Vol 88, No 3 (2017)
Research paper
Published online: 2017-03-31

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Relationship between maternal blood ceruloplasmin level, catalase and myeloperoxidase activity and neural tube defects

Orkun Cetin, Erbil Karaman, Baris Boza, Numan Cim, Murat Alisik, Ozcan Erel, Ismet Alkis, Recep Yildizhan, Ali Kolusari, Guler Hanım Sahin
Pubmed: 28397206
Ginekol Pol 2017;88(3):156-160.

Abstract

Objectives: The exact pathogenesis of neural tube defects (NTDs) is poorly understood. We aimed at evaluating maternal anti-oxidant capacity (ceruloplasmin level, myeloperoxidase and catalase activity) in pregnancies complicated by NTDs.

Material and methods: Fifty-four mothers with NTD-affected pregnancies and 61 healthy mothers, matched for gestational age, were recruited. Maternal venous blood samples were obtained after detailed fetal ultrasound examination to measure myeloperoxidase, catalase activity and ceruloplasmin levels. The clinical characteristics of all participants were collected.

Results: Maternal blood catalase activity was significantly lower in the study group (117.1 ± 64.8 kU/L) as compared to controls (152.2 ± 110.6 kU/L) (p = 0.044). Maternal blood ceruloplasmin levels were also significantly lower in the study group (180.5 ± 37.7 U/L) as compared to controls (197.9 ± 35.9 U/L) (p = 0.012). Myeloperoxidase activity was similar in both groups (112.6 ± 22.2 U/L vs. 113.6 ± 38.1 U/L) (p = 0.869).

Conclusions: In the present study, maternal blood ceruloplasmin level and catalase activity were found to be lower in NTD-affected pregnancies as compared to healthy controls. Thus, it seems safe to conclude that impaired antioxidant capacity may play a role in the development of NTDs during pregnancy, in addition to the genetic, environmental and metabolic factors.

References

  1. Copp AJ, Stanier P, Greene NDE. Neural tube defects: recent advances, unsolved questions, and controversies. Lancet Neurol. 2013; 12(8): 799–810.
  2. Daly LE, Kirke PN, Molloy A, et al. Folate levels and neural tube defects. Implications for prevention. JAMA. 1995; 274(21): 1698–1702.
  3. Perrone S, Longini M, Bellieni CV, et al. Early oxidative stress in amniotic fluid of pregnancies with Down syndrome. Clin Biochem. 2007; 40(3-4): 177–180.
  4. Finnell RH. Teratology: general considerations and principles. J Allergy Clin Immunol. 1999; 103(2): S337–S342.
  5. Agarwal A, Gupta S, Sekhon L, et al. Redox considerations in female reproductive function and assisted reproduction: from molecular mechanisms to health implications. Antioxid Redox Signal. 2008; 10(8): 1375–1403.
  6. Yazıcıoğlu C, Cebesoy FB, Balat O, et al. The relationship of ceruloplasmin and neural tube defects. J Turk Ger Gynecol Assoc. 2010; 11(2): 86–88.
  7. Pippenger CE. Pharmacology of neural tube defects. Epilepsia. 2003; 44 Suppl 3: 24–32.
  8. Uriu-Adams JY, Keen CL. Copper, oxidative stress, and human health. Mol Aspects Med. 2005; 26(4-5): 268–298.
  9. Góth L. A simple method for determination of serum catalase activity and revision of reference range. Clin Chim Acta. 1991; 196(2-3): 143–151.
  10. Bradley PP, Priebat DA, Christensen RD, et al. Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. J Invest Dermatol. 1982; 78(3): 206–209.
  11. Erel O. Automated measurement of serum ferroxidase activity. Clin Chem. 1998; 44(11): 2313–2319.
  12. Graf WD, Oleinik OE, Pippenger CE, et al. Comparison of erythrocyte antioxidant enzyme activities and embryologic level of neural tube defects. Eur J Pediatr Surg. 1995; 5 Suppl 1: 8–11.
  13. Zhao W, Mosley BS, Cleves MA, et al. Neural tube defects and maternal biomarkers of folate, homocysteine, and glutathione metabolism. Birth Defects Res A Clin Mol Teratol. 2006; 76(4): 230–236.
  14. Ishibashi M, Akazawa S, Sakamaki H, et al. Oxygen-induced embryopathy and the significance of glutathione-dependent antioxidant system in the rat embryo during early organogenesis. Free Radic Biol Med. 1997; 22(3): 447–454.
  15. Ornoy A. Embryonic oxidative stress as a mechanism of teratogenesis with special emphasis on diabetic embryopathy. Reprod Toxicol. 2007; 24(1): 31–41.
  16. Arslan M, Melek M, Demir H, et al. Relationship of antioxidant enzyme activities with myelomeningocele. Turk Neurosurg. 2012; 22(3): 300–304.