We investigated whether swim training modifies the effects of tri-iodothyronine (T3) treatment on the metabolic response and oxidative damage of rat liver. Respiratory capacities, oxidative damage, levels of antioxidants, and susceptibility to oxidative challenge of liver homogenates were determined. Mitochondrial respiratory capacities, rates of H2O2 release, and oxidative damage were also evaluated. Training modified most of the measured parameters in both thyroid states, although the extent of changes was higher in hyperthyroid preparations. T3 treatment enhanced homogenate respiratory capacity, which was further enhanced by training despite the decrease in mitochondrial respiratory capacity. Hormonal treatment also induced liver oxidative damage and glutathione depletion, and increased tissue susceptibility to oxidative challenge. These effects were lower in trained animals. The extensive oxidative damage found in liver homogenates from hyperthyroid sedentary rats was due to low tissue antioxidant protection and high mitochondrial H2O2 production rate, which were increased and decreased respectively by animal training. The training effect on H2O2 production was associated with lower oxidative damage and susceptibility to Ca2+-induced swelling of mitochondria. Measurements with respiratory inhibitors indicated that the differences in H2O2 release in hyperthyroid groups were due to differences in mitochondrial content of autoxidizable electron carrier located at Complex III. We conclude that moderate training is able to reduce hyperthyroid state-linked cellular and subcellular oxidative damage in liver increasing its antioxidant defenses and decreasing the mitochondrial generation of reactive oxygen species.

Tri-iodothyronine treatment differently affects liver metabolic response and oxidative stress in sedentary and trained rats

VENDITTI, PAOLA;BARI, ANGELA;DI MEO, SERGIO
2008

Abstract

We investigated whether swim training modifies the effects of tri-iodothyronine (T3) treatment on the metabolic response and oxidative damage of rat liver. Respiratory capacities, oxidative damage, levels of antioxidants, and susceptibility to oxidative challenge of liver homogenates were determined. Mitochondrial respiratory capacities, rates of H2O2 release, and oxidative damage were also evaluated. Training modified most of the measured parameters in both thyroid states, although the extent of changes was higher in hyperthyroid preparations. T3 treatment enhanced homogenate respiratory capacity, which was further enhanced by training despite the decrease in mitochondrial respiratory capacity. Hormonal treatment also induced liver oxidative damage and glutathione depletion, and increased tissue susceptibility to oxidative challenge. These effects were lower in trained animals. The extensive oxidative damage found in liver homogenates from hyperthyroid sedentary rats was due to low tissue antioxidant protection and high mitochondrial H2O2 production rate, which were increased and decreased respectively by animal training. The training effect on H2O2 production was associated with lower oxidative damage and susceptibility to Ca2+-induced swelling of mitochondria. Measurements with respiratory inhibitors indicated that the differences in H2O2 release in hyperthyroid groups were due to differences in mitochondrial content of autoxidizable electron carrier located at Complex III. We conclude that moderate training is able to reduce hyperthyroid state-linked cellular and subcellular oxidative damage in liver increasing its antioxidant defenses and decreasing the mitochondrial generation of reactive oxygen species.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11588/308720
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