Abstract

N‐Acetyl‐5‐methoxytryptamine, commonly known as melatonin, was isolated and structurally identified by a dermatologist, Aaron B. Lerner, in 1958. His interest stemmed from the fact that melatonin has potent skin‐lightening effects in amphibians and some other non‐mammalian species. In humans, however, melatonin is not capable of lightening skin or in reducing pigmentation. While melatonin synthesis is the best known to occur in the pineal gland, it is also produced in several other organs including the skin. Melatonin is a powerful, multifaceted direct free radical scavenger and indirect antioxidant. Numerous studies have shown that melatonin production wanes with increasing age and its loss has been speculated to be consequential in free radical‐mediated cellular and organ deterioration that occurs in the elderly. Additionally, a number of free radical‐related diseases, e.g. Alzheimer's disease, Parkinsonism, cataract formation, etc., may in part be a consequence of the loss of endogenous melatonin production. The administration of melatonin in animal models of these diseases typically defers their progression and limits their severity. Likewise, due to its antioxidant properties and via other mechanisms, melatonin may reduce skin aging. Melatonin, when applied topically to the skin of humans, has obvious protective effects against ultraviolet (UV) light‐induced erythema. Also, lipid peroxidation in human skin fibroblasts due to their exposure to UV‐B is reduced when melatonin is present.

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