Oxidative Stress in the Pathogenesis of Skin Disease

Abstract

Skin is the largest body organ that serves as an important environmental interface providing a protective envelope that is crucial for homeostasis. On the other hand, the skin is a major target for toxic insult by a broad spectrum of physical (i.e. UV radiation) and chemical (xenobiotic) agents that are capable of altering its structure and function. Many environmental pollutants are either themselves oxidants or catalyze the production of reactive oxygen species (ROS) directly or indirectly. ROS are believed to activate proliferative and cell survival signaling that can alter apoptotic pathways that may be involved in the pathogenesis of a number of skin disorders including photosensitivity diseases and some types of cutaneous malignancy. ROS act largely by driving several important molecular pathways that play important roles in diverse pathologic processes including ischemia-reperfusion injury, atherosclerosis, and inflammatory responses. The skin possesses an array of defense mechanisms that interact with toxicants to obviate their deleterious effect. These include non-enzymatic and enzymatic molecules that function as potent antioxidants or oxidant-degrading systems. Unfortunately, these homeostatic defenses, although highly effective, have limited capacity and can be overwhelmed thereby leading to increased ROS in the skin that can foster the development of dermatological diseases. One approach to preventing or treating these ROS-mediated disorders is based on the administration of various antioxidants in an effort to restore homeostasis. Although many antioxidants have shown substantive efficacy in cell culture systems and in animal models of oxidant injury, unequivocal confirmation of their beneficial effects in human populations has proven elusive.

Oxidative Stress and Skin Cancer: An Overview

“…Studies have shown that UVB radiation produces a variety of adverse effects that includes DNA damage [14,15], mutations in key regulatory genes [16], inflammation [17,18], immuno-suppression [19,20], photo-aging and skin cancer [21,22]. UVB is directly absorbed by cellular DNA leading to the formation of DNA lesions primarily cyclobutane pyrimidine dimers and pyrimidine (6-4)-pyrimidone photoproducts [13,23].…”

Anti-aging Effects of Diospyros kaki Thunb. Extracts in UVA-irradiated Epidermal Keratinocytes

“…UVA와 UVB는 DNA 손상과 세포사멸 수용체 활성화, 그리고 활성산소종을 생성시켜 세포 사멸을 유도하고 (Assefa et al, 2005), UVA와 UVB에 의해 촉진된 활성산소종의 생산은 직접적 혹은 간접적으로 염증반 응, 광감작, 암화 등을 유도한다 (Bickers & Athar, 2006).…”

Protective effect of Schizandrin B against damage of UVB irradiated skin cells depend on inhibition of inflammatory pathways

“…15 Therefore, antioxidants that clear up ROS have been proposed as photoprotective agents. 16,17 More and more skin care products contained botanical agents, which have the potential antioxidant and the properties of anti-inflammatory and anti-carcinogenic, which can avoid damages of UV radiation damge to skin.…”