title: Role of oxidative tissue injury in the pathophysiology of experimentally induced equine laminitis: a comparison of 2 models.
abstract: BACKGROUND
  Oxidative stress reportedly plays a role in sepsis-induced organ dysfunction and failure in many species. In septic horses, laminae are targeted; evidence of laminar oxidative stress has been reported experimentally in the black walnut extract (BWE) model. Carbohydrate (CHO)-induced laminitis may be more similar to clinical sepsis-related laminitis than the BWE model in that animals with CHO-induced disease commonly develop laminar failure. The role of oxidative stress in the CHO model remains unknown.
  
  
  OBJECTIVE
  Markers of oxidative stress will be increased in laminae from horses with BWE- and CHO-induced laminitis.
  
  
  METHODS
  Banked laminar tissue from various time points from animals subjected to BWE (n = 15) and CHO (n = 20) protocols.
  
  
  METHODS
  Laminar 4-hydroxynonenal (4-HNE) and protein carbonyl content were evaluated by slot blot analysis. Laminar 3-nitrotyrosine (3-NT) immunohistochemistry was performed.
  
  
  RESULTS
  The number of laminar 3-NT (+) cells was increased at developmental and Obel grade 1 (OG1) time points in the BWE model (versus control [CON]; P= .013) and lower in OG1 tissues than CON in the CHO model (P = .04). No change in 4-HNE content was observed in the CHO model, and no increase in laminar protein carbonyl content was present in either model (P > .05).
  
  
  CONCLUSIONS
  These results do not support a prominent role for oxidative stress at examined time points in CHO-overload laminitis and support transient oxidative stress in the BWE model. Tissue oxidation does not appear to be a central early pathophysiologic event in CHO-associated laminitis.
authors.affiliation: Ohio State University College of Veterinary Medicine, Columbus, OH 43210, USA.
authors.forename: T A
authors.initials: TA
authors.lastname: Burns
authors.forename: T
authors.initials: T
authors.lastname: Westerman
authors.forename: G J
authors.initials: GJ
authors.lastname: Nuovo
authors.forename: M R
authors.initials: MR
authors.lastname: Watts
authors.forename: A
authors.initials: A
authors.lastname: Pettigrew
authors.forename: C
authors.initials: C
authors.lastname: Yin
authors.forename: J K
authors.initials: JK
authors.lastname: Belknap
mesh_terms: D000447:Aldehydes / Q000032:analysis / Q000378:metabolism; D000818:Animals; D015415:Biomarkers; D004195:Disease Models, Animal; D005534:Foot Diseases / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology / Q000662:veterinary*; D006724:Hoof and Claw / Q000187:drug effects*; D006734:Horse Diseases / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D006736:Horses; D007249:Inflammation / Q000139:chemically induced / Q000503:physiopathology / Q000662:veterinary*; D031324:Juglans / Q000737:chemistry; D015227:Lipid Peroxidation; D018384:Oxidative Stress / Q000502:physiology*; D010936:Plant Extracts / Q000737:chemistry / Q000633:toxicity; D011506:Proteins / Q000378:metabolism; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D013213:Starch / Q000008:administration & dosage / Q000633:toxicity; D014443:Tyrosine / Q000378:metabolism
chemical_list: D000447:Aldehydes; D015415:Biomarkers; D010936:Plant Extracts; D011506:Proteins; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D014443:Tyrosine; D013213:Starch; C027576:4-hydroxy-2-nonenal