Advanced hair damage model from ultra-violet radiation in the presence of copper.

OBJECTIVE: Damage to hair from UV exposure has been well reported in the literature and is known to be a highly complex process involving initiation via absorption of UV light followed by formation and propagation of reactive oxygen species (ROS). The objective of this work was to understand these mechanisms, explain the role of copper in accelerating the formation of ROS and identify strategies to reduce the hair damage caused by these reactive species. METHODS: The location of copper in hair was measured by Transmission electron microscopy-(TEM) X-ray energy dispersive spectroscopy (XEDS) and levels measured by ICP-OES. Protein changes were measured as total protein loss via the Lowry assay, and MALDI ToF was used to identify the biomarker protein fragments. TBARS assay was used to measure lipid peroxide formation. Sensory methods and dry combing friction were used to measure hair damage due to copper and UV exposure and to demonstrate the efficacy of N,N' ethylenediamine disuccinic acid (EDDS) and histidine chelants to reduce this damage. RESULTS: In this work, a biomarker protein fragment formed during UV exposure is identified using mass spectrometry. This fragment originates from the calcium-binding protein S100A3. Also shown is the accelerated formation of this peptide fragment in hair containing low levels of copper absorbed from hair during washing with tap water containing copper ions. Transmission electron microscopy (TEM) X-ray energy dispersive spectroscopy (XEDS) studies indicate copper is located in the sulphur-poor endo-cuticle region, a region where the S100A3 protein is concentrated. A mechanism for formation of this peptide fragment is proposed in addition to the possible role of lipids in UV oxidation. A shampoo and conditioner containing chelants (EDDS in shampoo and histidine in conditioner) is shown to reduce copper uptake from tap water and reduce protein loss and formation of S100A3 protein fragment. In addition, the long-term consequences of UV oxidation and additional damage induced by copper are illustrated in a four-month wear study where hair was treated with a consumer relevant protocol of hair colouring treatments, UV exposure and regular shampoo and conditioning. CONCLUSIONS: The role of copper in accelerating UV damage to hair has been demonstrated as well as the ability of chelants such as EDDS and histidine in shampoo and conditioner products to reduce this damage.

Role of copper in photochemical damage to hair.

OBJECTIVE: The objective of this work was to identify whether low levels of redox metals such as copper will accelerate damage to hair on exposure to UV irradiation and whether this damage can be prevented. METHODS: The methods used were proteomics to measure the protein damage via protein loss after different periods of exposure and mass spectroscopy methods to identify specific marker peptides that are specifically created by this type of damage. RESULTS: In this work, we have developed new insights into the mechanism of UV damage using these proteomic methods. A marker fragment in the hair protein loss extract was identified (m/z = 1279) that is unique to UV exposure and increases with time of UV exposure. We have also identified for the first time in hair the role of exogenous copper in increasing UV damage both in terms of total protein degradation and also increased formation of the marker fragment and proposed a mechanism of action. It has been demonstrated that shampoo treatment containing a chelant such as N,N'-ethylenediamine disuccinic acid (EDDS) reduced copper accumulation in hair. CONCLUSION: This work provides evidence for the role of copper in UV-induced damage to hair and strategies to reduce copper levels in hair using a chelant such as EDDS.

The role of chelants in controlling Cu(II)-induced radical chemistry in oxidative hair colouring products.

The catalytic formation of hydroxyl radicals in oxidative hair colourant systems in the presence of added copper ions was measured and quantified using a colorimetric probe N,N'-(5-nitro-1,3-phenylene)bisglutaramide. Also monitored in the same experiments was the decomposition of hydrogen peroxide. The first set of experiments was performed using aqueous model solutions containing the key oxidant actives in a hair colourant, ammonium hydroxide and hydrogen peroxide at pH 10, with added copper and calcium ions. The second set of experiments was performed in the presence of hair containing different levels of copper in conditions very close to those found during hair colouring. Both sets of experiments demonstrate the ability of copper ions to trigger the formation of hydroxyl radicals and catalyse the decomposition of hydrogen peroxide. The ability of chelants ethylenediamine tetraacetic acid (EDTA) and N,N'-ethylenediamine disuccinic acid (EDDS) to moderate the flux of hydroxyl radicals formed in solution systems was demonstrated in the presence of copper ions alone. However, only EDDS was successful in the presence of both calcium and copper ions. This was confirmed in the hair experiments where again only EDDS was successful at preventing hydroxyl radical formation where hair is added as the source of copper and calcium ions. These results are explained using metal speciation modelling and demonstrate the importance of the chelant to be able to specifically bind and prevent the one-electron redox chemistry of copper in the presence of high levels of calcium ions as found in hair. The formation of hydroxyl radicals during the colouring process was shown to lead to hair structure damage as measured by protein loss. EDDS was demonstrated to significantly reduce cuticle damage by suppressing the formation of the hydroxyl radicals in systems with realistic concentrations of calcium and copper.

The proteomic profile of hair damage.

BACKGROUND: Monilethrix is a congenital hair shaft disorder with associated fragility. Many of the changes seen in monilethrix hair on light microscopy and scanning electron microscopy are also seen in hair weathering and cosmetic damage to hair. OBJECTIVES: We used monilethrix as a model to investigate the relationship between hair protein structure and hair strength and resistance to cosmetic insult. METHODS: We applied proteomic techniques to identify novel peptide damage markers for chemical oxidative damage to hair. RESULTS: The findings suggest that specific sites in the protein structure of hair are targeted during oxidative damage from bleaching, a unique insight into how chemical damage compromises the structural integrity of the hair shaft at the molecular level. CONCLUSIONS: Applying proteomics to the study of congenital and acquired hair shaft disorders can deliver new insights into hair damage and novel strategies to strengthen hair.