Introduction: According to a review of the literature, there is a lack of data on the mechanisms that participate in the suppression of inflammation that accompanies polycystic ovary syndrome (PCOS). Additionally, the changes in oxidative status resulting from a low-calorie diet have not been studied in a group of women with PCOS, and the oxidation and reduction processes associated with PCOS have not been explained. Material and methods: The study involved 49 women who were diagnosed with PCOS according to Rotterdam’s criteria, and 24 women voluntarily agreed to a three-month dietary intervention. The dietary intervention was carried out for 3 months. Glutathione peroxidase (GPx3) activity, the Ferric reducing ability of plasma, and uric acid concentration were measured spectrophotometrically both before and after the intervention. Statistical analysis was performed with the Statistica 10.0 software package, and a Pearson’s correlation matrix was generated. Results: A lower concentration of GPx3 was observed in women with PCOS (before the dietetic intervention began) compared with the GPx3 levels in healthy women. A relationship was shown between GPx3 levels and the concentration of prolactin, insulin on fasting, and triglycerides. After the dietary intervention, increases in uric acid and GPx3 activity were noted, as well as numerous relationships between anthropometric and biochemical parameters. The ferric reducing/antioxidant power did not change significantly. Conclusions: Inhibiting the effect of prolactin (by the level of reactive oxygen species) on the activity of GPx3 could be a starting point for the increase in antioxidative stress and the development of the inflammatory state associated with PCOS pathophysiology. Following a low-calorie diet with a lower glycemic index is proposed to silence inflammation by increasing the concentration of uric acid. During GPx3 mobilization, women with PCOS have a higher demand for selenium, and its deficiencies may contribute to disordered thyroid hormone synthesis. The three-month dietary intervention did not silence redox processes in the examined group of women.

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Many researchers suggest an increased risk of atherosclerosis in women with polycystic ovary syndrome. In the available literature, there are no studies on the mediators of inflammation in women with PCOS, especially after dietary intervention. Eicosanoids (HETE and HODE) were compared between the biochemical phenotypes of women with PCOS (normal and high androgens) and after the 3-month reduction diet. Eicosanoid profiles (9(S)-HODE, 13(S)-HODE, 5(S)-HETE, 12(S)-HETE, 15(S)-HETE, 5(S)-oxoETE, 16(R)-HETE, 16(S)-HETE and 5(S), 6(R)-lipoxin A4, 5(S), 6(R), 15(R)-lipoxin A4) were extracted from 0.5 ml of plasma using solid-phase extraction RP-18 SPE columns. The HPLC separations were performed on a 1260 liquid chromatograph. No significant differences were found in the concentration of analysed eicosanoids in phenotypes of women with PCOS. These women, however, have significantly lower concentration of inflammatory mediators than potentially healthy women from the control group. Dietary intervention leads to a significant (p < 0.01) increase in the synthesis of proinflammatory mediators, reaching similar levels as in the control group. The development of inflammatory reaction in both phenotypes of women with PCOS is similar. The pathways for synthesis of proinflammatory mediators in women with PCOS are dormant, but can be stimulated through a reduction diet. Three-month period of lifestyle change may be too short to stimulate the pathways inhibiting inflammatory process.

Analysis of TNF-α showed that women with high testosterone negative correlation between level of TNF-α and the concentration of DHEA-SO4. Inflammatory state involving TNF-α in women with PCOS and high concentration of androgens is caused by intensified Δ4 (progesterone) pathway and omitted or limited Δ5 (dehydroepiandrosterone) pathway of testosterone biosynthesis.