Vitamin E provides protection for bone in mature hindlimb unloaded male rats

Calcif Tissue Int. 2005 Apr;76(4):272-9. doi: 10.1007/s00223-004-0269-8. Epub 2004 Mar 8.

Abstract

The deleterious effects of skeletal unloading on bone mass and strength may, in part, result from increased production of oxygen-derived free radicals and proinflammatory cytokines. This study was designed to evaluate the ability of vitamin E (alpha-tocopherol), a free-radical scavenger with antiinflammatory properties, to protect against bone loss caused by skeletal unloading in mature male Sprague-Dawley rats. A 2 x 3 factorial design was used with either hindlimb unloading (HU) or normal loading (ambulatory; AMB), and low-dose (LD; 15 IU/kg diet), adequate-dose (AD; 75 IU/kg diet), or high-dose (HD; 500 IU/kg diet) vitamin E (DL-alpha-tocopherol acetate). To optimize the effects of vitamin E on bone, dietary treatments were initiated 9 weeks prior to unloading and continued during the 4-week unloading period, at which time animals were euthanized and blood and tissue samples were collected. Serum vitamin E was dose-dependently increased, confirming the vitamin E status of animals. The HD treatment improved oxidation parameters, as indicated by elevated serum ferric-reducing ability and a trend toward reducing tissue lipid peroxidation. Histomorphometric analysis of the distal femur revealed significant reductions in trabecular thickness (TbTh), double-labeled surface (dLS/BS), and rate of bone formation to bone volume (BFR/BV) due by HU. AMB animals on the HD diet and HU animals on the LD diet had reduced bone surface normalized to tissue volume (BS/TV) and trabecular number (TbN); however, the HD vitamin E protected against these changes in the HU animals. Our findings suggest that vitamin E supplementation provides modest bone protective effects during skeletal unloading.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Antioxidants / therapeutic use*
  • Biomarkers / blood
  • Bone Demineralization, Pathologic / drug therapy*
  • Bone Demineralization, Pathologic / etiology
  • Bone Demineralization, Pathologic / metabolism
  • Bone Density / drug effects
  • Bone Density / physiology
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Free Radical Scavengers / therapeutic use*
  • Hindlimb Suspension / physiology*
  • Lipid Peroxidation
  • Male
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Tibia / drug effects
  • Tibia / metabolism
  • Vitamin E / therapeutic use*

Substances

  • Antioxidants
  • Biomarkers
  • Free Radical Scavengers
  • Vitamin E