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>Magister Scientiae - MSc / Hyperpigmentation disorders such as melasma, freckles and black-pigmented spots on the surface of the skin are often a result of increased over production and accumulation of melanin pigments in the skin. In melanin biogenesis, tyrosinase is the key enzyme that catalysis the synthesis of melanin, thus the most effective and easiest way to reduce melanin synthesis is by inhibiting tyrosinase. There are a large number of reported tyrosinase inhibitors, their identification and isolation from natural sources is highly important because when natural tyrosinase inhibitors are identified in natural sources, their production is relatively low in cost. Tyrosinase inhibitors are highly sought in the cosmetic industry because of their skin – whitening effects. Most common used tyrosinase inhibitors are kojic acid (KA), arbutin, hydroquinone and ascorbic acid. However, these inhibitors have side effects and lack clinical efficiency. These facts led us to focus our research work on the exploration of natural tyrosinase inhibitors. Due to the therapeutic potential of medical plants researchers are not only concerned with validating ethnopharmacological usage of plants, but also with identification, isolation and characterization of bioactive components. Sutherlandia frutescens and Psoralea aphylla are both examples of indigenous fynbos species, which have been applied by indigenous people for the benefit of their medicinal properties.

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No / Reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) are produced in the skin under the influence of UV radiation. These compounds are highly reactive and can induce DNA lesions in epidermal cells. Melanin is considered to protect human skin against DNA damage by absorbing UV radiation. We have investigated whether melanin can, in addition, offer protection against the effects of H2O2 in human melanocytes and HaCaT keratinocytes. In the present study, it was shown that 40 and 100 μM H2O2 increased the number of DNA strand breaks as measured using the comet assay, in melanocytes of Caucasian origin. In melanocytes of the same origin in which melanin levels were increased by culturing in presence of 10 mM NH4Cl and elevated l-tyrosine, H2O2-induced DNA damage was reduced compared to that in control melanocytes. Similarly, HaCaT cells that were loaded with melanin were better protected against H2O2-induced DNA strand breaks than control HaCaT cells. These protective effects of melanin were mimicked by the intracellular Ca2+-chelator BAPTA. Thus, BAPTA reduced the level of H2O2-induced DNA strand breaks in melanocytes. Like BAPTA, melanin is known to be a potent chelator of Ca2+ and this was confirmed in the present study. It was shown that melanin levels in melanocytic cells correlated directly with intracellular Ca2+ binding capacity and, in addition, correlated inversely with H2O2-induced increases in intracellular Ca2+. Our results show that melanin may have an important role in regulating intracellular Ca2+ homeostasis and it is suggested that melanin protects against H2O2-induced DNA strand breaks in both melanocytes and keratinocytes and through its ability to bind Ca2+.

No / Background Hair is degraded by the action of both dermatophytic and nondermatophytic microorganisms. The importance of understanding hair sample condition in archaeological and forensic investigation highlights the need for a detailed knowledge of the sequence of degradation in samples that have been either buried or left exposed at the ground surface. Objectives To investigate the sequence of biodegradative change to human terminal scalp hair from archaeological and forensic contexts. Methods Cut modern scalp hair from three individuals with caucasoid-type hair was inoculated with soil microorganisms through soil burial in the field and under laboratory conditions to produce experimentally degraded samples. The degraded hair fibres were subjected to detailed histological examination using a combination of high-resolution light microscopy, transmission electron microscopy and scanning electron microscopy to investigate the nature and sequence of degradative change to hair structural components. Results/discussion Degradation was found to occur first within the least structurally robust components that afford the least resistance to microbial/chemical attack. The sequence of degradation (most to least-reflecting degree of vulnerability) in the hair cuticle was as follows: (1) intercellular 6-layer (cell membrane complex); (2) endocuticle; (3) cell membrane ß-layers; (4) exocuticle; (5) epicuticle; and (6) A-layer. In the hair cortex this was as follows: (I) intercellular 6-layer (cell membrane complex); (II) cell membrane ß-layers; (III) intermacrofibrillar matrix/nuclear remnants; (IV) microfibrils; (V) intermicrofibrillar matrix; and (VI) pigment granules (the hair fibre component that was the least vulnerable to degradation). Conclusions The selective progress of degradation in the hair shaft has been charted and this provides a basis for further histological work in better understanding the condition of hair fibres derived from archaeological or forensic contexts as well as being relevant to investigation of diseased hair, in particular hair infected by dermatophytes and hair weakened by genetic hair shaft abnormalities.

No / The present invention relates to compositions and methods useful in studying or modulating melanin pigmentation in the skin. Particularly, the invention relates to compositions comprising a substance capable of modulating the activity or expression of ALK6 (SEQ ID 2) or Cdc42 which in turn are capable of modulation of the transfer of melanin from melanocytes to keratinocytes and potentially from keratinocytes to keratinocytes. The invention also relates to assays for identifying such compositions, and methods of modulating skin pigmentation.

Yes / Melanin is the predominant pigment responsible for skin colour, and is synthesized by the melanocyte in the basal layer of the epidermis and then transferred to surrounding keratinocytes. Despite its optical properties, melanin is barely detectable in unstained sections of human skin. However, identification and localization of melanin is of importance for the study of skin pigmentation in health and disease. Current methods for the histologic quantification of melanin are suboptimal, and are associated with significant risk of misinterpretation. The aim of this study was to re-assess the existing literature, and to develop a more effective histological method of melanin quantification in human skin. Moreover, we confirm that Warthin-Starry (WS) stain provides a much more sensitive and more specific melanin detection method than the common-place Fontana-Masson (FM) stain. For example, WS staining sensitivity allowed the visualization of melanin even in very pale Caucasian skin that was missed by FM or Von Kossa (VK) stains. From our re-assessment of the histologyrelated literature we conclude that so-called ‘melanin dust’ is most likely an artefact of discoloration due to non-specific silver deposition in the stratum corneum. Unlike FM and VK, WS was not associated with this non-specific stratum corneum darkening, misinterpreted previously as ‘degraded’ or so-called ‘dust’ melanin. Finally, WS melanin particle counts were largely similar to manual counts by transmission electron microscopy, in contrast to both FM and VK. Together these findings allow us to propose a new histology/Image J-informed method for the accurate and precise quantification of epidermal melanin in skin.

Yes / Background: Melanin is synthesized by melanocytes in the basal layer of the epidermis. When transferred to surrounding keratinocytes it is the key UVR-protective biopolymer responsible for skin pigmentation. Most melanin is observable in the proliferative basal layer of the epidermis, and only sparsely distributed in the stratifying/differentiating epidermis. The latter has been explained, despite formal evidence, to ‘melanin degradation’ in supra-basal layers. Objectives: Our aim was to re-evaluate this currently-accepted basis for melanin distribution in the human skin epidermis, and whether this pattern is altered after a regenerative stimulus. Methods: Normal epidermis of adult human skin, at rest and after tape-stripping, was analysed by a range of (immuno)histochemical and high-resolution microscopy techniques. In vitro models of melanin granule uptake by human keratinocytes were attempted. Results: We propose a wholly different fate for melanin in the human epidermis. Our evidence indicates that the bulk of melanin is inherited only by the non-differentiating daughter cell post mitosis in progenitor keratinocytes, via asymmetric organelle inheritance. Moreover, this preferred pattern of melanin distribution can switch to a symmetric or equal daughter cell inheritance mode under conditions of stress including regeneration. Conclusions: We provide in this preliminary report a plausible and histologically-supportable explanation for how human skin pigmentation is efficiently organized in the epidermis. Steady state epidermis pigmentation may involve much less redox-sensitive melanogenesis than previously thought, and at least some pre-made melanin may be available for re-use. The epidermal-melanin unit may be an excellent example to study organelle distribution via asymmetric or symmetric inheritance in response to micro-environment and tissue demands. / Walgreens Boots Alliance