الفهرس 
Introduction and aim of the work
Patients And MethodsOnly 14 pages are availabe for public view
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Abstract
Cutaneous aging includes two distinct phenomena: True aging, also termed intrinsic aging, is universal, affecting the skin in a manner similar to other organ. It is an inevitable change attributable to the passage of time alone; photoaging is the superposition on intrinsic aging of changes attributable to chronic sun exposure, which are neither universal nor inevitable (Yaar and Gilchrest, 2001a). The underlying mechanisms of UVRinduced cutaneous effects are complex, and result from the interaction of UVR with a variety of molecules, including nucleic acids, membrane lipids and proteins. UVR can directly damage DNA following the absorption of photons by DNA, while UVRgenerated reactive oxygen species cause indirect oxidative damage to DNA, lipid membranes and other structures in their vicinity. DNA lesions if not repaired can lead to mutations and carcinogenesis. Both UVA and UVB are known to generate reactive oxygen species (Larsson etal., 2005). Enzymic and nonenzymic antioxidants interact in providing photoprotection in both intracellular and extracellular space of the skin. Antioxidant enzymes such as glutathione peroxidase and glutathione reductase reduce hydrogen peroxide and lipid hyDROPeroxides using gluthatione. Catalase interacts with hydrogen peroxide and the superoxide dismutases with superoxide. Nonenzymic antioxidants include Lascorbic acid in the fluid phase, gluthatione in the cellular compartment, vitamin E in membranes, and ubiquinol in mitochondria (EberleinK(Rh(Bonig and Ring, 2005). This study was conducted on 60 subjects, 40 elderly and 20 young control. The elderly subjects were divided into photoaging group (group A) and agematched intrinsic aging group (group B). Male/Female ratio was 1:1.