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

Fang, Zhijia; Zhao, Min; Zhao, Hong; Chen, Lifeng; Shi, Ping; Huang, Zhiwei

doi:10.1371/journal.pone.0103194

Cited by 139 publications

(84 citation statements)

References 45 publications

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“…increased γ-H2AX, a sensitive indicator of DNA DSB, in Caco-2 cells (Thompson et al, 2012). Therefore, Cr(VI)-induced DNA damage may be responsible for cell cycle delay, as observed in MG-63 cells in the present study through the positive correlation between the increasing showed that Cr(VI) induced DNA DSB in normal human dermal fibroblasts (Ha, Ceryak, & Patierno, 2004), HeLa cells (Wakeman et al, 2004) and T-lymphocyte Jurkat cells (Fang et al, 2014), as well as Cr-DNA, DNA-DNA and DNA-protein crosslinks in normal human lung cells (LL 24 cell cline) (Fang et al, 2014;Xu, Bubley, Detrick, Blankenship, & Patierno, 1996). In studies by Ha et al (2004), Wakeman et al (2004) and Xu et al (1996) In previous studies using non-osteoblasts, treatments with K 2 Cr 2 O 7 for 24-30 hours induced chromosome breaks as well as aneuploidy after a short post-exposure time of 24-30 hours (Figgitt et al, 2010;Güerci, Seoane, & Dulout, 2000;Seoane, Güerci, & Dulout, 2002).…”

Section: Discussionsupporting

confidence: 66%

“…Using the same cell line other authors found that Cr(VI) changed the expression of proteins involved in energy metabolism, stress signalling and proliferation (cytoskeletal proteins) (Raghunathan, Grant, & Ellis, ). Although genotoxic effects have been detected in several human cell types exposed to Cr(VI) (Fang et al, ; Novotnik, Ščančar, Milačič, Filipič, & Žegura, ; Thompson et al, ; Wise, Holmes, Liou, Adam, & Wise, ) it is pertinent the thorough investigation of such effects in human osteoblasts as they are also targets of Cr(VI). The aim of this work was to evaluate the effects of clinically relevant concentrations of Cr(VI) in human osteoblasts, by integrating genotoxicity results with possible changes in the cell cycle and cell viability, and assess the usefulness of these endpoints as reliable clinical biomarkers of Cr(VI)‐induced toxicity in bone tissues of patients using MoM prostheses.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 66%

Section: Introductionmentioning

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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“…34 There is growing evidence that chromium (III) is genotoxic 35 , highlighting the importance of measuring total chromium. In our study, we could not measure the valence state of chromium.…”

Section: Discussionmentioning

confidence: 99%

E-cigarettes as a source of toxic and potentially carcinogenic metals

Hess

Olmedo

Navas‐Acien

et al. 2017

Environmental Research

229

163

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Background and Aims The popularity of electronic cigarette devices is growing worldwide. The health impact of e-cigarette use, however, remains unclear. E-cigarettes are marketed as a safer alternative to cigarettes. The aim of this research was the characterization and quantification of toxic metal concentrations in five, nationally popular brands of cig-a-like e-cigarettes. Methods We analyzed the cartomizer liquid in 10 cartomizer refills for each of five brands by Inductively Coupled Plasma Mass Spectrometry (ICP-MS). Results All of the tested metals (cadmium, chromium, lead, manganese and nickel) were found in the e-liquids analyzed. Across all analyzed brands, mean (SD) concentrations ranged from 3.20 (0.454) to 1960 (1540) μg/L for lead, 53.9 (6.95) to 2110 (5220) μg/L for chromium and 115 (49.4) to 22600 (24400) μg/L for nickel. Manganese concentrations ranged from 28.7 (9.79) to 6919 (12200) μg/L. We found marked variability in nickel and chromium concentration within and between brands, which may come from nichrome heating elements. Conclusion Additional research is needed to evaluate whether e-cigarettes represent a relevant exposure pathway for toxic metals in users.

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“…Once inside the cells, CrVI is readily converted into CrIII by AOXs such as ascorbate, glutathione (GSH), and cysteine. CrIII was initially thought to be relatively non-toxic, however, it was found to be more damaging than CrVI in causing genotoxicity in cell free systems (Fang et al, 2014). CrIII interacts with DNA and induces DNA strand breaks, DNA-protein crosslinks and oxidative DNA base modifications (Nickens et al, 2010; Fang et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol protects the ovary against chromium-toxicity by enhancing endogenous antioxidant enzymes and inhibiting metabolic clearance of estradiol

Banu

Stanley

Sivakumar

et al. 2016

Toxicology and Applied Pharmacology

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Resveratrol (RVT), a polyphenolic component in grapes and red wine, has been known for its cytoprotective actions against several diseases. However, beneficial effects of RVT against early exposure to endocrine disrupting chemicals (EDCs) have not been understood. EDCs are linked to several ovarian diseases such as premature ovarian failure, polycystic ovary syndrome, early menopause and infertility in women. Hexavalent chromium (CrVI) is a heavy metal EDC, and widely used in >50 industries. Environmental contamination with CrVI in the US is rapidly increasing, predisposing the human to several illnesses including cancers and still birth. Our lab has been involved in determining the molecular mechanism of CrVI-induced female infertility and intervention strategies to mitigate CrVI effects. Lactating mother rats were exposed to CrVI (50 ppm potassium dichromate) from postpartum days 1–21 through drinking water with or without RVT (10 mg/kg body wt., through oral gavage daily). During this time, F1 females received respective treatments through mother’s milk. On postnatal day (PND) 25, blood and the ovary, kidney and liver were collected from the F1 females for analyses. CrVI increased atresia of follicles by increasing cytochrome C and cleaved caspase-3; decreasing antiapoptotic proteins; decreasing estradiol (E2) biosynthesis and enhancing metabolic clearance of E2, increasing oxidative stress and decreasing endogenous antioxidants. RVT mitigated the effects of CrVI by upregulating cell survival proteins and AOXs; and restored E2 levels by inhibiting hydroxylation, glucuronidation and sulphation of E2. This is the first study to report the protective effects of RVT against any toxicant in the ovary.

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

Cited by 139 publications

References 45 publications

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

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

E-cigarettes as a source of toxic and potentially carcinogenic metals

Resveratrol protects the ovary against chromium-toxicity by enhancing endogenous antioxidant enzymes and inhibiting metabolic clearance of estradiol

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