Level of nitric oxide and its synthases activity in the thyroid tissue of Graves’ disease patients

Abstract

The authors have studied the level of nitric oxide metabolites and its synthase activity (constitutive and inducible ones, сNOS and іNOS) in thyroid tissue of patients  with Graves’ disease. It has been established the highest level of nitric oxide metabolites in the tissue of toxic goiter compared with that in the unmodified thyroid  tissue of patients with euthyroid nodular pathology, which did not depend on the structure of follicular tissue, hyperplastic process or severity of thyroiditis, presence  of fibro-sclerotic changes in stroma, as well as excess in gland volume above the age norm. In thyroid tissue with severe disease there are no significant changes in  nitric oxide levels, whereas in case of moderate disease it is increased more than two-fold. сNOS activity in the tissue of toxic goiter is increased only in case of focal  thyroiditis and in tissue of maсrofolliсular structure, whereas a statistically significant increase in іNOS activity is confirmed in pathologically modified tissue in case of  concomitant thyroiditis, focal hyperplasia of thyroid epithelium, in tissue of patients with an increase in gland’s volume up to 300% above the normal volume and in  patients with mild disease; it does not depend on the peculiarities of tissue follliсular structure and presence of fibro-sclerotic stroma. іNOS induction is  absent in case  of a marked hyperplastic process, in the presence of a significant excess of gland volume (300-800% above normal) and in patients with severe Graves’ disease.  Changes in functional state of nitric oxide system, which combines the properties of the active  radical with functions of signaling molecule and mediator, in toxic  goiter tissue may be associated both with an increased activity of the gland, presence of inflammatory or autoimmune processes, and with endothelial  dysfunction of thyroid vessels, and mechanisms of regulation of thyroid cell proliferation and thyroid cell death.