COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE in VS .NET

Maker QR Code in VS .NET COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE

COSMETIC DERMATOLOGY: PRINCIPLES AND PRACTICE
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264 Overvad K, Thorling EB, Bjerring P, et al Selenium inhibits UV-light-induced skin carcinogenesis in hairless mice Cancer Lett 1985;27:163 265 Burke KE, Combs GF Jr, Gross EG, et al The effects of topical and oral Lselenomethionine on pigmentation and skin cancer induced by ultraviolet irradiation Nutr Cancer 1992;17:123 266 Rafferty TS, Beckett GJ, Walker C, et al Selenium protects primary human keratinocytes from apoptosis induced by exposure to ultraviolet radiation Clin Exp Dermatol 2003;28: 294 267 McKenzie RC, Rafferty TS, Beckett GJ Selenium: an essential element for immune function Immunol Today 1998; 19:342 268 Clark LC, Combs GF Jr, Turnbill BW, et al Effects of selenium supple-
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mentation for cancer prevention in patients with carcinoma of the skin A randomized controlled trial Nutritional Prevention of Cancer Study Group JAMA 1996;276:1957 Institute of Medicine, Food and Nutrition Board Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids Washington, DC: National Academy Press; 2000 Koller LD, Exon JH The two faces of selenium-deficiency and toxicity are similar in animals and man Can J Vet Res 1986;50:297 McKenzie RC Selenium, ultraviolet radiation and the skin Clin Exp Dermatol 2000;25:631 Stewart MS, Spallholz JE, Neldner KH, et al Selenium compounds have disparate abilities to impose oxidative
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stress and induce apoptosis Free Radic Biol Med 1999;26:42 273 Pinnell SR, Lin F-H, Lin J-Y, et al Ferulic acid stabilizes a solution of vitamins A and E and doubles its photoprotection of skin J Invest Dermatol 2005;125:826 274 Greul AK, Grundmann JU, Heinrich F, et al Photoprotection of UV-irradiated human skin: an antioxidative combination of vitamins E and C, carotenoids, selenium and proanthocyanidins Skin Pharmacol Appl Skin Physiol 2002;15: 307 275 Passi S, De Pita O, Grandinetti M, et al The combined use of oral and topical lipophilic antioxidants increases their levels both in sebum and stratum corneum Biofactors 2003;18:289
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CHAPTER 34 ANTIOXIDANTS
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CHAPTER 35 Anti-In ammatory Agents
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Mari Paz Castanedo-Tardan, MD Leslie Baumann, MD DEFINING INFLAMMATION
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Inflammation, from the Latin word inflammatio (to set on fire), is a dynamic vascular and cellular reflexive response of the living tissue to injury; such injury may present in the form of infection, chemical damage (eg, toxins, irritants), physical damage (eg, heat, cold, radiation, mechanical trauma), and the binding of antibodies to antigens within the body1 Inflammation is therefore a protective mechanism of the organism intended to remove such injurious stimuli as well as to initiate the healing process of the damaged tissue Localized vasodilation, increased vascular permeability, extravasation of plasmatic proteins, and migration of leukocytes into the affected tissue produce what Cornelius Celsius defined in the first century as the cardinal signs of acute inflammation: calor (heat), dolor (pain), rubor (redness), and tumor (swelling)2 Functio laesa (loss of function) was later added to the definition of inflammation by Rudolf Virchow in the 19th century3 A basic sequence of events characterizes virtually all types of inflammatory responses regardless of the provocative stimuli4 The initial reaction is vasodilation followed by transient vasoconstriction The microvascular endothelium then becomes more permeable to plasma proteins, which leak out into the extravascular compartment thus establishing an inflammatory exudate Inflammatory mediators released in the area induce the expression of selectintype adhesion molecules on the endothelial cells Recruited leukocytes then interact with such adhesion molecules, bind to the inflamed endothelium, and extravasate into the tissue where they respond to the insult through phagocytosis and degranulation Finally, the inflammatory response must be actively terminated when no longer essential to prevent unnecessary damage to tissue The process of inflammation, both vascular and cellular, is orchestrated by a large array of inflammatory mediators, which will be reviewed below These mediators include the following: (1) cellular-derived products, such as vasoactive amines (eg, histamine), cytokines, eicosanoids (eg, prostaglandins, thromboxanes, and leukotrienes), enzymes, and oxygen radicals and (2) plasmaderived mediators, which include complement cascade components, kinins, and fibrinopeptides (1) Cyclooxygenase pathway: All eicosanoids with ring structures, that is, the PGs, TXs, and prostacyclins, are synthesized via the cyclooxygenase pathway Two cyclooxygenases have been identified: COX-1 and COX-2 The former is ubiquitous and constitutive, whereas the latter is induced in response to inflammatory stimuli The products of these and subsequent reactions in this pathway are summarized in Fig 35-2 (2) Lipoxygenase pathway: Several lipoxygenase enzymes can act on AA to form different peroxidated derivatives (the hydroperoxyeicosatetraenoic [HPETE] acids 5-HPETE, 12-HPETE, and 15-HPETE) depending on which carbon of AA they insert or attach oxygen HPETEs are then rapidly reduced to hydroxylated derivatives (HETEs), LTs, or lipoxins, depending on the tissue
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