Abstract
Background: The paper presents the data on a condition and a role of inflammation mediators and the antioxidant protection system in blood plasma for endometriosis genitalis (EG) in women of reproductive age. The material for the research included results from the survey of 104 women of reproductive age, divided into two groups (control group and clinical group). It is shown in the paper that EG occurs with the development of oxidative stress (OS) caused by activation of lipid peroxidation and the cytokine system with a simultaneous reduction in the antioxidant defense system.

Aims and Objective: To define the condition and the role of inflammation mediators of lipid and cytokine natures and the antioxidant protection system in the development of EG in women of reproductive age.

Materials and Methods: The research was carried out among 104 women of reproductive age, divided into control and clinical groups. The clinical groups included women with adenomyosis and EG externa. EG was verified with clinical findings, ultrasound examinations of pelvic organs, hysteroscopies, and diagnostic laparoscopies. Statistik, version 6.0, was used for statistical analysis. Diagnostic techniques included spectrophotometric, biochemical, and enzyme immunodetection methods.

Results: Imbalance between radical processes and antioxidant protection systems causes the development of OS for EG; imbalance between pro-inflammatory and anti-inflammatory cytokines leads to inflammation activation and increased activities of triggers that develop endometrioid focuses.

Conclusion: Due to unclear mechanisms of its development, EG is problematic in its respond to treatment while the OS contribution into the pathophysiological basis is highly reasonable. Components of menstrual blood are triggers for OS. With failed mechanisms in the cleansing system, the macrophage reaction gets stronger followed by a release of cytokines.

Key words: Endometriosis Genitalis; Oxidative Stress; Lipid Peroxidation; Antioxidant Protection System; Cytokines; Interleukins