Ureaplasma parvum infection alters the placental redox status and may contribute to spontaneous abortion: a case-control study.

INTRODUCTION

This study aimed to investigate markers of oxidative stress in the placenta in the context of spontaneous abortion (SA) associated with Ureaplasma parvum infection.

MATERIAL &

METHODS

Placental samples from 89 women with spontaneous abortion (SA) and 20 with full-term delivery (C) were analyzed based on U. parvum (UP) infection status. Tissues underwent oxidative/nitroxidative stress, antioxidant, gene expression, and immunohistochemical analyses, with data integrated via PCA. After Kolmogorov-Smirnov testing, 2x2 comparisons were performed using Student's t-test or Mann-Whitney, as appropriate.

RESULTS

The results indicated oxidative lesions, protein, and lipid damage. Infection in the SA group contributed to the reduction of thiobarbituric acid-reactive substances (p < 0.0001), an increase in protein carbonylation (p < 0.01) and nitrite levels (p < 0.01), and a tendency for elevated 8-OHdG (p > 0.05). It also increased superoxide dismutase (SOD) activity (p < 0.05) and the SOD/GPx ratio (p < 0.05) while reducing catalase (CAT) (p < 0.01), glutathione peroxidase (GPx) (p < 0.0001), the SOD/CAT ratio (p < 0.0001), and nuclear factor erythroid 2-related factor 2 immunostaining (p < 0.05). Gene expression analysis revealed that the SA group with UP infection showed increased Copper/zinc-SOD/CAT (p < 0.01) and Manganese-SOD/CAT (p < 0.01) ratios and decreased Copper/zinc-SOD/GPx (p < 0.05) and Manganese-SOD/GPx (p < 0.0001) ratios. In the PCA, samples from the SA groups with and without infection exhibited similarities, standing out for their higher concentrations of manganese, copper, and zinc.

CONCLUSION

These findings suggest that U. parvum infection may result in a dynamic oxidative imbalance and significant variability in the placenta, which may, in turn, contribute to the development of SA.