Comparative Genotoxicity and Cytotoxicity of Four Hexavalent Chromium Compounds in Human Bronchial Cells

Overview

Journal Chem Res Toxicol

Publisher American Chemical Society

Specialty Toxicology

Date 2009 Dec 17

PMID 20000473

Citations 17

Authors

Sandra S Wise

Amie L Holmes

Qin Qin

Hong Xie

Spiros P Katsifis

W Douglas Thompson

John Pierce Wise Sr

Affiliations

Soon will be listed here.

Abstract

Hexavalent chromium (Cr(VI)) compounds are well-established human lung carcinogens. Solubility plays an important role in their carcinogenicity with the particulate Cr(VI) compounds being the most carcinogenic. Epidemiology and animal studies suggest that zinc chromate is the most potent particulate Cr(VI) compound; however, there are few comparative data to support these observations. The purpose of this study was to compare the genotoxicity of zinc chromate with two other particulate Cr(VI) compounds, barium chromate and lead chromate, and one soluble Cr(VI) compound, sodium chromate. The clastogenic effects of barium chromate and zinc chromate were similar, but lead chromate induced significantly less damage. The levels of DNA damage measured by gamma-H2A.X foci formation were similar for the three particulate chromium compounds. Corrected for chromium uptake differences, we found that zinc chromate and barium chromate were the most cytotoxic, and lead chromate and sodium chromate were less cytotoxic. Zinc chromate was more clastogenic than all other chromium compounds, and lead chromate was the least clastogenic. There was no significant difference between any of the compounds for the induction of DNA double strand breaks. All together, these data suggest that the difference in the carcinogenic potency of zinc chromate over the other chromium compounds is not due solely to a difference in chromium ion uptake and that the zinc cation may in fact have an important role in its carcinogenicity.

Citing Articles

Particulate hexavalent chromium inhibits global transcription of genes in DNA repair pathways, particularly targeting homologous recombination repair, base excision repair, mismatch repair and microhomology-mediated end-joining.

Meaza I, Cahill C, Speer R, Kouokam J, Wise Sr J J Hazard Mater. 2024; 485:136892.

PMID: 39706010 PMC: 11794018. DOI: 10.1016/j.jhazmat.2024.136892.

Carcinogenic Mechanisms of Hexavalent Chromium: From DNA Breaks to Chromosome Instability and Neoplastic Transformation.

Meaza I, Williams A, Wise S, Lu H, Wise Sr J, Pierce Sr J Curr Environ Health Rep. 2024; 11(4):484-546.

PMID: 39466546 PMC: 11872169. DOI: 10.1007/s40572-024-00460-9.

Prolonged Particulate Hexavalent Chromium Exposure Induces DNA Double-Strand Breaks and Inhibits Homologous Recombination Repair in Primary Rodent Lung Cells.

Wise J, Lu H, Meaza I, Wise S, Williams A, Young Wise J Biol Trace Elem Res. 2024; 202(12):5653-5663.

PMID: 38499919 PMC: 11408706. DOI: 10.1007/s12011-024-04136-1.

Particulate hexavalent chromium alters microRNAs in human lung cells that target key carcinogenic pathways.

Speer R, Meaza I, Toyoda J, Lu Y, Xu Q, Walter R Toxicol Appl Pharmacol. 2022; 438:115890.

PMID: 35101437 PMC: 8938933. DOI: 10.1016/j.taap.2022.115890.

Particulate Hexavalent Chromium Inhibits E2F1 Leading to Reduced RAD51 Nuclear Foci Formation in Human Lung Cells.

Speer R, Toyoda J, Croom-Perez T, Liu K, Wise J Toxicol Sci. 2021; 181(1):35-46.

PMID: 33677506 PMC: 8081024. DOI: 10.1093/toxsci/kfab019.

References

Cheng W . Impact of inorganic nutrients on maintenance of genomic stability. Environ Mol Mutagen. 2009; 50(5):349-60. DOI: 10.1002/em.20489. View

Wise Sr J, Wise S, Little J . The cytotoxicity and genotoxicity of particulate and soluble hexavalent chromium in human lung cells. Mutat Res. 2002; 517(1-2):221-9. DOI: 10.1016/s1383-5718(02)00071-2. View

Waalkes M . Cadmium carcinogenesis in review. J Inorg Biochem. 2000; 79(1-4):241-4. DOI: 10.1016/s0162-0134(00)00009-x. View

Holmes A, Wise S, Xie H, Gordon N, Thompson W, Wise Sr J . Lead ions do not cause human lung cells to escape chromate-induced cytotoxicity. Toxicol Appl Pharmacol. 2005; 203(2):167-76. DOI: 10.1016/j.taap.2004.08.006. View

Ishikawa Y, Nakagawa K, Satoh Y, Kitagawa T, Sugano H, Hirano T . "Hot spots" of chromium accumulation at bifurcations of chromate workers' bronchi. Cancer Res. 1994; 54(9):2342-6. View

Langard S, NORSETH T . A cohort study of bronchial carcinomas in workers producing chromate pigments. Br J Ind Med. 1975; 32(1):62-5. PMC: 1008024. DOI: 10.1136/oem.32.1.62. View

Beaver L, Stemmy E, Constant S, Schwartz A, Little L, Gigley J . Lung injury, inflammation and Akt signaling following inhalation of particulate hexavalent chromium. Toxicol Appl Pharmacol. 2008; 235(1):47-56. PMC: 3640501. DOI: 10.1016/j.taap.2008.11.018. View

Holmes A, Wise S, Sandwick S, Lingle W, Negron V, Thompson W . Chronic exposure to lead chromate causes centrosome abnormalities and aneuploidy in human lung cells. Cancer Res. 2006; 66(8):4041-8. DOI: 10.1158/0008-5472.CAN-05-3312. View

. Chromium, nickel and welding. IARC Monogr Eval Carcinog Risks Hum. 1990; 49:1-648. PMC: 7681426. View

10.

Holmes A, Wise S, Sandwick S, Wise Sr J . The clastogenic effects of chronic exposure to particulate and soluble Cr(VI) in human lung cells. Mutat Res. 2006; 610(1-2):8-13. DOI: 10.1016/j.mrgentox.2006.06.006. View

11.

Davies J . Lung cancer mortality among workers making lead chromate and zinc chromate pigments at three English factories. Br J Ind Med. 1984; 41(2):158-69. PMC: 1009277. DOI: 10.1136/oem.41.2.158. View

12.

Klein C, Su L, Bowser D, Leszczynska J . Chromate-induced epimutations in mammalian cells. Environ Health Perspect. 2002; 110 Suppl 5:739-43. PMC: 1241236. DOI: 10.1289/ehp.02110s5739. View

13.

Filipic M, Fatur T, Vudrag M . Molecular mechanisms of cadmium induced mutagenicity. Hum Exp Toxicol. 2006; 25(2):67-77. DOI: 10.1191/0960327106ht590oa. View

14.

Patierno S, Banh D, Landolph J . Transformation of C3H/10T1/2 mouse embryo cells to focus formation and anchorage independence by insoluble lead chromate but not soluble calcium chromate: relationship to mutagenesis and internalization of lead chromate particles. Cancer Res. 1988; 48(18):5280-8. View

15.

Ishikawa Y, Nakagawa K, Satoh Y, Kitagawa T, Sugano H, Hirano T . Characteristics of chromate workers' cancers, chromium lung deposition and precancerous bronchial lesions: an autopsy study. Br J Cancer. 1994; 70(1):160-6. PMC: 2033298. DOI: 10.1038/bjc.1994.268. View

16.

Xie H, Holmes A, Young J, Qin Q, Joyce K, Pelsue S . Zinc chromate induces chromosome instability and DNA double strand breaks in human lung cells. Toxicol Appl Pharmacol. 2008; 234(3):293-9. PMC: 4075174. DOI: 10.1016/j.taap.2008.10.010. View

17.

Wise S, Holmes A, Moreland J, Xie H, Sandwick S, Stackpole M . Human lung cell growth is not stimulated by lead ions after lead chromate-induced genotoxicity. Mol Cell Biochem. 2005; 279(1-2):75-84. DOI: 10.1007/s11010-005-8217-0. View

18.

Paz-Y-Mino C, Davalos M, Sanchez M, Arevalo M, Leone P . Should gaps be included in chromosomal aberration analysis? Evidence based on the comet assay. Mutat Res. 2002; 516(1-2):57-61. DOI: 10.1016/s1383-5718(02)00021-9. View

19.

Morrison A, Highland J, Krogan N, Arbel-Eden A, Greenblatt J, Haber J . INO80 and gamma-H2AX interaction links ATP-dependent chromatin remodeling to DNA damage repair. Cell. 2004; 119(6):767-75. DOI: 10.1016/j.cell.2004.11.037. View

20.

Sheffet A, Thind I, Miller A, Louria D . Cancer mortality in a pigment plant utilizing lead and zinc chromates. Arch Environ Health. 1982; 37(1):44-52. DOI: 10.1080/00039896.1982.10667532. View