| Studies on the Effects of Natural Chemicals to theMelanogenesis and Expressions of Specific DifferentialMolecules of Melanocytes at the Hair Follicles the Lesions ofVitiligoSurface pigmentation by melanin is the result of a chain of events beginning with the migration of neural crest precursors to populate the epidermis and its associated structures, such as hair bulbs, with melanoblasts, which undergo differentiation to give rise to the melanocyte population of the skin. Melanocytes possess the specialized cytoplasmic organization and the biosynthetic apparatus to generate melanin.The process of the melanogenesis may be summarized in ten stages difined as:l Migration of pigment cell precursors from the neural crest. 2 Clonal population of skin by melanocytes. 3 Induction of melanogenic genes,including tyrosinase, tyrosinase related proteins, and melanosomal matrix components. 4 Synthesis of tyrosinase and related melanogenic proteins. 5 Posttranslational processing and glycosylation of tyrosinase. 6 fusion of vesicles to form melanosomes and initiation of melanogenesis. 7 Control of tyrosinase activity. 8 Control of activity of tyrosinase-related proteins. 9 Posttyrosinase modification of biosynthesis. 10 Modification of melanin. Hypopigmentaion or hyperpigmentation may arise from interference with any of these processes. Inhibition of migration results in regional depigmentation(as waardenburg's syndrome). The distribution of pigmentation is influenced by clonal properties of melanocytes and the composition of their environment. An important factor in melanocyte differentiation is the induction of pigment gene expression in the appropriate location. The most significant cause of partial or sequential depigmentation is the absence of melanocytes in the affected region. This can beeither congenital or acquired .During melanogenesis, the major melanogenic enzyme is tyrosinase. Tyrosinase is synthesized as a transmembrane protein. Genetic abnormalities with reduced catalytic function of the protein result in general hypopigmentation. Hypopigmentation also may result from abnormalities of TRP1 and TRP2. Tyrosinase activity may be inhibited by chelation of active-site copper atoms or by competitive occupancy of the catalytic site. Sometimes, it also can be subjected to competitive feed back regulation by intermediate products of melanogenesis. In China, herbs such as Genus ligusticum, Largehead atractylodes rhizome, Common bletilla tuber and Agaric et al have been widely used in the treatment of pigment disorders of the skin,. But which chemicals of these herbs functions predominantly as a inhibitor still keeps unknown. Natural chemicals such as Aloin, Cinnamic acid and Sophorcardipine et al are key reactive elements of those plants. Thus, a study was performed to evaluate their effect to the tyrosinase in vitro.Vitiligo is an acquired melanin pigmentary disorder manifesting itself by expanding depigmented lesions of the skin. The onset is mostly early in life and it has an estimated worldwide incidence of 0.5-4%. While the etiology of vitiligo is as yet unknown/while the literature is replete with structural and morphological some or all features. Such as absence of melanin and melanocytes from affected epidermis,degeneration of melancoytes and /or basal/supra-basal keratinocytes. Most of these early studies concluded that fully white vitiligo skin is characterized microscopically by the complete absence of melanocytes. However there are some conflicting reports indicating that vitiligo lesions are not totally devoid of melanocytes. Significantly residual amounts of the melanocyte-specific enzyme tyrosinase have been detected in lesional vitiligo skin, providing unambiguous evidence for the presence of these cells. Since the depigmentationprocess can be reversible, either spontaneously or by using various therapeutic approaches, It seemed justifiable to readdress the issue and to reexplore a possible reservoir of melanocytes.pigmentation in mammals is due to melanin. These pig...
|
PDF Full Text Request