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Abstract

Allergic contact dermatitis is mediated in most cases by small molecular substances which are not complete antigens, unlike proteins. According to the concept of the hapten hypothesis derived from the classical studies by Landsteiner, it is generally accepted that small molecules require covalent binding to macro-molecular proteins to become immunogens [1], However, most small molecular compounds are chemically inert and are therefore not able to bind to high molecular proteins by themselves. One possibility is for them to be metabolized to highly reactive species by xenobiotica-metabolizing enzymes [1, 2]. Most xenobiotica are metabolized in the liver. However, the skin has also been recognized to be an important site of extrahepatic metabolism of xenobiotica [3–5]. This is especially the case for the epidermis (the outer layer of the skin), which weighs approximately 225 g and constitutes the major interface between the body and the environment with a surface area of 1.5–2.0 m2 [6, 7]. Immunocompetent cells such as peripheral blood monocytes and lymphocytes have also been shown to possess xenobiotica-metabolizing enzymes [8,9].

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© 1998 Springer-Verlag Berlin Heidelberg

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Merk, H.F. (1998). Skin Metabolism. In: Lepoittevin, JP., Basketter, D.A., Goossens, A., Karlberg, AT. (eds) Allergic Contact Dermatitis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80331-4_5

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  • DOI: https://doi.org/10.1007/978-3-642-80331-4_5

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