Purification of human skin tyrosinase and its protein inhibitor: Properties of the enzyme and the mechanism of inhibition by protein

Vijayan, Elimban; Husain, Intisar; Ramaiah, Arunachalam; Madan, N. C.

doi:10.1016/0003-9861(82)90555-0

Cited by 42 publications

(17 citation statements)

References 29 publications

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“…Several reports have provided evidence in favour of the existence of endogenous melanogenic inhibitors (Farooqui, Robb, Boyce, Warden, & Nordlund, 1995;Vijayan, Husain, Ramaiah, & Madan, 1982). In addition, in the search for safe, effective, and natural whitening agents, specific molecules have been identified as candidates, including arbutin, hydroquinone, linoleic acid, ascorbic acid, kojic acid or buthionine sulphoximine (Chang, 2012;Galvan, Wakamatsu, Alonso-Alvarez, & Solano, 2014;Lim et al, 2009;Palumbo, d'Ischia, Misuraca, & Prota, 1991;Park et al, 2009).…”

Section: Discussionmentioning

confidence: 98%

Effects of the melanogenic inhibitor, uracil, derived from Lactobacillus plantarum TWK10-fermented soy milk on anti-melanogenesis in B16F0 mouse melanoma cells

Chang

Dai

Leu

et al. 2015

Journal of Functional Foods

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Section: Discussionmentioning

confidence: 98%

Effects of the melanogenic inhibitor, uracil, derived from Lactobacillus plantarum TWK10-fermented soy milk on anti-melanogenesis in B16F0 mouse melanoma cells

Chang

Dai

Leu

et al. 2015

Journal of Functional Foods

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“…Numerous reports have suggested the existence of endogenous melanogenic inhibitors, [177,178] but few specific molecules have been identified. One group of inhibitors includes sphingolipids, a class of membrane associated lipids that act as signal transducers (reviewed in [179]).…”

Section: Melanogenic Inhibitorsmentioning

confidence: 99%

Cellular mechanisms regulating human melanogenesis

Park

Kosmadaki

Yaar

et al. 2009

Cell. Mol. Life Sci.

315

354

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The major differentiated function of melanocytes is the synthesis of melanin, a pigmented heteropolymer that is synthesized in specialized cellular organelles termed melanosomes. Mature melanosomes are transferred to neighboring keratinocytes and are arranged in a supranuclear cap, protecting the DNA against incident ultraviolet light (UV) irradiation. The synthesis and distribution of melanin in the epidermis involves several steps: transcription of melanogenic proteins, melanosome biogenesis, sorting of melanogenic proteins into the melanosomes, transport of melanosomes to the tips of melanocyte dendrites and finally transfer into keratinocytes. These events are tightly regulated by a variety of paracrine and autocrine factors in response to endogenous and exogenous stimuli, principally UV irradiation.

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“…In addition, the amount of cytochromes P450 (P450s) in the skin is limited, and this makes an arene oxide less attractive as a cause of skin rash. The skin does contain other metabolic enzymes such as peroxidases (Strohm and Kulkarni, 1986), sulfotransferases (Kudlacek et al, 1995;Higashi et al, 2004), and tyrosinase (Pomerantz and Ances, 1975;Vijayan et al, 1982;Wittbjer et al, 1991).…”

mentioning

confidence: 99%

Possible Bioactivation Pathways of Lamotrigine

Lu¹,

Uetrecht²

2007

Drug Metab Dispos

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ABSTRACT:The anticonvulsant lamotrigine is associated with idiosyncratic drug reactions, especially skin rashes. Most idiosyncratic reactions are believed to be caused by reactive metabolites. Previous studies have found evidence that an arene oxide is formed in rats; however, when we incubated radiolabeled lamotrigine with rat liver microsomes virtually no covalent binding was detected, and the expected downstream phenolic metabolites are not observed in humans. Rare cases of agranulocytosis have been associated with lamotrigine therapy, and we found that lamotrigine is oxidized to two different N-chloro products by HOCl. The more reactive Nchloro metabolite forms an adduct with N-acetylhistidine, and covalent binding was observed when radiolabeled lamotrigine was incubated with myeloperoxidase/H 2 O 2 /Cl ؊ . Another lamotrigine metabolite is an N-oxide. If this N-oxide were sulfated, it might be sufficiently reactive to bind to protein. The synthetic N-sulfate reacted with N-acetylserine; however, no covalent binding was detected when the radiolabeled N-oxide was incubated with sulfotransferase. We also investigated the possibility that lamotrigine might be oxidized to a free radical by other peroxidases or oxidized by other enzymes such as prostaglandin H synthase or tyrosinase, but no evidence of oxidation was found, and lamotrigine did not cause any detectable increase in lipid peroxidation in vivo. In view of the virtual lack of covalent binding to hepatic microsomes and the lack of any other likely pathway leading to metabolic activation in the skin, it is possible that the parent drug rather than a reactive metabolite causes lamotrigine-induced skin rashes.

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Purification of human skin tyrosinase and its protein inhibitor: Properties of the enzyme and the mechanism of inhibition by protein

Cited by 42 publications

References 29 publications

Effects of the melanogenic inhibitor, uracil, derived from Lactobacillus plantarum TWK10-fermented soy milk on anti-melanogenesis in B16F0 mouse melanoma cells

Effects of the melanogenic inhibitor, uracil, derived from Lactobacillus plantarum TWK10-fermented soy milk on anti-melanogenesis in B16F0 mouse melanoma cells

Cellular mechanisms regulating human melanogenesis

Possible Bioactivation Pathways of Lamotrigine

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