Plant System

Aneuploidogenic effects and DNA oxidation induced in vitro by differently sized gold nanoparticles

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