We investigated the effects of thyroid state on the mechanisms underlying rat heart mitochondrial capacity to remove H2O2 produced by an exogenous source. The removal rates were higher in the presence of respiratory substrates independently from thyroid state and were higher in hyperthyroid than in hypothyroid preparations. The thyroid state-linked changes in H2O2 removal rates, mirrored those in H2O2 release rates, showing that endogenous and exogenous H2O2 do not compete for the removing system. Mitochondrial content of coenzyme Q9 and Q10 was lower in hypothyroidism and higher in hyperthyroidism suggesting that the thyroid state-linked changes in the rates of H2O2 production are due to changes in the ubiquinone mitochondrial content. The rates of H2O2 removal in the presence of antioxidant enzyme inhibitors indicated that the contribution of each antioxidant is dependent on the thyroid state. This was supported by enzymatic activity measurements. Pharmacological inhibition also showed that the overall percentage contribution of the enzymatic processes, as well as that of non-enzymatic processes, is not affected by thyroid state. Cytochrome levels, inferred by light emission measurements, and western blot determination of cytochrome c, were lower in hypothyroid and higher in hyperthyroid preparations supporting the idea that the levels of reducing compounds were modified in opposite way by the changes in thyroid state. Further support was obtained showing that the whole antioxidant capacity, which provides an evaluation of capacity of the systems, different from cytochromes, assigned to H2O2 scavenging, was lower in hyperthyroid than in hypothyroid state.

Thyroid state affects H2O2 removal by rat heart mitochondria / Venditti, P; Napolitano, G; Fasciolo, G; Di Meo, S. - In: ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS. - ISSN 0003-9861. - 662:(2019), pp. 61-67. [10.1016/j.abb.2018.11.025]

Thyroid state affects H2O2 removal by rat heart mitochondria.

Venditti P
Writing – Review & Editing
;
Napolitano G
Methodology
;
Fasciolo G;
2019

Abstract

We investigated the effects of thyroid state on the mechanisms underlying rat heart mitochondrial capacity to remove H2O2 produced by an exogenous source. The removal rates were higher in the presence of respiratory substrates independently from thyroid state and were higher in hyperthyroid than in hypothyroid preparations. The thyroid state-linked changes in H2O2 removal rates, mirrored those in H2O2 release rates, showing that endogenous and exogenous H2O2 do not compete for the removing system. Mitochondrial content of coenzyme Q9 and Q10 was lower in hypothyroidism and higher in hyperthyroidism suggesting that the thyroid state-linked changes in the rates of H2O2 production are due to changes in the ubiquinone mitochondrial content. The rates of H2O2 removal in the presence of antioxidant enzyme inhibitors indicated that the contribution of each antioxidant is dependent on the thyroid state. This was supported by enzymatic activity measurements. Pharmacological inhibition also showed that the overall percentage contribution of the enzymatic processes, as well as that of non-enzymatic processes, is not affected by thyroid state. Cytochrome levels, inferred by light emission measurements, and western blot determination of cytochrome c, were lower in hypothyroid and higher in hyperthyroid preparations supporting the idea that the levels of reducing compounds were modified in opposite way by the changes in thyroid state. Further support was obtained showing that the whole antioxidant capacity, which provides an evaluation of capacity of the systems, different from cytochromes, assigned to H2O2 scavenging, was lower in hyperthyroid than in hypothyroid state.
2019
Thyroid state affects H2O2 removal by rat heart mitochondria / Venditti, P; Napolitano, G; Fasciolo, G; Di Meo, S. - In: ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS. - ISSN 0003-9861. - 662:(2019), pp. 61-67. [10.1016/j.abb.2018.11.025]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/739635
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