Effect of Thyroid State on the Morphof unctional Properties of Heart Mitochondria

Abstract

For an evaluation of the effect of thyroid hormone on the mitochondrial compartment of heart, we have studied morphological and functional characteristics of mitochondria within the heart of rats in different thyroid states. In particular, the relationship between membrane-bound proteins, such as the cytochromes, and the surface of inner mitochondrial membranes has been investigated. By quantitative electron microscopy it has been shown, according to our previous data, that thyroidectomy causes an increase in several parameters such as the specific mitochondrial mass (mg mitochondrial protein/g tissue), the number and inner membrane surface of mitochondria per unit volume of heart, without any significant variation of the ratio between the surface of the inner membranes and the volume of mitochondria. The treatment with substitutive doses of triiodothyronine (T₃) tends to restore the normal pattern. On the other hand, mitochondria isolated from thyroidectomized rats show lower oxygen consumption due to a lower content of cytochromes, which are distributed at lower density on the inner membranes. Also in this case the pattern is reversed by T₃ treatment. It is concluded that thyroid hormone causes an increase of mitochondrial cytochrome content, which, notwithstanding the decrease of the mitochondrial mass, leads to a higher respiratory rate and to a larger capacity of oxidative metabolism in the heart.

Role of Oxidative Stress in Thyroid Hormone-Induced Cardiomyocyte Hypertrophy and Associated Cardiac Dysfunction: An Undisclosed Story

“…THs also regulate the synthesis of nuclear- as well as mitochondrial-encoded mitochondrial proteins via a nuclear mechanism [ 62 ]. Regardless of a decline in the number of mitochondria per cell in the hyperthyroid heart [ 63 ], there is a rise in respiratory chain proteins of the mitochondria [ 64 ]. These proteins can significantly contribute to the TH-provoked stimulation of mitochondrial respiration [ 59 , 64 ] and cause enhanced ROS generation [ 53 ].…”

“…Regardless of a decline in the number of mitochondria per cell in the hyperthyroid heart [ 63 ], there is a rise in respiratory chain proteins of the mitochondria [ 64 ]. These proteins can significantly contribute to the TH-provoked stimulation of mitochondrial respiration [ 59 , 64 ] and cause enhanced ROS generation [ 53 ]. Effectively, Asayama et al reported increased mitochondrial oxidative metabolism in hypertrophied hyperthyroid rat hearts and proposed a key role for this observation in TH-induced myocardial dysfunction [ 25 , 43 , 44 ].…”