**1. Introduction**

Hashimoto's disease (HT) is known as chronic lymphocytic thyroiditis. It is an autoimmune-mediated disease characterized by dense infiltrations of the thyroid gland by plasma cells, macrophages and, particularly, lymphocytes [1,2]. The T and B lymphocytes are stimulated against thyroglobulin and thyroid peroxidase, and induce a number of biochemical processes that lead to progressive destruction of thyrocytes, fibrosis, reduction of the thyroid gland size and its hypofunction [3]. Growing evidence indicates that HT is linked to lowered cellular antioxidant potential and enhanced oxidative stress (OS) [2–4].

OS is a situation in which balance between reactive oxygen species (ROS) and the body's ability to neutralize them is shifted in favor of oxidants [5]. This leads to a temporary or chronic elevation of ROS concentration as well as disturbed cell metabolism and degradation of cell components [5].

Evidence showed an altered antioxidant potential and enhanced OS in the plasma of HT patients. Lassoued et al. [6] demonstrated increased plasma malondialdehyde (MDA) concentration as well as the activities of superoxide dismutase (SOD) and catalase (CAT) compared to the controls. Rostami et al. [2] observed decreased reduced glutathione (GSH) concentration in the plasma of newly diagnosed hypothyroid HT patients. This study showed that GSH depletion initiates OS and development of immunological intolerance in the course of HT. Ates et al. [4] argued that higher OS levels in patients progressing to overt hypothyroidism may be evidence of redox balance shift towards oxidative reactions and could thus serve as a significant factor in the initiation and progression of this disease. Interestingly, in the study performed by Nanda et al. [7], OS levels were higher in the thyroid antibody-positive hypothyroid group than in the thyroid antibody-negative hypothyroid group. The authors concluded that the presence of autoimmune antibodies is a key factor for enhanced ROS production and increased concentrations of oxidative biomolecular modifications, while thyroid hormone levels are of secondary importance.

Systemic inflammation, elevated levels of thyroid antibodies, disturbed concentrations of thyroid hormones and chronically raised ROS levels in the course of HT lead to numerous systemic complications, including cardiological diseases, insulin resistance, mood disorders and salivary gland diseases [2,4,8].

Agha-Hosseini et al. [8] demonstrated significantly reduced unstimulated saliva flow rate and xerostomia among HT women in euthyreosis vs. healthy controls. The cause of salivary gland dysfunction in the course of HT has not been explained yet. It is noteworthy that they observed salivary gland dysfunction in patients in euthyreosis. Abnormalities in both the composition and the amount of the secreted saliva negatively affects oral health and the condition of the entire body. Therefore, it is important to understand the mechanisms leading to salivary gland dysfunction in the course of the described disease. Moreover, the oral cavity is exposed to numerous oxidizing agents capable of generating large amounts of ROS. Evidence showed that salivary and, to some extent, plasma antioxidants, constitute an important part of the antioxidant barrier in both oral cavity and the entire body. Salivary peroxidase (Px), together with catalase (CAT), neutralizes H2O2 formed in a dismutation reaction catalyzed by superoxide dismutase (SOD). Reduced glutathione (GSH) is the most important low molecular weight salivary antioxidant responsible for maintaining thiol groups of salivary proteins at a reduced level. Forty percent of the total salivary antioxidant barrier is provided by bloodborne uric acid (UA) [5]. Failure of these antioxidant systems may result in the development of oral cavity diseases, including periodontitis [9,10], precancerous lesions [11] and cancers [12]. Previous studies showed the alteration in the salivary antioxidants barrier and the contribution of OS in the development and progression of salivary gland dysfunction in the course of other autoimmune diseases: psoriasis vulgaris, systemic sclerosis, rheumatoid arthritis, diabetes type 1, multiple sclerosis, Sjögren's syndrome and systemic lupus erythematosus [13–21]. In general, reduced/elevated levels of endogenous, non-enzymatic antioxidants or enhanced/weakened activity of antioxidant enzymes and increased oxidative modification of salivary cell components are observed in the saliva of patients with autoimmune diseases. The salivary antioxidants in HT have not yet been determined, so in the light of the above, it appears necessary to assess the antioxidant potential of saliva and the role of OS in the development of salivary gland dysfunction in the course of HT.

The aim of this study was to evaluate antioxidative defense parameters and measurable oxidative stress effects in unstimulated and stimulated saliva and plasma/erythrocytes of patients with HT in euthyreosis and to compare the obtained results with those in the control group.
