Hypothyroidism maintained reactive oxygen species-steady state in the kidney of rats intoxicated with ethylene glycol: effect related to an increase in the glutathione that maintains the redox environment.

Our objective was to determine whether hypothyroidism protects against ethylene glycol (EG)-induced renal damage and whether the redox environment participates in the protection process. We used 36 male Wistar rats divided into four groups: (1) euthyroid, (2) euthyroid + 0.75% EG, (3) hypothyroid, and (4) hypothyroid + 0.75% EG. Hypothyroidism occurred 2 weeks after thyroidectomy. The parathyroid gland was reimplanted. EG was administrated for 21 days in drinking water. On day 21, the renal function was assessed and then the rats were decapitated. The left kidney was processed for histology, and the right kidney was used to determine the redox environment, oxidative stress, and the testing of the antioxidant enzymatic system. EG in euthyroid rats reduced the hydric and electrolytic balance and it also caused oxidative stress and renal damage. Hypothyroidism per se modifies the renal function causing a low osmolal and potassium clearance and the filtered load of potassium and sodium. In addition, there was an enhanced redox state because hypothyroidism increases the reduced glutathione concentration caused by a high activity of γ-glutamylcysteine synthase. Hypothyroidism is a protective state against EG because the changes in the renal function were smaller than in the euthyroid state. The oxidative stress and cellular damage were ameliorated by the hypothyroid condition. Also, the hypothyroidism-enhanced redox environment protects against EG-induced oxidative stress, renal damage, and renal dysfunction.