Toxicity of hair dyes in human keratinocytes Effects of Basic Yellow 57 in combination with Resorcinol and Hydrogen Peroxide
DOI:
https://doi.org/10.26481/marble.2014.v2.325Abstract
Background. In the United States and Europe, more than 30% of women over 18 years and approximately 10% of men over 40 years are using hair colouring products. Previous studies have shown that low concentrations of the semi-permanent hair dye Basic Yellow 57 (BY57) lead to toxicity in human keratinocytes. The aim of this study is to investigate the DNA damaging effects of BY57 in combination with other (oxidizing) components, such as hydrogen peroxide (a bleach component) and resorcinol (a colour coupler) in human keratinocyte (HaCaT) cells. Furthermore, another aim of the present study is to evaluate the potential DNA damaging mechanisms caused by these hair dye components. Methods. The HaCaT cells were exposed to different concentrations BY57 (0-100 µg/ml), hydrogen peroxide (0-100 µM), resorcinol (0-100 µg/ml) and to the possible combinations of these components. Diphenyleneiodonium (DPI; 10 and 50 µg/ml) and hydroxyurea (HU; 10 mM) were added to the keratinocytes to evaluate the potential DNA damaging mechanisms. DPI was applied as an NADPH oxidase inhibitor and HU functions as an DNA polymerase inhibitor. In the present study, the tested concentrations are based on the proportion of the hair dye components as present in commercially available hair dye products. In order to detect potential DNA fragmentation after treating the cells with the different hair dye components, the single cell gel electrophoresis (comet) assay was used. Results. Treatment of the HaCaT cells with hydrogen peroxide (100 µM) and Basic Yellow 57 (100 µg/ml) lead to a significant induction of DNA fragmentation in human keratinocytes. The combination of BY57 together with hydrogen peroxide and resorcinol lead to a significant induction in DNA damage. However, this induction was approximately equal to the DNA damaging effects caused by hydrogen peroxide only. Furthermore, the addition of DPI lead to an unexpected induction of DNA fragmentation. Conclusion. The present results showed that the exposure of human keratinocytes to Basic Yellow 57, hydrogen peroxide and the combination treatments of the hair dye components containing hydrogen peroxide lead to an induction of DNA fragmentation. However, the possible working mechanisms of DNA damaging effects caused by BY57 remains unclear. The DNA damaging effects of DPI could suggest an inhibition of the DNA repair system via the inhibition of NADPH oxidase. Since this effect is not confirmed by the results of the DNA repair inhibitor (HU), no conclusion could be drawn from these findings. To elucidate the possible DNA damaging mechanisms of BY57 on human keratinocytes, further research is needed.References
National Cancer Institute (NCI). Hair Dyes and Cancer Risk 2011. Available from: http://www.cancer.gov/cancertopics/factsheet/Risk/hair-dyes#r1.
American Cancer Society. Hair Dyes 2011. Available from: http://www.cancer.org/cancer/cancercauses/othercarcinogens/intheworkplace/hair-dyes.
Czene K, Tiikkaja S, Hemminki K. Cancer risks in hairdressers: assessment of carcinogenicity of hair dyes and gels. International journal of cancer. 2003;105(1):108-12.
SCCS. Opinion on Basic Yellow 57. Colipia nº C10. Directorate-General for Health & Consumers. 2010.
SCCS. Opinion of the scientific committee on cosmetic products and non-food products intended for consumers concerning basic yellow 57. Colipia nº C10. 2003.
Veal EA, Day AM, Morgan BA. Hydrogen peroxide sensing and signaling. Molecular cell. 2007;26(1):1-14.
Re-evaluation of Some Organic Chemicals, Hydrazine and Hydrogen Peroxide: World Health Organization International Agency For Research On Cancer; 1999.
SCCS. Hair dyes and hydrogen peroxide. 2011.
Public Health England. Hydrogen Peroxide: General Information. Toxicology Department. 2009.
Hahn S, Kielhorn J, Koppenhöfer J, Wibbertmann A, Mangelsdorf I. Concise International Chemical Assessment Document 71: Resorcinol. World Health Organization. 2006.
PubChem Compound. Compund Summary: Resorcinol. Pharmacology and Biomedical Effects and Toxicology: NCBI; [cited 2009]. Available from: https://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5054&loc=ec_rcs#x395.
SCCS. Opinion on Resorcinol. Colipa nº A11. 2010.
Li Y, Trush MA. Diphenyleneiodonium, an NAD (P) H oxidase inhibitor, also potently inhibits mitochondrial reactive oxygen species production. Biochemical and biophysical research communications. 1998;253(2):295-9.
Day III RS. Deoxyguanosine reverses inhibition by hydroxyurea of repair of UV-irradiated adenovirus 5. Mutation Research/DNA Repair. 1993;293(3):215-23.
Mercken EM, Hageman GJ, Schols AM, Akkermans MA, Bast A, Wouters EF. Rehabilitation decreases exerciseinduced oxidative stress in chronic obstructive pulmonary disease. American journal of respiratory and critical care medicine. 2005;172(8):994-1001.
Lambert AJ, Buckingham JA, Boysen HM, Brand MD. Diphenyleneiodonium acutely inhibits reactive oxygen species production by mitochondrial complex I during reverse, but not forward electron transport. Biochimica et Biophysica Acta (BBA)-Bioenergetics. 2008;1777(5):397-403.
Pines A, Perrone L, Bivi N, Romanello M, Damante G, Gulisano M, et al. Activation of APE1/Ref-1 is dependent on reactive oxygen species generated after purinergic receptor stimulation by ATP. Nucleic acids research. 2005;33(14):4379-94.
Riganti C, Gazzano E, Polimeni M, Costamagna C, Bosia A, Ghigo D. Diphenyleneiodonium inhibits the cell redox metabolism and induces oxidative stress. Journal of Biological Chemistry. 2004;279(46):47726-31.
Li J-M, Shah AM. ROS generation by nonphagocytic NADPH oxidase: potential relevance in diabetic nephropathy. Journal of the American Society of Nephrology. 2003;14(suppl 3):S221-S6.
