Serum micro- and macroelements levels in women with polycystic ovary syndrome associated with pelvic inflammatory disease Original paper

What was studied?

This clinical study investigated the serum levels of essential macro- and microelements, specifically magnesium, copper, manganese, nickel, zinc, chromium, selenium, and vanadium, in women diagnosed with polycystic ovary syndrome (PCOS), both with and without concurrent pelvic inflammatory disease (PID). The primary goal was to determine whether the concentrations of these elements differed in PCOS patients and to evaluate their possible role in the pathophysiology of PCOS, especially concerning oxidative stress, inflammation, and reproductive dysfunction.

Who was studied?

The study population consisted of three distinct groups: 30 women with PCOS and PID (Group I), 22 women with PCOS but no inflammatory pelvic disease (Group II), and 25 healthy controls (Group III). All participants were of reproductive age. The research was conducted in Ukraine and used serum samples analyzed via mass spectrometry following microwave digestion. The analysis focused on comparing element levels across the groups and interpreting their biological significance in the context of PCOS-associated metabolic and inflammatory disturbances.

What were the most important findings?

The study found that women with PCOS, regardless of inflammatory status, had significantly elevated levels of serum zinc and nickel, and decreased levels of manganese, compared to healthy controls. Magnesium, chromium, selenium, and vanadium levels did not differ significantly between groups. Zinc and nickel were especially elevated in women with concurrent PID, pointing to a synergistic relationship between inflammation and trace element dysregulation.

Mechanistically, elevated zinc and nickel levels are implicated in exacerbating oxidative stress through increased lipid peroxidation and suppression of antioxidant systems. Nickel, in particular, may damage cellular membranes, disrupt mitochondrial and DNA integrity, and impair transcription processes, collectively impairing folliculogenesis and ovulation. Elevated zinc levels may also result from the action of pro-inflammatory cytokines (IL-1, IL-6, IL-18, TNF-α), which stimulate zinc accumulation via metallothionein upregulation. Meanwhile, reduced manganese, an essential cofactor for mitochondrial antioxidant enzymes, may compromise cellular redox balance and energy metabolism. These patterns may contribute to the hormonal imbalance, chronic inflammation, and reproductive dysfunction seen in PCOS.

In microbiome terms, such trace element imbalances could promote gut dysbiosis. For example, nickel excess is known to enrich pathobionts like Proteobacteria and suppress beneficial anaerobes like Faecalibacterium prausnitzii. A similar trend with excess zinc may reduce Bifidobacterium spp. populations and increase intestinal permeability. Reduced manganese availability may impair SCFA-producing microbes, further disrupting gut-immune-endocrine signaling.

What are the implications of this study?

This study provides strong evidence that trace element imbalances, particularly elevated serum zinc and nickel and decreased manganese, may play a critical role in the pathogenesis of PCOS, especially in cases compounded by inflammation. The findings suggest that these elements influence oxidative stress, mitochondrial function, and immune activity, potentially contributing to reproductive dysfunction. Clinically, this underscores the value of monitoring serum trace elements in PCOS patients, especially those with comorbid inflammatory pelvic conditions. Moreover, nutritional strategies, such as reducing dietary sources of nickel and zinc while increasing manganese intake, may serve as adjunctive interventions. Given the known link between trace elements and microbiota composition, this study also opens a pathway to integrate trace element modulation as part of microbiome-based therapeutic approaches for PCOS.