Presented in part as a research abstract at the 2011 American College Veterinary Internal Medicine Forum, Denver, CO, June 17, 2011.
Effect of N-Acetylcysteine Supplementation on Intracellular Glutathione, Urine Isoprostanes, Clinical Score, and Survival in Hospitalized Ill Dogs
Version of Record online: 4 MAR 2013
Copyright © 2013 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 27, Issue 2, pages 250–258, March/April 2013
How to Cite
Viviano, K.R. and VanderWielen, B. (2013), Effect of N-Acetylcysteine Supplementation on Intracellular Glutathione, Urine Isoprostanes, Clinical Score, and Survival in Hospitalized Ill Dogs. Journal of Veterinary Internal Medicine, 27: 250–258. doi: 10.1111/jvim.12048
- Issue online: 15 MAR 2013
- Version of Record online: 4 MAR 2013
- Manuscript Accepted: 7 JAN 2013
- Manuscript Revised: 24 NOV 2012
- Manuscript Received: 19 JUN 2012
- Lipid peroxidation;
- Oxidative stress;
- Vitamin E
Antioxidant depletion and lipid peroxidation have been correlated with disease severity and associated with poor outcomes.
Supplementing dogs with N-acetylcysteine (NAC) during the first 48 hours of hospitalization will increase cysteine, normalize glutathione concentrations, and decrease the degree of lipid peroxidation associated with illness.
Sixty systemically ill hospitalized client-owned dogs and 14 healthy control dogs.
Randomized investigator-blinded, placebo-controlled prospective study. Dogs were randomized to treatment with NAC (n = 30) versus placebo (n = 30). Antioxidants, urine 8-isoprostane/creatinine (IP/Cr), and clinical score were determined before and after treatment with NAC. Glutathione, cysteine, and vitamin E concentrations were quantified using high-performance liquid chromatography. Atomic absorption spectroscopy and enzyme-linked immunosorbent assays were used to quantify selenium and isoprostane concentrations, respectively.
Ill dogs had significantly lower vitamin E concentrations (27 versus 55 μg/mL; P = .0005) as well as elevated IP/Cr ratios (872 versus 399 pg/mg; P = .0007) versus healthy dogs. NAC supplementation significantly increased plasma cysteine (8.67 versus 15.1 μM; P < .0001) while maintaining glutathione concentrations. Dogs in the placebo group experienced a statistically significant decrease in glutathione concentrations (1.49 versus 1.44 mM; P = .0463). Illness severity and survival were unchanged after short duration NAC supplementation.
Ill dogs experience systemic oxidative stress. Supplementation with NAC during the first 48 hours of hospitalization stabilized erythrocyte glutathione concentrations. The clinical impact of this supplementation and glutathione concentration stabilization was undetermined.