Branter E., Drescher N., Padilla M., et al.
Journal of veterinary internal medicine / American College of Veterinary Internal Medicine, 2012. 26(3): p.582-8.
BACKGROUND: Reversible antioxidant depletion is found in hyperthyroid humans, and antioxidant depletion increases the risk of methimazole toxicosis in rats. OBJECTIVES: 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. ANIMALS: Hyperthyroid cats presented for radioiodine treatment (n = 44) and healthy mature adult control cats (n = 37). METHODS: Prospective, controlled, observational study. Red blood cell glutathione (GSH), plasma ascorbate (AA), plasma free retinol (vitamin A), alpha-tocopherol (vitamin E), and urinary free 8-isoprostanes in hyperthyroid cats were compared to healthy cats and to hyperthyroid cats 2 months after treatment. RESULTS: Blood antioxidants were not significantly different in hyperthyroid cats (mean GSH 1.6 +/- 0.3 mM; AA 12.8 +/- 4.9 muM, and vitamin E, 25 +/- 14 mug/mL) compared to controls (GSH 1.4 +/- 0.4 mM; AA 15.0 +/- 6.6 muM, and vitamin E, 25 +/- 17 mug/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 mug/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.