Abstract
Recent studies have shown that antioxidant enzyme expression and activity are drastically reduced in most human skin diseases, leading to propagation of oxidative stress and continuous disease progression. However, antioxidants, an endogenous defense system against reactive oxygen species (ROS), can be induced by exogenous sources, resulting in protective effects against associated oxidative injury. Many studies have shown that the induction of antioxidants is an effective strategy to combat various disease states. In one approach, a SOD mimetic was applied topically to mouse skin in the two-stage skin carcinogenesis model. This method effectively reduced oxidative injury and proliferation without interfering with apoptosis. In another approach, Protandim, a combination of 5 well-studied medicinal plants, was given via dietary administration and significantly decreased tumor incidence and multiplicity by 33% and 57%, respectively. These studies suggest that alterations in antioxidant response may be a novel approach to chemoprevention. This paper focuses on how regulation of antioxidant expression and activity can be modulated in skin disease and the potential clinical implications of antioxidant-based therapies.
Highlights
Antioxidant enzyme expression is known to decrease with aging, which has been theorized to contribute to age-related diseases
This paper focuses on the therapeutic potential of exogenous antioxidant inducers, the use of SOD mimetics as a chemopreventive agent, and dietary mechanisms of antioxidant induction in skin carcinogenesis
Several studies have shown that TPA can induce manganese superoxide dismutase (MnSOD) expression; by direct activation of protein kinase C (PKC) or through the production reactive oxygen species that can act as cell signaling molecules activating redox-sensitive transcription factors such as activator protein-1 (AP-1) and NF-κB [11,12,13]
Summary
Antioxidant enzyme expression is known to decrease with aging, which has been theorized to contribute to age-related diseases. The reactive oxidants of ROS include superoxide anion (O2−), singlet oxygen (O2), hydrogen peroxide (H2O2), and the hydroxyl radical (OH). These molecules can act as signaling molecules, they can participate in cellular damage, such as lipid peroxidation and DNA damage that trigger altered downstream signaling and apoptotic pathways. The skin consists of various antioxidant enzymes such as glutathione reductase, catalase, and superoxide dismutase. These enzymes are often activated to maintain homeostasis and to minimize the damaging effects of ROS. Alterations in the expression/activity of these antioxidants increase the susceptibility of skin to ROS-mediated injury that contributes to skin disease. This paper focuses on the therapeutic potential of exogenous antioxidant inducers, the use of SOD mimetics as a chemopreventive agent, and dietary mechanisms of antioxidant induction in skin carcinogenesis
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