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Glutathione plays an important role in preventing oxidative damage to the skin. In addition to its many recognized biological functions, glutathione has also been associated with skin lightening ability. The role of glutathione as a skin whitener was discovered as a side effect of large doses of glutathione. Glutathione utilizes different mechanisms to exert its action as a skin whitening agent at various levels of melanogenesis. It inhibits melanin synthesis by means of stopping the neurotransmitter precursor L-DOPA's ability to interact with tyrosinase in the process of melanin production. Glutathione inhibits the actual production as well as agglutination of melanin by interrupting the function of L-DOPA. Another study found that glutathione inhibits melanin formation by direct inactivation of the enzyme tyrosinase by binding and chelating copper within the enzyme's active site. Glutathione's antioxidant property allows it to inhibit melanin synthesis by quenching of free radicals and peroxides that contribute to tyrosinase activation and melanin formation. Its antioxidant property also protects the skin from UV radiation and other environmental as well as internal stressors that generate free radicals that cause skin damage and hyperpigmentation. In most mammals, melanin formation consists of eumelanin (brown-black pigment) and pheomelanin ( yellow-red pigment) as either mixtures or co-polymers. Increase in glutathione level may induce the pigment cell to produce pheomelanin instead of eumelanin pigments. A research by Te-Sheng Chang found lowest levels of reduced glutathione to be associated with eumelanin type pigmentation, whereas the highest ones were associated with the pheomelanin. As a result, it is reasonable to assume that depletion of glutathione would result in eumelanin formation. Prota observed that decreased glutathione concentration led to the conversion of L-Dopaquinone to Dopachrome, increasing the formation of brown-black pigment (eumelanin).

Gamma-glutamylcysteine (GGC) is the immediate precursor to GSH. GGC supplementation would circumvent feedback inhibitory control of GCL by the end product GSH. Accordingly, a method of elevating GSH levels with the notable advantage of bypassing negative feedback inhibition has been described. Because of this, GGC has been the focus of therapeutic efforts since Puri and Meister 1983. The first documented use of GGC in brains appears to be Pileblad and Magnusson, 1992. Astroglia cells are capable of utilising GGC. Direct delivery of the GSH precursor GCC to brain has been reported to effectively replenish levels of GSH in the brain. Most of the work done on GGC has been preclinical, based on in vivo animal models, or in vitro brain cultures. In order for the therapeutic value of GGC elevation against AD to be vindicated, three empirical hurdles have to be cleared. The first is to demonstrate that delivery of GGC into the brain can indeed increase GSH. The second is to demonstrate that the increase in GGC can indeed reduce oxidative stress in the brain, a condition frequently linked with cognitive decline.

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