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Title: Hexavalent chromium is cytotoxic and genotoxic to hawksbill sea turtle cells

Abstract

Sea turtles are a charismatic and ancient ocean species and can serve as key indicators for ocean ecosystems, including coral reefs and sea grass beds as well as coastal beaches. Genotoxicity studies in the species are absent, limiting our understanding of the impact of environmental toxicants on sea turtles. Hexavalent chromium (Cr(VI)) is a ubiquitous environmental problem worldwide, and recent studies show it is a global marine pollutant of concern. Thus, we evaluated the cytotoxicity and genotoxicity of soluble and particulate Cr(VI) in hawksbill sea turtle cells. Particulate Cr(VI) was both cytotoxic and genotoxic to sea turtle cells. Concentrations of 0.1, 0.5, 1, and 5 μg/cm{sup 2} lead chromate induced 108, 79, 54, and 7% relative survival, respectively. Additionally, concentrations of 0, 0.1, 0.5, 1, and 5 μg/cm{sup 2} lead chromate induced damage in 4, 10, 15, 26, and 36% of cells and caused 4, 11, 17, 30, and 56 chromosome aberrations in 100 metaphases, respectively. For soluble Cr, concentrations of 0.25, 0.5, 1, 2.5, and 5 μM sodium chromate induced 84, 69, 46, 25, and 3% relative survival, respectively. Sodium chromate induced 3, 9, 9, 14, 21, and 29% of metaphases with damage, and caused 3, 10, 10, 16,more » 26, and 39 damaged chromosomes in 100 metaphases at concentrations of 0, 0.25, 0.5, 1, 2.5, and 5 μM sodium chromate, respectively. These data suggest that Cr(VI) may be a concern for hawksbill sea turtles and sea turtles in general. - Highlights: • Particulate Cr(VI) is cytotoxic and clastogenic to hawksbill sea turtle cells. • Soluble Cr(VI) is cytotoxic and clastogenic to hawksbill sea turtle cells. • Cr(VI) may be a risk factor for hawksbill sea turtle health.« less

Authors:
 [1];  [2];  [2];  [1];  [2];  [2];  [3];  [4];  [2];
  1. Wise Laboratory of Environmental and Genetic Toxicology, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103 (United States)
  2. (United States)
  3. Graduate School of Agricultural Sciences, Tohoku University, Laboratory of Animal Breeding and Genetics, Second Research Building, Rm 112, 1-1 Amamiyamachi, Aoba-ku, Sendai 981-8555 (Japan)
  4. Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103 (United States)
Publication Date:
OSTI Identifier:
22439810
Resource Type:
Journal Article
Resource Relation:
Journal Name: Toxicology and Applied Pharmacology; Journal Volume: 279; Journal Issue: 2; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; CHROMIUM; CHROMOSOMAL ABERRATIONS; CHROMOSOMES; COASTAL REGIONS; CONCENTRATION RATIO; CORAL REEFS; ECOSYSTEMS; GRAMINEAE; HAZARDS; LEAD; MITOSIS; POLLUTANTS; SEAS; SODIUM; TOXICITY; TURTLES

Citation Formats

Wise, Sandra S., E-mail: sandra.wise@maine.edu, Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Xie, Hong, E-mail: hongxie@usm.maine.edu, Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Fukuda, Tomokazu, E-mail: tomofukuda009@gmail.com, Douglas Thompson, W., E-mail: dougt@usm.maine.edu, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, and and others. Hexavalent chromium is cytotoxic and genotoxic to hawksbill sea turtle cells. United States: N. p., 2014. Web. doi:10.1016/J.TAAP.2014.06.008.
Wise, Sandra S., E-mail: sandra.wise@maine.edu, Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Xie, Hong, E-mail: hongxie@usm.maine.edu, Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Fukuda, Tomokazu, E-mail: tomofukuda009@gmail.com, Douglas Thompson, W., E-mail: dougt@usm.maine.edu, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, & and others. Hexavalent chromium is cytotoxic and genotoxic to hawksbill sea turtle cells. United States. doi:10.1016/J.TAAP.2014.06.008.
Wise, Sandra S., E-mail: sandra.wise@maine.edu, Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Xie, Hong, E-mail: hongxie@usm.maine.edu, Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, Fukuda, Tomokazu, E-mail: tomofukuda009@gmail.com, Douglas Thompson, W., E-mail: dougt@usm.maine.edu, Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103, and and others. Mon . "Hexavalent chromium is cytotoxic and genotoxic to hawksbill sea turtle cells". United States. doi:10.1016/J.TAAP.2014.06.008.
@article{osti_22439810,
title = {Hexavalent chromium is cytotoxic and genotoxic to hawksbill sea turtle cells},
author = {Wise, Sandra S., E-mail: sandra.wise@maine.edu and Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103 and Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103 and Xie, Hong, E-mail: hongxie@usm.maine.edu and Maine Center for Toxicology and Environmental Health, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103 and Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103 and Fukuda, Tomokazu, E-mail: tomofukuda009@gmail.com and Douglas Thompson, W., E-mail: dougt@usm.maine.edu and Department of Applied Medical Science, University of Southern Maine, Science Building, 96 Falmouth Street, Portland, ME 04103 and and others},
abstractNote = {Sea turtles are a charismatic and ancient ocean species and can serve as key indicators for ocean ecosystems, including coral reefs and sea grass beds as well as coastal beaches. Genotoxicity studies in the species are absent, limiting our understanding of the impact of environmental toxicants on sea turtles. Hexavalent chromium (Cr(VI)) is a ubiquitous environmental problem worldwide, and recent studies show it is a global marine pollutant of concern. Thus, we evaluated the cytotoxicity and genotoxicity of soluble and particulate Cr(VI) in hawksbill sea turtle cells. Particulate Cr(VI) was both cytotoxic and genotoxic to sea turtle cells. Concentrations of 0.1, 0.5, 1, and 5 μg/cm{sup 2} lead chromate induced 108, 79, 54, and 7% relative survival, respectively. Additionally, concentrations of 0, 0.1, 0.5, 1, and 5 μg/cm{sup 2} lead chromate induced damage in 4, 10, 15, 26, and 36% of cells and caused 4, 11, 17, 30, and 56 chromosome aberrations in 100 metaphases, respectively. For soluble Cr, concentrations of 0.25, 0.5, 1, 2.5, and 5 μM sodium chromate induced 84, 69, 46, 25, and 3% relative survival, respectively. Sodium chromate induced 3, 9, 9, 14, 21, and 29% of metaphases with damage, and caused 3, 10, 10, 16, 26, and 39 damaged chromosomes in 100 metaphases at concentrations of 0, 0.25, 0.5, 1, 2.5, and 5 μM sodium chromate, respectively. These data suggest that Cr(VI) may be a concern for hawksbill sea turtles and sea turtles in general. - Highlights: • Particulate Cr(VI) is cytotoxic and clastogenic to hawksbill sea turtle cells. • Soluble Cr(VI) is cytotoxic and clastogenic to hawksbill sea turtle cells. • Cr(VI) may be a risk factor for hawksbill sea turtle health.},
doi = {10.1016/J.TAAP.2014.06.008},
journal = {Toxicology and Applied Pharmacology},
number = 2,
volume = 279,
place = {United States},
year = {Mon Sep 01 00:00:00 EDT 2014},
month = {Mon Sep 01 00:00:00 EDT 2014}
}
  • Cadmium nitrate decreased the viability of Chinese hamster ovary (CHO) cells in a concentration-dependent manner; 50% inhibition (IC{sub 50}) was achieved at 0.015 mM. In contrast, lead nitrate appeared to be less toxic. Neither cadmium nitrate nor lead nitrate significantly increased frequencies of binucleated CHO cells with micronuclei (MN). However, both cadmium nitrate and lead nitrate could augment sister chromatid exchanges (SCEs). Cadmium nitrate induced SCEs with a potency approximately equal to that of mitomycin C and more than 10 times higher than lead nitrate. Cadmium nitrate also increased chromosome aberrations (CAs), which included breaks, acentrics, interchanges, and dicentrics ofmore » chromosomes. In addition, cadmium nitrate induced a decrease in the mitotic index (MI), but lead nitrate increased it. In summary, it appears that both of these two heavy metal salts have cytogenetic toxicities with different degrees of effects on the cytotoxicity, MN, CAs, and SCEs and CHO cells. However, SCE was the most sensitive endpoint for indicating mutagenetic effects of cadmium and lead in the present study. 31 refs., 3 figs., 3 tabs.« less
  • Human lymphocytes (HL) as well as lymphocytes (RL), hepatocytes (RH), and gastric mucosa cells (GM) of Sprague-Dawley rats were treated in vitro for 1 h with methylmercury chloride (MMC, 0.5 -4 [mu]g/ml) and dimethylmercury (DMM, 5-40 [mu]g/ml). The cytotoxicity of the two organic mercury compounds was assessed by dye exclusion, and the extent of induced DNA fragmentation was measured with a single-cell microgel electrophoresis assay. Both MMC and DMM induced DNA damage and cytotoxicity in a dose-related manner in HL, RL, and GM. MMC was more effective in causing a significant increase in median DNA migration than DMM at dosesmore » yielding approximately the same degree of cytotoxicity. In rat hepatocytes the MMC-induced DNA damage was, however, lower than in the other cells. An analysis of repair kinetics following exposure to 2 [mu]g/ml MMC was carried out in human lymphocytes obtained from an adult male donor. The bulk of DNA repair occurred 90 min after in vitro exposure, and it was about complete by 120 min following cessation of exposure. Finally, in order to have a basis for extrapolating to the human situation, in vivo studies were performed with Sprague-Dawley rats, also assessing the DNA damage and cytotoxicity in the lymphocytes and gastric mucosa cells. These in vivo results after oral exposure may be directly compared to the in vitro data obtained in the same cells. 27 refs., 9 figs., 1 tab.« less
  • Thio-dimethylarsinate (thio-DMA), a recently discovered urine metabolite in humans, was investigated for its cytotoxic, genotoxic and cell-cycle disruptive effects in the cultured human hepatocarcinoma cell line, HepG2, and Syrian hamster embryo cells. In addition, the role of glutathione (GSH) on the cytotoxic effects of thio-DMA was investigated in terms of the effects of GSH depletion and the effects of exogenously added GSH. LC{sub 50} values of arsenicals for cells incubated for 48 h were 0.026 mM for thio-DMA, 0.343 mM for DMA and 3.66 mM for dithio-DMA. Depletion of cell GSH reduced the cytotoxic effects of thio-DMA. The cytotoxic effectsmore » of 0.02 mM and 0.05 mM thio-DMA were enhanced markedly when used in combination with 1 to 3 mM GSH, but decreased again when combined with 5 mM GSH. These results suggested that cytotoxic intermediates were generated by the interaction of thio-DMA with GSH, while an excessive amount of GSH suppressed the generation of these intermediates. Flow-cytometry showed that thio-DMA was an inducer of cells with 4N DNA and hypo 2N DNA. The results also demonstrated that cells arrested in the mitotic phase had abnormalities in their spindle organization and centrosome integrity. In addition, cells arrested in mitosis by thio-DMA had chromosome structural aberrations, such as chromatid gaps, chromatid breaks and chromatid exchanges. Moreover, the cytotoxic effects of thio-DMA may in part be associated with an apoptotic mode of cell death that was evaluated by the appearance of nucleosome level DNA fragmentations and an 85-kDa cleavage fragment of poly (ADP-ribose) polymerase. These findings suggest that the presence of thio-DMA in human urine has implications for human health in terms of arsenic metabolism and toxicity.« less
  • Hexavalent chromium (CrVI) has been widely used in industries throughout the world. Increased usage of CrVI and atmospheric emission of CrVI from catalytic converters of automobiles, and its improper disposal causes various health hazards including female infertility. Recently we have reported that lactational exposure to CrVI induced a delay/arrest in follicular development at the secondary follicular stage. In order to investigate the underlying mechanism, primary cultures of rat granulosa cells were treated with 10 {mu}M potassium dichromate (CrVI) for 12 and 24 h, with or without vitamin C pre-treatment for 24 h. The effects of CrVI on intrinsic apoptotic pathway(s)more » were investigated. Our data indicated that CrVI: (i) induced DNA fragmentation and increased apoptosis, (ii) increased cytochrome c release from the mitochondria to cytosol, (iii) downregulated anti-apoptotic Bcl-2, Bcl-XL, HSP70 and HSP90; upregulated pro-apoptotic BAX and BAD, (iv) altered translocation of Bcl-2, Bcl-XL, BAX, BAD, HSP70 and HSP90 to the mitochondria, (v) upregulated p-ERK and p-JNK, and selectively translocated p-ERK to the mitochondria and nucleus, (vi) activated caspase-3 and PARP, and (vii) increased phosphorylation of p53 at ser-6, ser-9, ser-15, ser-20, ser-37, ser-46 and ser-392, increased p53 transcriptional activation, and downregulated MDM-2. Vitamin C pre-treatment mitigated CrVI effects on apoptosis and related pathways. Our study, for the first time provides a clear insight into the effect of CrVI on multiple pathways that lead to apoptosis of granulosa cells which could be mitigated by vitamin C.« less
  • Hexavalent chromium [Cr(VI)] is an important human carcinogen associated with pulmonary diseases and lung cancer. Exposure to Cr(VI) induces DNA damage, cell morphological change and malignant transformation in human lung epithelial cells. Despite extensive studies, the molecular mechanisms remain elusive, it is also not known if Cr(VI)-induced transformation might accompany with invasive properties to facilitate metastasis. We aimed to study Cr(VI)-induced epithelial–mesenchymal transition (EMT) and invasion during oncogenic transformation in lung epithelial cells. The results showed that Cr(VI) at low doses represses E-cadherin mRNA and protein expression, enhances mesenchymal marker vimentin expression and transforms the epithelial cell into fibroblastoid morphology.more » Cr(VI) also increases cell invasion and promotes colony formation. Further studies indicated that Cr(VI) uses multiple mechanisms to repress E-cadherin expression, including activation of E-cadherin repressors such as Slug, ZEB1, KLF8 and enhancement the binding of HDAC1 in E-cadherin gene promoter, but DNA methylation is not responsible for the loss of E-cadherin. Catalase reduces Cr(VI)-induced E-cadherin and vimentin protein expression, attenuates cell invasion in matrigel and colony formation on soft agar. These results demonstrate that exposure to a common human carcinogen, Cr(VI), induces EMT and invasion during oncogenic transformation in lung epithelial cells and implicate in cancer metastasis and prevention. - Graphical abstract: Epithelial–mesenchymal transition during oncogenic transformation induced by hexavalent chromium involves reactive oxygen species-dependent mechanisms in lung epithelial cells. - Highlights: • We study if Cr(VI) might induce EMT and invasion in epithelial cells. • Cr(VI) induces EMT by altering E-cadherin and vimentin expression. • It also increases cell invasion and promotes oncogenic transformation. • Catalase reduces Cr(VI)-induced EMT, invasion and transformation.« less