Allergy to hair dye.
Ontology highlight
ABSTRACT:
SUBMITTER: McFadden JP
PROVIDER: S-EPMC1790769 | biostudies-literature | 2007 Feb
REPOSITORIES: biostudies-literature
Publications
Allergy to hair dye.
McFadden John P JP White Ian R IR Frosch Peter J PJ Sosted Heidi H Johansen Jenne D JD Menne Torkil T
BMJ (Clinical research ed.) 20070201 7587
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Project description:Most commercial permanent hair dyeing technologies are based on the oxidative process of p-phenylenediamine and its derivative materials. However, concerns about their toxicological issues have been raised throughout the years. Herein, we report an innovative surface coloration strategy for fabricating melanin-mimetic multicolor and low-toxicity hair dyes through sodium periodate-induced rapid deposition of eumelanin-like polydopamine (PDA) and pheomelanin-like PDA/cysteine co-deposited coatings on the hair surface. The color and morphology of the resulting hair were characterized in detail by several spectroscopy methods and the possible mechanism for the multi-coloring effects and structural differences of the melanin-mimetic coating was proposed. Our strategy eliminates the use of toxic dye precursors or organic solvents, and the favorable safety of the PDA-based formulations is demonstrated. The fabricated dyes can be applied to hair simply by combing, resulting in uniform multi-coloring effects within a short time. Furthermore, the melanin-mimetic hair dyes have excellent durability and ultraviolet protection performance. This work provides a facile and versatile methodology to develop the next generation of safe, sustainable and multicolor hair dyes and pave new avenues for advancing the field of surface coloration, nanoreactors, nanogenerators, energy storage materials and biomimetic sensing devices.
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Project description:The styryl pyridinium dyes, FM1-43 and AM1-43, are fluorescent molecules that can permeate the mechanotransduction channels of hair cells, the sensory receptors of the inner ear. When these dyes are applied to hair cells, they enter the cytoplasm rapidly, resulting in a readily detectable intracellular fluorescence that is often used as a molecular indication of mechanotransduction channel activity. However, such dyes can also permeate the ATP receptor, P2X(2). Therefore, we explored the contribution of P2X receptors to the loading of hair cells with AM1-43. The chick inner ear was found to express P2X receptors and to release ATP, similar to the inner ear of mammals, allowing for the endogenous stimulation of P2X receptors. The involvement of these receptors was evaluated pharmacologically, by exposing the sensory epithelium of the chick inner ear to 5 microM AM1-43 under different experimental conditions and measuring the fluorescence in hair cells after fixation of the tissue. Pre-exposure of the tissue to 5 mM EGTA for 15 min, which should eliminate most of the gating "tip links" of the mechanotransduction channels, deceased fluorescence by only 44%. In contrast, P2X receptor antagonists (pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid [PPADS], suramin, 2',3'-O-(2,4,6-trinitrophenyl) ATP [TNP-ATP], and d-tubocurarine) had greater effects on dye loading. PPADS, suramin, and TNP-ATP all decreased intracellular AM1-43 fluorescence in hair cells by at least 69% when applied at a concentration of 100 microM. The difference between d-tubocurarine-treated and control fluorescence was statistically insignificant when d-tubocurarine was applied at a concentration that blocks the mechanotransduction channel (200 microM). At a concentration that also blocks P2X(2) receptors (2 mM), d-tubocurarine decreased dye loading by 72%. From these experiments, it appears that AM1-43 can enter hair cells through endogenously activated P2X receptors. Thus, the contribution of P2X receptors to dye entry should be considered when using styryl pyridinium dyes to detect hair cell mechanotransduction channel activity, especially in the absence of explicit mechanical stimulation of stereocilia.
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Project description:To evaluate the risks of hair dye exposure, we investigated cellular and molecular effects of Arianor Ebony dye, which is a mixture of azo and anthraquinone dyes, used in the composition of the black color. Cytotoxicity, genotoxicity, and gene expression of relevant molecules of apoptotic and oxidative stress mechanisms were investigated in HepG2 cells exposed to Arianor Ebony. Results showed that the dye did not induce cytotoxicity to exposed cells at a concentration up to 50 µg/mL compared to the negative control. However, genotoxic assays indicated that the dye was able to damage the genetic material at a concentration of 25 µg/mL, with induction factor values of exposed cells two- to five-fold higher than those recorded for the negative control. Moreover, the lowest observed effect concentration was 12.5 µg/mL. For gene expression, relevant changes were observed in cytochrome c and caspase 9, which decreased in cells incubated with the dye in a dose-dependent manner when compared with the negative control. In parallel, the expression of genes for antioxidant enzymes was increased in exposed cells, suggesting the presence of metabolic routes that protect cells against the toxic effect of the dye, avoiding exacerbated cellular death. Results suggested that the dye disrupted cellular homeostasis through mitochondrial dysfunction, which may be hazardous to human health. Thus, further investigations are necessary to deeply understand the mechanisms of action of the dye, considering its toxic potential found in our ex vivo assays.
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