Display options
Cite
Udensi UK, Graham-Evans BE, Rogers C, et al. Cytotoxicity patterns of arsenic trioxide exposure on HaCaT keratinocytes. Clin Cosmet Investig Dermatol. 2011;4:183-90doi: 10.2147/CCID.S24677.
Udensi, U. K., Graham-Evans, B. E., Rogers, C., & Isokpehi, R. D. (2011). Cytotoxicity patterns of arsenic trioxide exposure on HaCaT keratinocytes. Clinical, cosmetic and investigational dermatology, 4183-90. https://doi.org/10.2147/CCID.S24677
Udensi, Udensi K, et al. "Cytotoxicity patterns of arsenic trioxide exposure on HaCaT keratinocytes." Clinical, cosmetic and investigational dermatology vol. 4 (2011): 183-90. doi: https://doi.org/10.2147/CCID.S24677
Udensi UK, Graham-Evans BE, Rogers C, Isokpehi RD. Cytotoxicity patterns of arsenic trioxide exposure on HaCaT keratinocytes. Clin Cosmet Investig Dermatol. 2011;4:183-90. doi: 10.2147/CCID.S24677. Epub 2011 Dec 09. PMID: 22253543; PMCID: PMC3257883.
Copy Download .nbib Format: NLM
Share it on

Clin Cosmet Investig Dermatol. 2011;4:183-90. doi: 10.2147/CCID.S24677. Epub 2011 Dec 09.

Cytotoxicity patterns of arsenic trioxide exposure on HaCaT keratinocytes.

Clinical, cosmetic and investigational dermatology

Udensi K Udensi, Barbara E Graham-Evans, Christian Rogers, Raphael D Isokpehi

Affiliations

  1. RCMI-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, Jackson, MS 39217.

PMID: 22253543 PMCID: PMC3257883 DOI: 10.2147/CCID.S24677

Abstract

BACKGROUND: Arsenic is a ubiquitous environmental toxicant, and abnormalities of the skin are the most common outcomes of long-term, low-dose, chronic arsenic exposure. If the balance between keratinocyte proliferation, differentiation, and death is perturbed, pathologic changes of the epidermis may result, including psoriasis, atopic dermatitis, and certain forms of ichthyosis. Therefore, research investigations using in vitro human epidermal cells could help elucidate cellular and molecular processes in keratinocytes affected by arsenic. Data from such investigations could also provide the basis for developing cosmetic intervention for skin diseases caused by arsenic.

METHODS: The viability of HaCaT keratinocyte cultures with or without prior exposure to low-dose arsenic trioxide was compared for varying concentrations of arsenic trioxide over a time course of 14 days because in untreated control cultures, approximately 2 weeks is required to complete cell differentiation. Long-term cultures were established by culturing HaCaT cells on collagen IV, and cells were subsequently exposed to 0 parts per million (ppm), 1 ppm, 5 ppm, 7.5 ppm, 10 ppm, and 15 ppm of arsenic trioxide. The percentages of viable cells as well as DNA damage after exposure were determined on Day 2, Day 5, Day 8, and Day 14.

RESULTS: Using both statistical and visual analytics approaches for data analysis, we have observed a biphasic response at a 5 ppm dose with cell viability peaking on Day 8 in both chronic and acute exposures. Further, a low dose of 1 ppm arsenic trioxide enhanced HaCaT keratinocyte proliferation, whereas doses above 7.5 ppm inhibited growth.

CONCLUSION: The time course profiling of arsenic trioxide cytotoxicity using long-term HaCaT keratinocyte cultures presents an approach to modeling the human epidermal cellular responses to varying doses of arsenic trioxide treatment or exposure. A low dose of arsenic trioxide appears to aid cell growth but concomitantly disrupts the DNA transcription process.

Keywords: DNA damage; HaCaT; arsenic trioxide; chronic exposure; keratinocyte; visual analytics

References

  1. Clin Dermatol. 2011 Jul-Aug;29(4):360-76 - PubMed
  2. Am J Epidemiol. 2011 Feb 1;173(3):345-54 - PubMed
  3. J Invest Dermatol. 2004 Jan;122(1):125-9 - PubMed
  4. Cancer Treat Rev. 2007 Oct;33(6):542-64 - PubMed
  5. Cytogenet Genome Res. 2008;122(3-4):297-307 - PubMed
  6. J Assoc Physicians India. 2010 Oct;58:617-24, 629 - PubMed
  7. J Vis Exp. 2011 Jan 02;(47): - PubMed
  8. Toxicol Pathol. 2003 Nov-Dec;31(6):575-88 - PubMed
  9. Int J Biochem Cell Biol. 2009 May;41(5):963-8 - PubMed
  10. Toxicol Appl Pharmacol. 2006 Dec 1;217(2):161-7 - PubMed
  11. Int J Environ Res Public Health. 2004 Sep;1(2):83-9 - PubMed
  12. Biomark Insights. 2011 Feb 08;6:7-16 - PubMed
  13. IEEE Comput Graph Appl. 2009 Mar-Apr;29(2):84-7 - PubMed
  14. J Cell Biol. 1988 Mar;106(3):761-71 - PubMed
  15. Toxicol Sci. 2011 Jan;119(1):73-83 - PubMed
  16. Skin Pharmacol Physiol. 2010;23(2):68-78 - PubMed
  17. Environ Health Perspect. 2000 May;108(5):393-7 - PubMed
  18. Carcinogenesis. 2003 Apr;24(4):747-56 - PubMed
  19. Anticancer Drugs. 2003 Nov;14(10):825-8 - PubMed
  20. Huan Jing Ke Xue. 2010 Dec;31(12):3036-42 - PubMed
  21. Cell. 1987 Sep 25;50(7):1131-7 - PubMed
  22. J Cell Biol. 1990 Dec;111(6 Pt 2):2807-14 - PubMed
  23. Genomics. 2006 Oct;88(4):513-20 - PubMed
  24. Chem Res Toxicol. 2004 Jul;17(7):871-8 - PubMed
  25. Am J Pathol. 2011 May;178(5):2066-76 - PubMed
  26. Int J Environ Res Public Health. 2010 May;7(5):1970-83 - PubMed
  27. Toxicol Appl Pharmacol. 1999 Aug 15;159(1):65-75 - PubMed
  28. Toxicol Sci. 2002 Oct;69(2):306-16 - PubMed
  29. Sci Total Environ. 2011 Aug 1;409(17):3092-7 - PubMed
  30. Toxicol Appl Pharmacol. 2010 Apr 15;244(2):234-41 - PubMed
  31. Environ Health Perspect. 2006 Aug;114(8):1193-8 - PubMed
  32. Sci Total Environ. 2006 Nov 1;370(2-3):310-22 - PubMed
  33. Int J Epidemiol. 1998 Oct;27(5):871-7 - PubMed
  34. Dermatol Clin. 2011 Jan;29(1):45-51 - PubMed
  35. Br J Haematol. 1998 Dec;103(4):1092-5 - PubMed
  36. J Biol Chem. 2011 May 27;286(21):18969-81 - PubMed
  37. Biochimie. 2005 Jul;87(7):613-24 - PubMed
  38. Environ Int. 2002 Feb;27(7):597-604 - PubMed
  39. Curr Protoc Cell Biol. 2001 May;Chapter 10:Unit 10.2 - PubMed
  40. Carcinogenesis. 2003 Nov;24(11):1811-7 - PubMed
  41. Int J Dermatol. 2002 Dec;41(12):841-6 - PubMed

Publication Types

Grant support