Skin atrophy in cytoplasmic SOD-deficient mice and its complete recovery using a vitamin C derivative

Biochem Biophys Res Commun. 2009 May 1;382(2):457-61. doi: 10.1016/j.bbrc.2009.03.053. Epub 2009 Mar 14.

Abstract

Intrinsic skin ageing is characterized by atrophy and loss of elasticity. Although the skin hypertrophy induced by photoageing has been studied, the molecular mechanisms of skin atrophy during ageing remain unclear. Here, we report that copper/zinc superoxide dismutase (CuZn-SOD)-deficient mice show atrophic morphology in their skin. This atrophy is accompanied by the degeneration of collagen and elastic fibers, and skin hydroxyproline is also significantly reduced in deficient mice. These imply that the dysfunction of collagen and elastin biosynthesis are involved in the progression of skin thinning. Furthermore, transdermal administration of a vitamin C derivative which can permeate through the membrane, completely reversed the skin thinning and deterioration of collagen and elastin in the mutant mice. These indicate that the vitamin C derivative is a powerful agent for alleviating skin ageing through regeneration of collagen and elastin. The CuZn-SOD-deficient mice might be applicable to evaluation of therapeutic medicines against skin ageing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ascorbic Acid / analogs & derivatives*
  • Ascorbic Acid / pharmacology
  • Ascorbic Acid / therapeutic use
  • Atrophy / drug therapy
  • Atrophy / genetics
  • Atrophy / pathology
  • Collagen / metabolism
  • Cytoplasm
  • Elastin / metabolism
  • Mice
  • Mice, Knockout
  • Skin / drug effects*
  • Skin / enzymology
  • Skin / pathology
  • Skin Aging / drug effects*
  • Skin Aging / genetics
  • Superoxide Dismutase / genetics*
  • Superoxide Dismutase-1

Substances

  • 6-O-palmitol-ascorbate-2-O-phosphate
  • Collagen
  • Elastin
  • Sod1 protein, mouse
  • Superoxide Dismutase
  • Superoxide Dismutase-1
  • Ascorbic Acid