title: 17β-estradiol protects human skin fibroblasts and keratinocytes against oxidative damage.
abstract: BACKGROUND
  Reactive oxygen species (ROS) cause severe damage to extracellular matrix and to molecular structure of DNA, proteins and lipids. Accumulation of these molecular changes apparently constitutes the basis of cell ageing. 17b-estradiol (E2) has a key role in skin ageing homeostasis as evidenced by the accelerated decline in skin appearance seen in the perimenopausal years. Oestrogens improve many aspects of the skin such as skin thickness, vascularization, collagen content and quality. Despite these clinical evidences, the effects of oestrogens on skin at the cellular level need further clarification.
  
  
  METHODS
  HaCaT and human fibroblasts were cultured under various conditions with E2 and H2 O2 ; then were subjected to immunofluorescence and western blot analysis. Lipoperoxidation was investigated using BODIPY.
  
  
  RESULTS
  In human fibroblasts oxidative stress decreases procollagen-I synthesis, while E2 significantly increases it. Fibroblasts and HaCaT cells viability in the presence of E2 demonstrates a notably increased resistance to H2 O2 effects. Furthermore E2 is able to counteract H2 O2 -mediated lipoperoxidation and DNA oxidative damage in skin cells.
  
  
  CONCLUSIONS
  In this study we highlight that the menopause-associated oestrogens decline is involved in reduced collagen production and that E2 could counteract the detrimental effects of oxidative stress on the dermal compartment during skin aging. Furthermore, our data show that physiological concentrations of oestrogens are able to interfere with ROS-mediated cell viability reduction and to protect human skin cells against oxidative damage to cellular membranes and nucleic acids structure.
  
  
  CONCLUSIONS
  Our experimental data show that the presence of 17β-estradiol may protect skin cells against oxidative damage and that the dramatic lowering of oestrogen levels during menopause, could render skin more susceptible to oxidative damage.
authors.affiliation: Department of Critical Care Medicine and Surgery, Division of Clinical, Preventive and Oncology Dermatology, University of Florence, Florence, Italy Department of Clinical Physiopathology, Andrology Unit, and Center of Excellence 'DeNothe', University of Florence, Florence, Italy Dermatology and Venereology Division, University of Rome "G. Marconi", Rome, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Bottai
authors.forename: R
authors.initials: R
authors.lastname: Mancina
authors.forename: M
authors.initials: M
authors.lastname: Muratori
authors.forename: P
authors.initials: P
authors.lastname: Di Gennaro
authors.forename: T
authors.initials: T
authors.lastname: Lotti
mesh_terms: D002460:Cell Line; D002478:Cells, Cultured; D024042:Collagen Type I / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology*; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D015603:Keratinocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology
chemical_list: D024042:Collagen Type I; D017382:Reactive Oxygen Species; D004958:Estradiol