Sağlıklı ve preeklamptik gebelerde oksidatif stres parametrelerinin ve nitrik oksitin değerlendirilmesi

Year 2022, , 94 - 98, 31.08.2022

Özlem Aydın Berktaş , Sadettin Oğuzhan Tutar

https://doi.org/10.31590/ejosat.1092209

Abstract

Bu çalışmada preeklamptik gebelerde oksidatif hasar parametreleri araştırıldı ve sağlıklı dokularla karşılaştırıldı. 53 preeklamptik ve 53 sağlıklı gebe plasentada antioksidan enzimler belirlendi. Plasenta dokusunda serbest oksijen radikallerinin hasarı, antioksidan enzim sistemleri (lipid peroksidasyon (LPO), glutatyon (GSH) ve katalaz (CAT) miktarları, miyeloperoksidaz (MPx) enzim aktiviteleri ve nitrik oksit düzeyleri ölçülerek belirlendi. Preeklampsi geçirmiş gebede LPO düzeyleri sağlıklı gebelere göre yükselmiştir. Sağlıklı plasenta dokularında GSH miktarı yüksek iken, preeklampsi dokularında oldukça düşük bulundu. Preeklampsili kadınların plasental dokularında CAT, MPx enzim aktiviteleri ve NO düzeyleri oldukça yüksek iken, sağlıklı dokularda düşük bulunmuştur. Plasental dokularda antioksidan enzim aktiviteleri ve miktarları gruplar arasında önemli farklılıklar göstermektedir. Bu veriler doğrultusunda oksidatif stres parametrelerinin doku düzeyindeki hasarı oldukça iyi gösterdiğini söyleyebiliriz. Sonuç olarak elde edilen veriler plasenta dokusunda oksidatif hasarı göstermekte ve antioksidan mekanizmanın çalıştığını göstermektedir.

Keywords

Preeklampsi, Oksidatif hasar, Reaktif oksijen türleri, antioksidan enzimler

The evaluation of oxidative stress parameters and nitric oxide in healthy and preeclamptic pregnant women

Abstract

In the present study, oxidative damage parameters in preeclamptic pregnant women were investigated and compared with healthy tissues. Antioxidant enzymes were determined in 53 preeclamptic and 53 healthy pregnant placentas. The damage of free oxygen radicals in the placental tissue was determined by measuring by antioxidant enzyme systems (The amounts of lipid peroxidation (LPO), glutathione (GSH) and catalase (CAT), myeloperoxidase (MPx) enzyme activities and nitric oxide levels (NO)). The LPO levels increased in the pregnant woman who has had preeclampsia compared with healthy pregnant. While the amount of GSH was high in healthy placental tissues, it was found to be quite low preeclampsia tissues. While CAT, MPx enzyme activities and levels of NO were quite high in the placental tissues of women with preeclampsia, they were found to be low in healthy tissues. The antioxidant enzyme activities and amounts show significant differences between groups in placental tissues. In line with these data, we can say that oxidative stress parameters show the damage at the tissue level quite well. As a result, the data obtained show oxidative damage in the placental tissue and indicate that the antioxidant mechanism works.

Keywords

Preeclampsia, Oxidative damage, Reactive oxygen species, Antioxidant enzymes

References

• Adiga, U., D’souza, V., Kamath, A., & Mangalore, N. (2007). Antioxidant activity and lipid peroxidation in preeclampsia. J Chin Med Assoc, 70, 435–438. doi: 10.1016/S1726-4901(08)70034-0.
• Aebi, H. (1984). Catalase in vitro. In Method Enzymol, Lester, P., Ed. Academic Press: Vol. Volume 105, 121-126. doi: 10.1016/s0076-6879(84)05016-3.
• Bowen, R.S., Moodley, J., Dutton, M.F., & Theron, A.J. (2001). Oxidative stress in pre-eclampsia. Acta Obstet Gynecol Scand, 80, 719–725. 20. doi: 10.1034/j.1600-0412.2001.080008719.x.
• Burton, G.J., & Jauniaux, E. (2015). What is the placenta? American Journal of Obstetrics and Gynecology, 213:S6.e1- S6. e4. doi: 10.1016/j.ajog.2015.07.050.
• Chamy, V.M., Lepe, J., Catalan, A., Retama,l D., Escobar, J.A., & Madrid, E.M. (2006). Oxidative stress is closely related to clinical severity of pre-eclampsia. Biol Res, 39:229–236. disease. doi: 10.4067/s0716-97602006000200005.
• Furchgott, R.F., & Zawadzki, J.V. (1980). The obligatory role of the endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature, 288:373-376. DOI: 10.1038/288373a0.
• Gitto, E., Pellegroni, S., Gitto, P., Barberi, I., & Reiter, R.J. (2009). Oxidative stress of the newborn in the pre- and postnatal period and the clinical utility of melatonin. J Pineal Res, 46: 128–139. doi: 10.1111/j.1600-079X.2008.00649.x.
• Hauth, J.C., Ewell, M.G., & Levine, R.J, et al. Pregnancy outcomes in healthy nulliparas who developed hypertension. (2000). Calcium for Preeclampsia Prevention Study Group. Obstet Gynecol, 95:24–8. doi: 10.1016/s0029-7844(99)00462-7.
• Hung, T.H., Skepper, J.N., & Charnock-Jones, D.S, et al. (2002). Hypoxia– reoxygenation: a potent inducer of apoptotic changes in the human placenta and possible etiological factor in preeclampsia. Circ Res, 90:1274–81. doi: 10.1161/01.res.0000024411.22110.aa.
• Lanoix, D., Beghdadi, H., Lafond, J., & Vaillancourt, C. (2008). Human placental trophoblasts synthesize melatonin and express its receptors. Journal of Pineal Research, 45:50–60. doi: 10.1111/j.1600-079X.2008.00555.x. Epub 2008 Feb 25.
• Lowe, D.T. (2000). Nitric oxide dysfunction in the pathophysiology of pre-eclampsia. Nitric Oxide, 4(4):441–448. doi: 10.1006/niox.2000.0296.
• Miranda, K.M., Espey. M,G., Wink, D.A. (2001). “A rapid, simple spectrophotometric method for simultaneous detection of nitrate and nitrite”. Nitric Oxide, 5(1):62-71. doi: 10.1006/niox.2000.0319.
• Moncada, S. (1992). The L-arginine: nitric oxide pathway. Acta Physiol Scand, 145:201–227. doi:10.1111/ j.1748-1716.1992.tb09359.x doi: 10.1111/j.1748-1716.1992.tb09359.x.
• Myatt, L. (2006). Placental adaptive responses and fetal programming. J Physiol, 25-30. doi: 10.1113/jphysiol.2006.104968.
• Ohishi, H., & Yagi, K. (1979). Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem, 95:351-358. doi: 10.1016/0003-2697(79)90738-3.
• Palmer, R.M.J., Ferrige, A.G., & Moncada, S. (1987). Nitric oxide release account for the biological activity of endothelium-derived relaxing factor. Nature, 327:524-526. doi: 10.1038/327524a0.
• Priebat, P.P., Christensen, D.A., & Rothstein, R.D. (1982). Measurement of cutaneous inflammation: Estimation of neutrophil content with an enzyme marker. J Invest Dermatol, 78,206–20. doi: 10.1111/1523-1747.ep12506462.
• Saugstad, O.D. (1996). Mechanisms of tissue injury by oxygen radicals: implications for neonatal disease. Acta Paediatr, 85:1–4. doi: 10.1111/j.1651-2227.1996.tb13880.x.
• Sedlak, J., & Lindsay, R.H. (1968). Estimation of total, protein-bound, and nonprotein sulfhydryl groups in tissue with Ellman's reagent. Anal Biochem, 25(1):192-205. DOI: 10.1016/0003-2697(68)90092-4.
• Syme, M.R., Paxton, W., & Keelan, J.A. (2004). Drug transfer and metabolism by the human placenta. Clin Pharmacokinet, 43(8): 487-514. doi: 10.2165/00003088-200443080-00001.
• Tresguerres, J.A., Kireev, R., Tresguerres, A.F., Borras, C., Vara, E., Ariznavarreta, C. (2008). Molecular mechanisms involved in the hormonal prevention of aging in the rat. J Steroid Biochem Mol Biol, 108(3-5):318-326. doi: 10.1016/j.jsbmb.2007.09.010.
• Walsh, S.W. (1997). The role of oxidative stress and antioxidants in preeclampsia. Contemporary OB/GYN, 42:113–124. 48.
• Young, B.C., Levine, R.J., Karumanchi, S.A. (2010). Pathogenesis of Preeclampsia. Annu Rev Pathol, 5:173–92. doi: 10.1146/annurev-pathol-121808-102149.