Alfredo Pontecorvi

Thyroid Hormones and Antioxidant Systems: Focus on Oxidative Stress in Cardiovascular and Pulmonary Diseases

In previous works we demonstrated an inverse correlation between plasma Coenzyme Q10 (CoQ10) and thyroid hormones; in fact, CoQ10 levels in hyperthyroid patients were found among the lowest detected in human diseases. On the contrary, CoQ10 is elevated in hypothyroid subjects, also in subclinical conditions, suggesting the usefulness of this index in assessing metabolic status in thyroid disorders. A Low-T3 syndrome is a condition observed in several chronic diseases: it is considered an adaptation mechanism, where there is a reduction in pro-hormone T4 conversion. Low T3-Syndrome is not usually considered to be corrected with replacement therapy. We review the role of thyroid hormones in regulation of antioxidant systems, also presenting data on total antioxidant capacity and Coenzyme Q10. Published studies suggest that oxidative stress could be involved in the clinical course of different heart diseases; our data could support the rationale of replacement therapy in low-T3 conditions.

Hormonal influence on coenzyme Q(10) levels in blood plasma.

Coenzyme Q10 (CoQ10), also known as ubiquinone for its presence in all body cells, is an essential part of the cell energy-producing system. However, it is also a powerful lipophilic antioxidant protecting lipoproteins and cell membranes. Due to these two actions, CoQ10 is commonly used in clinical practice in chronic heart failure, male infertility, and neurodegenerative disease. However, it is also taken as an anti-aging substance by healthy people aiming for long-term neuroprotection and by sportsmen to improve endurance. Many hormones are known to be involved in body energy regulation, in terms of production, consumption and dissipation, and their influence on CoQ10 body content or blood values may represent an important pathophysiological mechanism. We summarize the main findings of the literature about the link between hormonal systems and circulating CoQ10 levels. In particular the role of thyroid hormones, directly involved in the regulation of energy homeostasis, is discussed. There is also a link with gonadal and adrenal hormones, partially due to the common biosynthetic pathway with CoQ10, but also to the increased oxidative stress found in hypogonadism and hypoadrenalism.

Non-Thyroidal Illness: Physiopathology and Clinical Implications

In critical illness, several abnormalities in thyroid hormone (TH) secretion, metabolism and action have been described in patients without previous diagnosis of intrinsic thyroid disease and are collectively called “Non thyroidal syndrome” (NTIS) [1]; this term is now largely employed, in the place of “euthyroid sick syndrome” [2-4] or “low-T3 syndrome”, due to the most common abnormality, a decreased level of serum total triiodothyronine (T3), which can be detected very early, within 2 hours after the onset of severe physical stress [5-7]. However, T3 lowering is only one of the endocrine picture described is such a situation; therefore the term NTIS seems to be more appropriate, also strengthening its extrathyroidal source.

Relationship between growth hormone deficiency and oxidative stress in patients with heart failure: Preliminary data.

It is well known that heart failure is associated with oxidative stress (OS). Reactive oxygen species in fact influence sarcolemmal and mitochondrial ione channels, which are responsible for cardiomyocyte excitability and are important in myocardial remodeling after a myocardial infarction. The decrease of anabolic axes can have a role in the progression of the illness. In order to evaluate the relationship between growth hormone deficiency (GHD) and indexes of OS, we have performed a dynamic GH evaluation and determined oxidized form of coenzyme Q10 (CoQ10) (component of mitochondrial respiratory chain also endowed with antioxidant properties) in a group of 12 patients (10 male e 2 female, age 49-73) affected by heart failure (NYHA II-III; EF<40%).