This work was performed at the University of Wisconsin-Madison, School of Veterinary Medicine.
Antioxidant Status in Hyperthyroid Cats before and after Radioiodine Treatment
Version of Record online: 17 MAR 2012
Copyright © 2012 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 26, Issue 3, pages 582–588, May-June 2012
How to Cite
Branter, E., Drescher, N., Padilla, M. and Trepanier, L.A. (2012), Antioxidant Status in Hyperthyroid Cats before and after Radioiodine Treatment. Journal of Veterinary Internal Medicine, 26: 582–588. doi: 10.1111/j.1939-1676.2012.00903.x
Preliminary data in abstract form presented at the Annual Meeting of the American College of Veterinary Internal Medicine, 2011, Denver, CO.
- Issue online: 2 MAY 2012
- Version of Record online: 17 MAR 2012
- Manuscript Accepted: 24 JAN 2012
- Manuscript Revised: 1 DEC 2011
- Manuscript Received: 26 SEP 2011
- Waltham Foundation
- Feline plasma;
- Oxidative stress
Reversible antioxidant depletion is found in hyperthyroid humans, and antioxidant depletion increases the risk of methimazole toxicosis in rats.
To determine whether abnormalities in concentrations of blood antioxidants or urinary isoprostanes were present in hyperthyroid cats, and were reversible after radioiodine treatment. To determine whether or not antioxidant abnormalities were associated with idiosyncratic methimazole toxicosis.
Hyperthyroid cats presented for radioiodine treatment (n = 44) and healthy mature adult control cats (n = 37).
Prospective, controlled, observational study. Red blood cell glutathione (GSH), plasma ascorbate (AA), plasma free retinol (vitamin A), α-tocopherol (vitamin E), and urinary free 8-isoprostanes in hyperthyroid cats were compared to healthy cats and to hyperthyroid cats 2 months after treatment.
Blood antioxidants were not significantly different in hyperthyroid cats (mean GSH 1.6 ± 0.3 mM; AA 12.8 ± 4.9 μM, and vitamin E, 25 ± 14 μg/mL) compared to controls (GSH 1.4 ± 0.4 mM; AA 15.0 ± 6.6 μM, and vitamin E, 25 ± 17 μg/mL). Urinary isoprostanes were increased in hyperthyroid cats (292 ± 211 pg/mg creatinine) compared to controls (169 ± 82 pg/mg; P = .006), particularly in hyperthyroid cats with a USG < 1.035. Plasma free vitamin A was higher in hyperthyroid cats (0.54 ± 0.28 μg/mL versus 0.38 ± 0.21 in controls; P = .007). Both abnormalities normalized after radioiodine treatment. No association was found between oxidative status and prior idiosyncratic methimazole toxicosis.
Conclusion and Clinical Importance
Increased urinary isoprostane could reflect reversible renal oxidative stress induced by hyperthyroidism, and this requires additional evaluation.