PMID- 21418321
OWN - NLM
STAT- MEDLINE
DCOM- 20110929
LR  - 20161125
IS  - 1939-1676 (Electronic)
IS  - 0891-6640 (Linking)
VI  - 25
IP  - 3
DP  - 2011 May-Jun
TI  - Role of oxidative tissue injury in the pathophysiology of experimentally induced 
      equine laminitis: a comparison of 2 models.
PG  - 540-8
LID - 10.1111/j.1939-1676.2011.0706.x [doi]
AB  - 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. HYPOTHESIS/OBJECTIVES: Markers 
      of oxidative stress will be increased in laminae from horses with BWE- and 
      CHO-induced laminitis. ANIMALS: 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 AND 
      CLINICAL IMPORTANCE: 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.
CI  - Copyright (c) 2011 by the American College of Veterinary Internal Medicine.
FAU - Burns, T A
AU  - Burns TA
AD  - Ohio State University College of Veterinary Medicine, Columbus, OH 43210, USA.
FAU - Westerman, T
AU  - Westerman T
FAU - Nuovo, G J
AU  - Nuovo GJ
FAU - Watts, M R
AU  - Watts MR
FAU - Pettigrew, A
AU  - Pettigrew A
FAU - Yin, C
AU  - Yin C
FAU - Belknap, J K
AU  - Belknap JK
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110321
PL  - United States
TA  - J Vet Intern Med
JT  - Journal of veterinary internal medicine
JID - 8708660
RN  - 0 (Aldehydes)
RN  - 0 (Biomarkers)
RN  - 0 (Plant Extracts)
RN  - 0 (Proteins)
RN  - 0 (Reactive Nitrogen Species)
RN  - 0 (Reactive Oxygen Species)
RN  - 42HK56048U (Tyrosine)
RN  - 9005-25-8 (Starch)
RN  - K1CVM13F96 (4-hydroxy-2-nonenal)
SB  - IM
MH  - Aldehydes/analysis/metabolism
MH  - Animals
MH  - Biomarkers
MH  - Disease Models, Animal
MH  - Foot Diseases/chemically induced/metabolism/physiopathology/*veterinary
MH  - Hoof and Claw/*drug effects
MH  - Horse Diseases/chemically induced/*metabolism/physiopathology
MH  - Horses
MH  - Inflammation/chemically induced/physiopathology/*veterinary
MH  - Juglans/chemistry
MH  - Lipid Peroxidation
MH  - Oxidative Stress/*physiology
MH  - Plant Extracts/chemistry/toxicity
MH  - Proteins/metabolism
MH  - Reactive Nitrogen Species
MH  - Reactive Oxygen Species
MH  - Starch/administration & dosage/toxicity
MH  - Tyrosine/metabolism
EDAT- 2011/03/23 06:00
MHDA- 2011/10/01 06:00
CRDT- 2011/03/23 06:00
PHST- 2011/03/23 06:00 [entrez]
PHST- 2011/03/23 06:00 [pubmed]
PHST- 2011/10/01 06:00 [medline]
AID - 10.1111/j.1939-1676.2011.0706.x [doi]
PST - ppublish
SO  - J Vet Intern Med. 2011 May-Jun;25(3):540-8. doi: 10.1111/j.1939-1676.2011.0706.x. 
      Epub 2011 Mar 21.