Thyroid hormones (TH) are major contributor to oxidative stress in mammals because they (1) stimulate reactive oxygen species generation (ROS), (2) impair antioxidant defenses, and (3) increase the susceptibility to free radicals of most tissues. Unlike mammals, THs seem to diminish mitochondrial ROS while they have limited effect on the antioxidant machinery in birds. However, how THs modify the susceptibility to ROS has never been explored in an avian model, and very little is known about their effect on oxidative balance in birds. Therefore, the objective of our study was to examine the effect of chronic pharmacological hypo␣ and hyperthyroidism on (i) the susceptibility of mitochondrial membranes to ROS; and (ii) the level of oxidative stress assessed by measuring oxidative damage to lipids, nucleic acids and proteins in the gastrocnemius muscle of ducklings. We show that hypothyroidism had no effect on the susceptibility of mitochondrial membranes to free radicals. Hypothyroid ducklings had lower oxidized lipids (-31%) and DNA (+25%) but a similar level of protein carbonylation relative to controls. Conversely, mitochondrial membranes of hyperthyroid ducklings exhibited higher unsaturation (þ12%) and peroxidation (þ31%) indexes than in controls indicating a greater susceptibility to free radicals. However, hyperthyroid ducklings exhibited more oxidative damages on proteins (+67%) only, whereas lipid damages remained unchanged, and there was a slight reduction (-15%) in damages to DNA compared to euthyroid controls. Our results indicate that birds and mammals present fundamental differences in their oxidative stress response to thyroid status.