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AGI Dermatics Data Shows the 8 Oxo-Guanine Repair Enzyme OGG1,Encapsulated in Liposomes, Reduces MMP-1 and TNF-alpha in UV,Irradiated Skin Cells

Clinical Data Presented at the Society for Investigative Dermatology

FREEPORT, N.Y., May 16, 2007 /PRNewswire-FirstCall/ -- AGI Dermatics today announced new clinical research that the 8-oxo-guanine DNA glycosylase (OGG1) encapsulated in liposomes enhances DNA repair and reduces MMP-1 and TNF-alpha in UV irradiated skin cells. The data was presented at the 68th Annual Meeting of the Society for Investigative Dermatology, May 9 - 12, in Los Angeles, CA.

"Our clinical study suggests that OGGI liposomes enhance DNA repair in skin cells," said Daniel Yarosh, PhD, President, AGI Dermatics. "This is particularly exciting when we consider that existing data shows that 8-oxo- guanine causes the most significant damage to mitochondrial DNA, which manifests as nearly all signs of premature aging."

The study examined the question of, if by damaging DNA with reactive oxygen species (ROS) would there be an increase of either/both matrix metalloproteinase-1 (MMP-1) and tumor necrosis factor, two factors known to play roles in photoaging. The formation of 8-oxo-G is induced by ROS from UVA irradiation, cigarette smoke, environmental stressors, endogenous enzymatic peroxidation reactions and normal mitochondrial metabolism. Those mentioned account for nearly all of the symptoms of premature skin aging. Long-term exposure consequences include photodamage, fine lines and wrinkles.

Natural cellular repair of the oxidative damage entails complete removal of 8-oxo-G from DNA via the enzyme OGGI. For the test, OOGI encapsulated in liposomes showed that the delivery of this enzyme into fibroblasts increases the rate of repair of 8-oxo-G, and reduces mitochondrial toxicity and analyzed mRNA content and protein secretion of MMP-1 and TNF-alpha, with real-time RT- PCR and ELISA.

Normal human dermal fibroblasts (NHDF) were irradiated with solar- stimulating (ss) UV (UVA340 bulb) to induce MMP-1. Following irra
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