Free Radical Generator Identified by Nu Skin Scientists
Posted by on May 15th, 2008 at 01:19pm
New research funded by Nu Skin Enterprises on internal causes of aging has identified a previously unknown source of superoxide free radicals. Free radicals from external triggers, such as sun exposure and cigarette smoke, have expanded been known to damage skin cells and components of the skin’s extracellular matrix, including collagen and elastin.
Scientists from Nu Skin Enterprises and Purdue University report their novel research findings on age-related NADH oxidase (arNOX) that week in Kyoto, Japan, at universal Investigative Dermatology 2008 (IID2008), a major scientific venue for the latest knowledge on skin biology. The scientists present compelling evidence that arNOX, an enzyme associated with cell membranes, is present and active on skin cells. Significantly, arNOX activity increases during the “aging” years of about 45-70.
“Identifying skin-associated arNOX and its increasing activity with age is a breakthrough discovery in understanding skin aging,” said Zoe Diana Draelos, MD, primary investigator with Dermatology Consulting Services, member of the Nu Skin Scientific Advisory Board and one of the study authors. “Currently, most dermatological research focuses on correcting skin damage after it occurs. Identifying an internal source of free radicals in skin, and advancing an understanding of how and why they are generated, adds to our ability to address fundamental mechanisms that may combine with external sources to lead to accelerated skin aging.”
“Evidence of arNOX in the skin provides further insights into potentially revolutionary therapies for skin care, particularly considering its activity correlates with the ages when public start to see their skin lose its elasticity and firmness, and notice increasingly discoloration and lines and wrinkles,” remarked Helen Knaggs, PhD, vice president of Nu Skin global research and development. “whether we can develop innovative ways to inhibit arNOX activity and prevent the production of free radicals in the first place, thereupon we can address both sides of the equation — correcting free radical damage from external sources, while at the same moment preventing free radical production from internal sources.”
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