The pathogenesis of chronic obstructive pulmonary disease (COPD) encompasses a number of injurious processes, including an abnormal inflammatory response in the lungs to inhaled particles and gases. Other processes, such as failure to resolve inflammation, abnormal cell repair, apoptosis, abnormal cellular maintenance programs, extracellular matrix destruction (protease/antiprotease imbalance), and oxidative stress (oxidant/antioxidant imbalance) also have a role. The inflammatory responses to the inhalation of active and passive tobacco smoke and urban and rural air pollution are modified by genetic and epigenetic factors. The subsequent chronic inflammatory responses lead to mucus hypersecretion, airway remodeling, and alveolar destruction. This article provides an update on the cellular and molecular mechanisms of these processes in the pathogenesis of COPD. During the past decade a plethora of studies have unravelled the multiple roles of nitric oxide (NO) in airway physiology and pathophysiology. In the respiratory tract, NO is produced by a wide variety of cell types and is generated via oxidation ofL-arginine that is catalyzed by the enzyme NO synthase (NOS). NOS exist in three distinct are forms: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). NO derived from the constitutive are forms of NOS (nNOS and eNOS) and other NO-adduct molecules (nitrosothiols) have been shown to be modulators of bronchomotor tone. On the other hand, NO derived from iNOS seems to be a proinflammatory mediator with immunomodulatory effects. Finally, the production of NO under oxidative stress conditions secondarily generates strong oxidizing agents (reactive nitrogen species) that may modulate the development of chronic inflammatory airway diseases and/or amplify the inflammatory response.

BACKGROUND: According to the World Health Organization (WHO), 10-15% of couples of reproductive age have infertility. According to researcher D. Sukhe (1999), hormonal infertility in the reproductive age of women was 33.6%, which was a large part of the cause of infertility. In recent years, the number of cases of endocrine disorders, including malignancy and sexually transmitted infections, has been increasing year by year. According to WHO reports, thyroid disorders have a prevalence of 49.3% for active reproductive age (30-50). According to the report of the Health Development Center in 2016, since the thyroid disorders are the second most common disease in endocrine gland disease, our study found that the infertility in reproductive age of women can be substantial due to the loss of thyroid gland. METHODS: The study was carried out by the couple of 20-45 year-olds and modeled as an analytical study model. The questionnaire was used for the couple’s interviews and some of the measurement of body and serum use of TOSOH Corporation AIA-360, Tokyo, Japan. On the serum, anti-TPO and аnti-TG carbohydrates are identified by the Cobas e-411 analyzer under the manufacturer’s accompanying protocol. RESULTS: 76.7% of women were diagnosed with infertility euthyroid, 0.7% hyperthyroidism, 22.6% hypothyroidism (3.8% with overt hypothyroidism and 18.8% subclinical hypothyroidism). Prevalence of TAI, in 6.7% isolated positive anti-Tg were found, and 14.3% had isolated positive TPO, In 3.7% of cases, both types of autoantibodies were present. We analysed binary logistic regression for anti-TPO and anti-TG autoantibody in the positive and negative group in past obstetrics history, evidence of positive of anti-TPO and anti-Tg was increased risk of miscarriage 2.2 times (OR = 2.2, p <0.01). CONCLUSIONS: Women with disorders in our study have high percentage of subclinical hypothyroidism and have higher rate of thyroid autobodies in serum which may be a problem for women with infertility and pregnancy complications due to the loss of thyroid gland. There is a need to develop a principle of recovery and treatment.