Human Skin Cells Are More Sensitive than Human Lung Cells to the Cytotoxic and Cell Cycle Arresting Impacts of Particulate and Soluble Hexavalent Chromium

Xie, Hong; Holmes, Amie L.; Wise, Sandra S.; Young, Jamie L.; Wise, James T.F.; Wise, John Pierce

doi:10.1007/s12011-015-0315-6

Cited by 17 publications

(7 citation statements)

References 27 publications

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“…These data are not surprising and are consistent with historical literature showing Cr(VI) is a clastogen (IARC 1990, De Flora et., 1990). Our study is also consistent with current studies using primary and immortalized lung and skin cell lines (Wise, J. et al, 2002; Wise, S. et al 2004, 2006a; Holmes et al, 2006a, 2006b; Xie et al, 2015). Difficulties arise in trying to compare the urothelial cells to these studies as different cell types require different media which can affect Cr(VI) reduction and dissolution.…”

Section: Discussionsupporting

confidence: 93%

Hexavalent chromium induces chromosome instability in human urothelial cells

Wise

Holmes

Liou

et al. 2016

Toxicology and Applied Pharmacology

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Numerous metals are well-known human bladder carcinogens. Despite the significant occupational and public health concern of metals and bladder cancer, the carcinogenic mechanisms remain largely unknown. Chromium, in particular, is a metal of concern as incidences of bladder cancer have been found elevated in chromate workers, and there is an increasing concern for patients with metal hip implants. However, the impact of Cr(VI) on bladder cells has not been studied. We compared chromate toxicity in two bladder cell lines; primary human urothelial cells and hTERT-immortalized human urothelial cells. Hexavalent chromium (Cr(VI)) induced a concentration- and time-dependent increase in chromosome damage in both cell lines, with the hTERT-immortalized cells exhibiting more chromosome damage than the primary cells. Chronic exposure to Cr(VI) also induced a concentration-dependent increase in aneuploid metaphases in both cell lines which was not observed after a 24 h exposure. Aneuploidy induction was higher in the hTERT-immortalized cells. When we correct for uptake, Cr(VI) induces a similar amount of chromosome damage and aneuploidy suggesting that the differences in Cr(VI) sensitivity between the two cells lines were due to differences in uptake. The increase in chromosome instability after chronic chromate treatment suggests this may be a mechanism for chromate-induced bladder cancer specifically and may be a mechanism for metal-induced bladder cancer in general.

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Section: Discussionsupporting

confidence: 93%

Hexavalent chromium induces chromosome instability in human urothelial cells

Wise

Holmes

Liou

et al. 2016

Toxicology and Applied Pharmacology

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“…To assess how the f-SatIII content associates with stress intensity, we used a previously tested model with human skin fibroblasts cultured in the presence of Cr(VI). Cr(VI) induces oxidative stress with severity depending on the Cr(VI) concentration (Carlisle et al, 2000; Veiko et al, 2005; Asatiani et al, 2011; Xie et al, 2015; Monteiro et al, 2019). The fifth-passage HSF-66, HSF-61, HSF-57, HSF-49, and HSF-41 cells were cultured in the presence of 4 or 6 µM of K 2 CrO 4 for 24 h. After the culture medium was changed to a fresh one, the cells were cultivated for the next 72 h. To assess their proliferative activity, the amount of DNA in the cells was measured ( Figure 5A ).…”

Section: Resultsmentioning

confidence: 99%

Copy Number Variation of Human Satellite III (1q12) With Aging

et al. 2019

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Introduction: Human satellite DNA is organized in long arrays in peri/centromeric heterochromatin. There is little information about satellite copy number variants (CNVs) in aging and replicative cell senescence (RS). Materials and Methods: Biotinylated pUC1.77 probe was used for the satellite III (f-SatIII) quantitation in leukocyte DNA by the non-radioactive quantitative hybridization for 557 subjects between 2 and 91 years old. The effect of RS and genotoxic stress (GS, 4 or 6 µM of K 2 CrO 4 ) on the f-SatIII CNV was studied on the cultured human skin fibroblast (HSF) lines of five subjects. Results: f-SatIII in leukocyte and HSFs varies between 5.7 and 40 pg/ng of DNA. During RS, the f-SatIII content in HSFs increased. During GS, HSFs may increase or decrease f-SatIII content. Cells with low f-SatIII content have the greatest proliferative potential. F-SatIII CNVs in different individuals belonging to the different generations depend on year of their birth. Children (born in 2005–2015 years) differed significantly from the other age groups by low content and low coefficient of variation of f-SatIII. In the individuals born in 1912–1925 and living in unfavorable social conditions (FWW, the Revolution and the Russian Civil War, SWW), there is a significant disproportion in the content of f-SatIII. The coefficient of variation reaches the maximum values than in individuals born in the period from 1926 to 1975. In the group of people born in 1990–2000 (Chernobyl disaster, the collapse of the Soviet Union, and a sharp decline in the population living standard), again, there is a significant disproportion of individuals in the content of f-SatIII. A similar disproportion was observed in the analysis of a group of individuals born in 1926–1975 who in their youth worked for a long time in high-radioactive environment. Conclusion: In generations that were born and who lived in childhood in a period of severe social perturbations or in conditions of environmental pollution, we found a significant increase in leukocyte DNA f-SatIII variability. It is hypothesized that the change of the f-SatIII content in the blood cells reflects the body response to stress of different nature and intensity.

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“…There are two possible explanations for this: (1) the previous studies focused on acute, high-Cr(VI) exposures and this change could be related to survival during acute Cr(VI) exposure, and (2) another report found that human lung and skin fibroblasts have different sensitivities to Cr(VI). 32…”

Section: Discussionmentioning

confidence: 99%

Investigating the Role of Mitochondrial Respiratory Dysfunction during Hexavalent Chromium-Induced Lung Carcinogenesis

Wise¹,

Wang²,

Alstott³

et al. 2018

J Environ Pathol Toxicol Oncol

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Hexavalent chromium [Cr(VI)] is a lung carcinogen and its complete mechanism of action remains to be investigated. Metabolic reprogramming of key energy metabolism pathways (e.g., increased anaerobic glycolysis in the presence of oxygen or “Warburg effect,” dysregulated mitochondrial function, and lipogenesis) are important to cancer cell and tumor survival and growth. In our current understanding of Cr(VI)-induced carcinogenesis, the role for metabolic reprogramming remains unclear. In this study, we treated human lung epithelial cells (BEAS-2B) with Cr(VI) for 6 months and obtained malignantly transformed cells from an isolated colony grown in soft agar. We also used Cr(VI)-transformed cells from two other human lung cell lines (BEP2D and WTHBF-6 cells). Overall, we found that all the Cr(VI)-transformed cells had no changes in their mitochondrial respiratory functions (measured by the Seahorse Analyzer) compared with passaged-matched control cells. Using a xenograft tumor growth model, we generated tumors from these transformed cells in Nude mice. Using cells obtained from the xenograft tumor tissues, we observed that these cells had decreased maximal mitochondrial respiration, spare respiratory capacity, and coupling efficiency. These results provide evidence that, although mitochondrial dysfunction does not occur during Cr(VI)-induced transformation of lung cells, it does occur during tumor development.

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Human Skin Cells Are More Sensitive than Human Lung Cells to the Cytotoxic and Cell Cycle Arresting Impacts of Particulate and Soluble Hexavalent Chromium

Cited by 17 publications

References 27 publications

Hexavalent chromium induces chromosome instability in human urothelial cells

Hexavalent chromium induces chromosome instability in human urothelial cells

Copy Number Variation of Human Satellite III (1q12) With Aging

Investigating the Role of Mitochondrial Respiratory Dysfunction during Hexavalent Chromium-Induced Lung Carcinogenesis

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