Studies on the genotoxic effect of chromium oxide (Cr VI): Interaction with deoxyribonucleic acid in solution

Khorsandi, Khatereh; Rabbani-Chadegani, Azra

doi:10.1016/j.mrgentox.2012.10.002

Cited by 20 publications

(5 citation statements)

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“…In this study, we demonstrated that Cr(III) likely also interferes with the stacking mode of DNA base pairs and causes DNA cleavage and degradation of DNA. Cr(VI) was previously suggested to interact with DNA via two modes of interaction: inducing structural changes and DNA compaction [11]. Our results further suggested that Cr(VI) can intercalate into the planes between DNA base pairs and cause DNA structural changes and degradation.…”

Section: Resultssupporting

confidence: 75%

Genotoxicity of Tri- and Hexavalent Chromium Compounds In Vivo and Their Modes of Action on DNA Damage In Vitro

et al. 2014

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Chromium occurs mostly in tri- and hexavalent states in the environment. Hexavalent chromium [Cr(VI)] compounds are extensively used in diverse industries, and trivalent chromium [Cr(III)] salts are used as micronutrients and dietary supplements. In the present work, we report that they both induce genetic mutations in yeast cells. They both also cause DNA damage in both yeast and Jurkat cells and the effect of Cr(III) is greater than that of Cr(VI). We further show that Cr(III) and Cr(VI) cause DNA damage through different mechanisms. Cr(VI) intercalates DNA and Cr(III) interferes base pair stacking. Based on our results, we conclude that Cr(III) can directly cause genotoxicity in vivo.

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Section: Resultssupporting

confidence: 75%

Genotoxicity of Tri- and Hexavalent Chromium Compounds In Vivo and Their Modes of Action on DNA Damage In Vitro

et al. 2014

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“…Similarly, Lou et al (), using human B lymphoblastoid cells, found comets with a significant increase of (%) DNA in the tail after exposure to a range of K 2 Cr 2 O 7 concentrations: 5‐15 μ m during 24 hours and 2.5‐15 μ m during 48 hours. Indeed, Cr(VI) was previously suggested to interact with DNA via two modes of interaction: inducing structural changes and DNA compaction indicating chromium oxide genotoxicity (Khorsandi & Rabbani‐Chadegani, ). Fang and co‐workers (2014) suggested that Cr(VI) could intercalate into the planes between DNA base pairs and cause DNA structural changes and degradation.…”

Section: Discussionmentioning

confidence: 99%

Cr(VI)‐induced genotoxicity and cell cycle arrest in human osteoblast cell line MG‐63

Monteiro

Santos

Bastos

et al. 2019

J of Applied Toxicology

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Occupational environments are major exposure routes to Cr(VI). However, Cr(VI) may also establish in bone tissues by ingestion or through Cr containing orthopaedic prostheses that, due to wear and corrosion, may release metal particles and ions potentially affecting bone tissue. The aim of this work was to evaluate the effects of clinically relevant concentrations of Cr(VI) in human osteoblasts, by integrating genotoxic effects, evaluated by the comet assay and cytokinesis‐blocked micronucleus assay (scoring the presence of micronucleus, nucleoplasmic bridges and nuclear division index), with the effects on cell cycle and cell viability. Human osteoblasts MG‐63 were in vitro exposed to Cr(VI) at concentrations ranging from 0.1 to 5 μm, for 24 and 48 hours. Results pointed out to a decrease of cell viability for both time exposures in a time‐ and dose‐dependent manner, which was related to cell cycle arrest and DNA damage. Chromosome abnormalities were also observed. Hence, these data suggest that cells arrested in the cell division with DNA damage may have followed cell death pathways, while some surviving ones still revealed DNA damage at chromosome level indicating abnormal cell division progression. In conclusion, Cr(VI) induced cytotoxic and genotoxic effects in human bone cells at concentrations that could be found in patients with metal‐on‐metal prostheses. In addition, the early onset of genotoxic damage induced by Cr(VI) at low concentrations after 24 hours of cell exposure alert to the relevance of periodic monitoring of patients for genotoxicity diagnosis after implantation of prostheses before clinical symptoms appear.

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“…Lipid metabolism was greatly affected by Cr (III) , especially cholesterol (Król et al 2012). Studies had shown that Cr (VI) could induce protein denaturation, nucleic acid precipitation, nuclear protein denaturation, DNA damage, and interference with the enzyme system (Khorsandi and Rabbani-Chadegani 2013), as well as genotoxicity (Wan et al 2017). At present, the research on Cr mainly focused on Cr (VI) compounds, and it had been confirmed that Cr (VI) could damage many systems in animal body to varying degrees and even cause organ cancer after long-term exposure (Jaroslav et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Antagonistic effects of nano-selenium on broilers hepatic injury induced by Cr(VI) poisoning in AMPK pathway

Zhang

Zhao

et al. 2020

Environ Sci Pollut Res

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Cr (chromium, with common valence states of III and VI) is one of the common broiler feed additives. Liver injury and metabolic disorders could be caused by Cr (VI) (hexavalent chromium) poisoning in broilers. Oxidative damage and metabolic disorders of organisms caused by heavy metals could be antagonized by nano-Se (nano-selenium). Nano-Se was chosen to study the antagonism of Cr (VI) poisoning in broilers. AMPK (Adenosine 5 , -monophosphate-activated protein kinase) is known as a "cell energy regulator" and plays a key regulatory role in carbohydrate and lipid metabolism. AMPK pathway and ACACA/CPT1A two genes were selected to study the prevention and treatment of nano-Se on Cr (VI) poisoning in broilers and its molecular mechanism. For this purpose, 180 1-day-old AA (Arbor Acres) broilers were selected and randomly divided into 6 groups (n = 30) for further testing. After feeding as planned for 35 days, the livers of such broilers were taken for further examination including histopathological examination, differential gene expression analysis, and further validation on both mRNA and protein levels using related techniques like RT-qPCR, western blot, and immunohistochemistry (IHC). The histopathological examination suggested that the liver cells of the Cr (VI) poisoning group were more severely injured than the nano-Se addition group. RT-qPCR results showed that the relative expression of ACACA gene in the Cr (VI) poisoning group was significantly increased (P < 0.05), while the CPT1A gene's expression was significantly decreased (P < 0.01). Those results were reversed in the nano-Se addition group. Western blot results were consistent with RT-qPCR and both suggested antagonism of nano-Se on Cr (VI) . Through morphological and histopathological observation, as well as the measurement of the mRNA and protein expression levels of ACACA and CPT1A genes in AMPK pathway, it was confirmed that nano-Se has certain preventive and protective effects on Cr (VI) poisoning in broiler chickens. Furthermore, the adverse effects of Cr (VI) on carbohydrate and lipid metabolism in broilers can be antagonized by nano-Se through AMPK pathway. A new method and experimental basis were provided to the future study of Cr (VI) poisoning in broilers. Keywords AMPK pathway . ACACA gene . CPT1A gene . Cr (VI) poisoning . High-throughput sequencing . Nano-selenium . Abbreviations . Nano-SeNano-selenium . CrChromium . Cr (III) Trivalent chromium . Cr (VI) Hexavalent chromium . AMPKAdenosine 5 , -monophosphate-activated protein kinase . K 2 Cr 2 O 7 Potassium dichromate . LD 50 Median lethal dose .

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Studies on the genotoxic effect of chromium oxide (Cr VI): Interaction with deoxyribonucleic acid in solution

Cited by 20 publications

References 20 publications

Genotoxicity of Tri- and Hexavalent Chromium Compounds In Vivo and Their Modes of Action on DNA Damage In Vitro

Genotoxicity of Tri- and Hexavalent Chromium Compounds In Vivo and Their Modes of Action on DNA Damage In Vitro

Cr(VI)‐induced genotoxicity and cell cycle arrest in human osteoblast cell line MG‐63

Antagonistic effects of nano-selenium on broilers hepatic injury induced by Cr(VI) poisoning in AMPK pathway

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