open access

Ahead of Print
Research paper
Published online: 2021-09-22
Get Citation

Can redox imbalance predict abnormal foetal development?

Marek Pietryga1, Kinga Tobola-Wrobel1, Piotr Dydowicz1, Sandra Radzicka-Mularczyk1, Katarzyna Ziolkowska1, Marta Napierala1, Ewa Florek1, Jacek Brazert1
DOI: 10.5603/GP.a2021.0122
Affiliations
  1. Poznan University of Medical Sciences, Poland, Poland

open access

Ahead of Print
ORIGINAL PAPERS Obstetrics
Published online: 2021-09-22

Abstract

Objectives: Based on the current state of knowledge, elevated levels of oxidative stress markers may be considered as risk factors for pregnancy complications. The aim of the research was to assess the correlation between selected oxidative stress biomarkers with the occurrence of foetal chromosomal aberration and congenital malformations.

Material and methods: This retrospective research lasted for two years. The purpose was to determine serum levels of selected oxidative stress markers, including total protein (TP), glutathione (GSH), S-nitrosothiols (RSNO), nitric oxide (NO), trolox equivalent antioxidant capacity (TEAC) and glutathione S-transferase (GST) at 11–13 + 6 gestational weeks in 38 women with confirmed foetal developmental abnormalities and in 34 healthy pregnancies in order to assess their utility as predictors of abnormal foetal development.

Results: Serum concentrations of TP (56.90 ± 5.30 vs 69.1 ± 15.30 mg/mL), TEAC (4.93 ± 0.82 vs 5.64 ± 0.74 μM/mL) and GST (15.94 ± 4.52 vs 21.72 ± 6.81 nM/min/mg) were statistically significantly (p < 0.05) lower in the group of patients with developmental abnormalities in the fetus, whereas GSH levels (6.43 ± 1.24 vs 4.98 ± 1.88 nM/mg) were significantly higher, compared to the group of healthy fetuses. There were no differences in the concentration of these markers between chromosomal aberrations and fetal dysmorphia in subjects. A significant difference in odds ratio obtained for GSH (OR = 0.57, 95% CL: 0.40–0.80) indicates that its higher concentration can relate to reduced risk of developmental abnormalities, whereas odds ratio for TP (OR=1.11, 95% CL: 1.04–1.17), TEAC (OR = 3.54, 95% CL: 1.56–8.05) and GST (OR = 1.18, 95% CL: 1.03–1.17) indicate that their elevation may increase the risk of developmental abnormalities

Conclusions: Elevated levels of TP, GST, TEAC and low GSH level may be relevant to predict congenital defects.

Abstract

Objectives: Based on the current state of knowledge, elevated levels of oxidative stress markers may be considered as risk factors for pregnancy complications. The aim of the research was to assess the correlation between selected oxidative stress biomarkers with the occurrence of foetal chromosomal aberration and congenital malformations.

Material and methods: This retrospective research lasted for two years. The purpose was to determine serum levels of selected oxidative stress markers, including total protein (TP), glutathione (GSH), S-nitrosothiols (RSNO), nitric oxide (NO), trolox equivalent antioxidant capacity (TEAC) and glutathione S-transferase (GST) at 11–13 + 6 gestational weeks in 38 women with confirmed foetal developmental abnormalities and in 34 healthy pregnancies in order to assess their utility as predictors of abnormal foetal development.

Results: Serum concentrations of TP (56.90 ± 5.30 vs 69.1 ± 15.30 mg/mL), TEAC (4.93 ± 0.82 vs 5.64 ± 0.74 μM/mL) and GST (15.94 ± 4.52 vs 21.72 ± 6.81 nM/min/mg) were statistically significantly (p < 0.05) lower in the group of patients with developmental abnormalities in the fetus, whereas GSH levels (6.43 ± 1.24 vs 4.98 ± 1.88 nM/mg) were significantly higher, compared to the group of healthy fetuses. There were no differences in the concentration of these markers between chromosomal aberrations and fetal dysmorphia in subjects. A significant difference in odds ratio obtained for GSH (OR = 0.57, 95% CL: 0.40–0.80) indicates that its higher concentration can relate to reduced risk of developmental abnormalities, whereas odds ratio for TP (OR=1.11, 95% CL: 1.04–1.17), TEAC (OR = 3.54, 95% CL: 1.56–8.05) and GST (OR = 1.18, 95% CL: 1.03–1.17) indicate that their elevation may increase the risk of developmental abnormalities

Conclusions: Elevated levels of TP, GST, TEAC and low GSH level may be relevant to predict congenital defects.

Get Citation

Keywords

oxidative stress; congenital malformations; chromosomal abnormalities; prenatal diagnostic

About this article
Title

Can redox imbalance predict abnormal foetal development?

Journal

Ginekologia Polska

Issue

Ahead of Print

Article type

Research paper

Published online

2021-09-22

DOI

10.5603/GP.a2021.0122

Keywords

oxidative stress
congenital malformations
chromosomal abnormalities
prenatal diagnostic

Authors

Marek Pietryga
Kinga Tobola-Wrobel
Piotr Dydowicz
Sandra Radzicka-Mularczyk
Katarzyna Ziolkowska
Marta Napierala
Ewa Florek
Jacek Brazert

References (33)
  1. Karlík M, Valkovič P, Hančinová V, et al. Markers of oxidative stress in plasma and saliva in patients with multiple sclerosis. Clin Biochem. 2015; 48(1-2): 24–28.
  2. Bilen H, Altinkaynak K, Sebin E, et al. Serum YKL-40 and MDA levels in Behcet disease. J Pak Med Assoc. 2016; 66(10): 1299–1302.
  3. Jakuš V, Sándorová E, Kalninová J, et al. Monitoring of glycation, oxidative stress and inflammation in relation to the occurrence of vascular complications in patients with type 2 diabetes mellitus. Physiol Res. 2014; 63(3): 297–309.
  4. Santulli P, Chouzenoux S, Fiorese M, et al. Protein oxidative stress markers in peritoneal fluids of women with deep infiltrating endometriosis are increased. Hum Reprod. 2015; 30(1): 49–60.
  5. Dennery PA. Effects of oxidative stress on embryonic development. Birth Defects Res C Embryo Today. 2007; 81(3): 155–162.
  6. Menezo YJR, Silvestris E, Dale B, et al. Oxidative stress and alterations in DNA methylation: two sides of the same coin in reproduction. Reprod Biomed Online. 2016; 33(6): 668–683.
  7. Pagano G, Castello G. Oxidative stress and mitochondrial dysfunction in Down syndrome. Adv Exp Med Biol. 2012; 724: 291–299.
  8. Maciejczyk M, Mikoluc B, Pietrucha B, et al. Oxidative stress, mitochondrial abnormalities and antioxidant defense in Ataxia-telangiectasia, Bloom syndrome and Nijmegen breakage syndrome. Redox Biol. 2017; 11: 375–383.
  9. Sultana Z, Maiti K, Aitken J, et al. Oxidative stress, placental ageing-related pathologies and adverse pregnancy outcomes. Am J Reprod Immunol. 2017; 77(5).
  10. Pietryga M, Dydowicz P, Toboła K, et al. Selected oxidative stress biomarkers in antenatal diagnosis as 11-14 gestational weeks. Free Radic Biol Med. 2017; 108: 517–523.
  11. Toboła-Wróbel K, Pietryga M, Dydowicz P, et al. Association of Oxidative Stress on Pregnancy. Oxid Med Cell Longev. 2020; 2020: 6398520.
  12. Pietryga M, Borowski D, Brązert J, et al. Polish Gynecological Society - Ultrasound Section Guidelines on ultrasound screening in uncomplicated pregnancy. Ginekol Pol. 2015; 86(7): 551–559.
  13. Pietryga M. Ultrasonografia prenatalna twarzoczaszki i aberracji chromosomowych. Exemplum, Poznań 2015: 153–279.
  14. Mazer Zumaeta A, Wright A, Syngelaki A, et al. First-trimester contingent screening for trisomies 21, 18 and 13 by biomarkers and maternal blood cell-free DNA testing. Fetal Diagn Ther. 2014; 35(3): 185–192.
  15. LOWRY OH, ROSEBROUGH NJ, FARR AL, et al. Protein measurement with the Folin phenol reagent. J Biol Chem. 1951; 193(1): 265–275.
  16. ELLMAN GL. Tissue sulfhydryl groups. Arch Biochem Biophys. 1959; 82(1): 70–77.
  17. Bonina FP, Puglia C, Frasca G, et al. Protective effects of a standardised red orange extract on air pollution-induced oxidative damage in traffic police officers. Nat Prod Res. 2008; 22: 1544.
  18. Kleinbongard P, Rassaf T, Dejam A, et al. Griess method for nitrite measurement of aqueous and protein-containing samples. Methods Enzymol. 2002; 359: 158–168.
  19. Re R, Pellegrini N, Proteggente A, et al. Antioxidant activity applying an improved ABTS radical cation decolorization assay. Free Radic Biol Med. 1999; 26(9-10): 1231–1237.
  20. Habig WH, Pabst MJ, Jakoby WB. Glutathione S-transferases. The first enzymatic step in mercapturic acid formation. J Biol Chem. 1974; 249(22): 7130–7139.
  21. Burton GJ, Jauniaux E. Oxidative stress. Best Pract Res Clin Obstet Gynaecol. 2011; 25(3): 287–299.
  22. Snijders RJ, Sundberg K, Holzgreve W, et al. Maternal age- and gestation-specific risk for trisomy 21. Ultrasound Obstet Gynecol. 1999; 13(3): 167–170.
  23. Miller A, Riehle-Colarusso T, Siffel C, et al. Maternal age and prevalence of isolated congenital heart defects in an urban area of the United States. Am J Med Genet A. 2011; 155A(9): 2137–2145.
  24. Hollier LM, Leveno KJ, Kelly MA, et al. Maternal age and malformations in singleton births. Obstet Gynecol. 2000; 96(5 Pt 1): 701–706.
  25. Rossner P, Milcova A, Libalova H, et al. Biomarkers of exposure to tobacco smoke and environmental pollutants in mothers and their transplacental transfer to the foetus. Part II. Oxidative damage. Mutat Res. 2009; 669(1-2): 20–26.
  26. Duhig K, Chappell LC, Shennan AH. Oxidative stress in pregnancy and reproduction. Obstet Med. 2016; 9(3): 113–116.
  27. Shahmohamadnejad S, Vaisi-Raygani A, Shakiba Y, et al. Association between butyrylcholinesterase activity and phenotypes, paraoxonase192 rs662 gene polymorphism and their enzymatic activity with severity of rheumatoid arthritis: correlation with systemic inflammatory markers and oxidative stress, preliminary report. Clin Biochem. 2015; 48(1-2): 63–69.
  28. Jakuš V, Sándorová E, Kalninová J, et al. Monitoring of glycation, oxidative stress and inflammation in relation to the occurrence of vascular complications in patients with type 2 diabetes mellitus. Physiol Res. 2014; 63(3): 297–309.
  29. Wrześniak M, Kepinska M, Królik M, et al. The Influence of Tobacco Smoke on Protein and Metal Levels in the Serum of Women during Pregnancy. PLoS One. 2016; 11(8): e0161342.
  30. Zdravkovic T, Genbacev O, McMaster MT, et al. The adverse effects of maternal smoking on the human placenta: a review. Placenta. 2005; 26 Suppl A: S81–S86.
  31. Shaamash AH, Elsnosy ED, Makhlouf AM, et al. Maternal and fetal serum nitric oxide (NO) concentrations in normal pregnancy, pre-eclampsia and eclampsia. Int J Gynecol Obstet. 2000; 68(3): 207–214.
  32. Savvidou MD, Hingorani AD, Tsikas D, et al. Endothelial dysfunction and raised plasma concentrations of asymmetric dimethylarginine in pregnant women who subsequently develop pre-eclampsia. Lancet. 2003; 361(9368): 1511–1517.
  33. Bartosz G. Druga twarz tlenu. Wolne rodniki w przyrodzie. PWN, Warszawa 2013.

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk
tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl