title: Vitamin E provides protection for bone in mature hindlimb unloaded male rats.
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.
authors.affiliation: Department of Surgery, Research University of Oklahoma Health Sciences Center, O'Donoghue Research Building, room 335, 1122 N.E. 13th St., Oklahoma City, OK 73117, USA. brenda-smith@ouhsc.edu
authors.forename: B J
authors.initials: BJ
authors.lastname: Smith
authors.forename: E A
authors.initials: EA
authors.lastname: Lucas
authors.forename: R T
authors.initials: RT
authors.lastname: Turner
authors.forename: G L
authors.initials: GL
authors.lastname: Evans
authors.forename: M R
authors.initials: MR
authors.lastname: Lerner
authors.forename: D J
authors.initials: DJ
authors.lastname: Brackett
authors.forename: B J
authors.initials: BJ
authors.lastname: Stoecker
authors.forename: B H
authors.initials: BH
authors.lastname: Arjmandi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D018488:Bone Demineralization, Pathologic / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D019417:Hindlimb Suspension / Q000502:physiology*; D015227:Lipid Peroxidation; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013977:Tibia / Q000187:drug effects / Q000378:metabolism; D014810:Vitamin E / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D016166:Free Radical Scavengers; D014810:Vitamin E