Evaluation of the Toxic Potency of Selected Cadmium Compounds on A549 and CHO-9 Cells

• Autorzy: Zapór L.
• Języki publikacji: EN

Abstrakty

EN

Cytotoxicity of cadmium sulphide, oxide and chloride was tested using A549 and CHO-9 cells. Metabolic activity of cells (MTT test) and cell membrane permeability (NRU test) were used as cytotoxicity endpoints. The results revealed unexpectedly low toxicity of cadmium sulphide as compared to chloride and oxide. This preliminary report does not provide any explanation for this effect, but the result may nevertheless be interesting for future studies of toxicity mechanisms of cadmium compounds. First cadmium compounds caused damage or change in the permeability of cell membranes, then inhibition of metabolic activity of mitochondria. It cannot be ruled out that the cell lysosomes are at first exposed to the effect of cadmium.

Słowa kluczowe

EN

cadmium sulphide; cadmium chloride; cadmium oxide

PL

siarczek kadmu; chlorek kadmu; tlenek kadmu

• Wydawca: Taylor & Francis
• Czasopismo: International Journal of Occupational Safety and Ergonomics
• Rocznik: 2014
• Tom: Vol. 20, No. 4
• Strony: 573--581
• Opis fizyczny: Bibliogr. 25 poz., wykr.

Twórcy

autor

Zapór L.

• Central Institute for Labour Protection – National Research Institute (CIOP-PIB), Poland

Bibliografia

• 1. International Agency for Research on Cancer (IARC). Cadmium and cadmium compounds (CAS number 7440-43-9). Lyon, France: IARC Press; 1993.
• 2. U.S. Department of Health and Human Services. Toxicological profile for cadmium. 2012. Retrieved September 4, 2014, from: http://www.atsdr.cdc.gov/toxprofiles/tp5.pdf.
• 3. Li KG, Chen JT, Bai SS, Wen X, Song SY, Yu Q, et al. Intracellular oxidative stress and cadmium ions release induce cytotoxicity of unmodified cadmium sulfide quantum dots. Toxicol In Vitro. 2009;23(6):1007–13.
• 4. Dopp E, Hartmann LM, Florea AM, von Recklinghausen U, Pieper R, Shokouhi B, et al.. Uptake of inorganic and organic derivatives of arsenic associated with induced cytotoxic and genotoxic effects in Chinese hamster ovary (CHO) cells. Toxicol Appl Pharmacol. 2004;201(2):156–65.
• 5. Huang X, Klein C, Costa M. Crystalline Ni3 S2 specifically enhances the formation of oxidants in the nuclei of CHO cells as detected by dichlorofluorescein. Carcinogenesis. 1994;15(3):545–8.
• 6. Döhr O, Sinning R, Vogel C, Münzel P, Abel J. Effect of transforming growth factor-β1 on expression of aryl hydrocarbon receptor and genes of Ah gene battery: clues for independent down-regulation in A549 cells. Mol Pharmacol. 1997;51(5):703–10. Retrieved September 4, 2014, from: http://molpharm.aspetjournals.org/content/51/5/703.full.pdf+html.
• 7. Foster KA, Oster CG, Mayer MM, Avery ML, Audus KL. Characterization of the A549 cell line as a type II pulmonary epithelial cell model for drug metabolism. Exp Cell Res. 1998;243(2):359–66.
• 8. Travaglione S, Bruni B, Falzano L, Paoletti L, Fiorentini C. Effects of the new-identified amphibole fluoro-edenite in lung epithelial cells. Toxicol in Vitro. 2003;17(5–6):547–52.
• 9. Wu SC, Yen GC. Effects of cooking oil fumes on the genotoxicity and oxidative stress in human lung carcinoma (A-549) cells. Toxicol in Vitro. 2004;18:571–80.
• 10. Walum E, Balls M, Bianchi V, Blaauboer B, Bolcsfoldi G, Guillouzo A, et al. ECITTS: an integrated approach to the application of in vitro test systems to the hazard assessment of chemicals. Altern Lab Anim. 1992;20:406–28.
• 11. Combes RD, Balls M. Integrated testing strategies for toxicity employing new and existing technologies. Altern Lab Anim. 2011;39(3):213–25.
• 12. Tennant JA. Evaluation of the trypan blue technique for determination of cell viability. Transplantation. 1964;2:685–94.
• 13. INVITTOX Protocol No. 64. The neutral red cytotoxicity assay. The ERGATT/FRAME data bank of in vitro techniques in toxicology. Nottingham, UK: INVITTOX; 1992.
• 14. INVITTOX Protocol No. 17. MTT assay. The ERGATT/FRAME data bank of in vitro techniques in toxicology. Nottingham, UK: INVITTOX; 1990.
• 15. PerOx (TOS/TOC) kit. Photometric test system for the determination of the total oxidative status/capacity (TOS/TOC) in EDTA-plasma, serum and other biological samples. Bensheim, Germany: Immundiagnostik; 2011.Retrieved September 4, 2014, from: http://www.immundiagnostik.com/fileadmin/pdf/Perox_KC5100.pdf.
• 16. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein dye binding. Anal Biochem. 1976;72:248–54.
• 17. Apostoli P, Huard C, Chaumontet C, Martel P, Alessio L, Mazzoleni G. Effects of four inorganic lead compounds on the proliferation and junctional coupling of cultured REL liver cells. Am J Ind Med. 2000;38(3):340–8.
• 18. Beyersmann D, Hartwig A. Carcinogenic metal compounds: recent insight into molecular and cellular mechanisms. Arch Toxicol. 2008;82(8):493–512.
• 19. Hack CE, Covington TR, Lawrence G, Shipp A, Gentry R. A pharmacokinetic model of the intracellular dosimetry of inhaled nickel. J Toxicol Environ Health A. 2007;70(5):445–64.
• 20. Schwerdtle T, Hartwig A. Bioavailability and genotoxicity of soluble and particulate nickel compounds in cultured human lung cells. Materials Science and Engineering Technology. 2006;37(6):521–5.
• 21. Kurowska E, Bal W. Toxicology of cadmium and nickel. In: Fishbein JC, editor. Advances in molecular toxicology. Amsterdam, The Netherlands: Elsevier; 2010. vol. 4, p. 85–12.
• 22. Glaser U, Klöppel H, Hochrainer D. Bioavailability indicators of inhaled cadmium compounds. Ecotoxicol Environ Saf. 1986;11(3):261–71.
• 23. Belyaeva AE, Glazunov VV, Korotkov MS. Cyclosporin A-sensitive permeability transition pore is involved in Cd2+-induced dysfunction of isolated rat liver mitochondria: doubts no more. Arch Biochem Biophys. 2002;405(2):252–64.
• 24. Pourahmad J, Brien JP. A comparison of hepatocyte cytotoxicity mechanisms for Cu+2 and Cd+2. Toxicology. 2000;143:263–73.
• 25. Fotakis G, Cemeli E, Anderson D, Timbrell JA. Cadmium chloride-induced DNA and lysosomal damage in a hepatoma cell line. Toxicol in Vitro. 2005;19(4):481–9.