online ISSN 2415-3176
print ISSN 1609-6371
logoExperimental and Clinical Physiology and Biochemistry
  • 5 of 10
Up
ECPB 2020, 90(2): 36–43
https://doi.org/10.25040/ecpb2020.02.036
Research articles

Pubertal development of male offspring born to mothers of different ages with fetoplacental insufficiency

N. Yu. SELIUKOVA1,2, N. М. BRECHKA1
Abstract

Today, the problem of male infertility or poor reproductive health is very relevant around the world. The formation of the reproductive system begins in the womb, when all the organs and systems are formed. Fetoplacental insufficiency – a clinical syndrome caused by morphological and functional changes in the placenta, manifested by disorders of the fetus, growth and development. To date, it is not known how fetoplacental insufficiency in mothers affects the condition and functioning of the reproductive system in adult male offspring. The purpose of this scientific work was to investigate the development of puberty in males-offspring born to mothers of different age with fetoplacental insufficiency and to evaluate efficacy of base and combined drug therapy during pregnancy. Materials. Healthy, mature Vistar females-mothers of young (3–4 months) and mature (8–10 months) reproductive age have been used in the experiment. Modeling of fetoplacental insufficiency has been carried out by subcutaneous daily introduction of 50% tetrachlomethane oil solution in dose of 2ml/kg of body weight from 12th to 18th day of pregnancy. General body masses and sexual development have been researched. The samples of blood serum with the aim to evaluate estradiol, testosterone and progesterone hormones levels have been taken. Results. Discussion. In the study of the reproductive weight of males, no changes were found, but at the autopsy of pubertal males were found animals in which the testicles were not lowered into the scrotum (cryptorchidism), such rats were born to young mothers with fetoplacental insufficiency. Such changes occurred against the background of hormonal imbalance, which manifested itself in a decrease in total testosterone and, conversely, increased estradiol and progesterone. There was a lag in sexual development in animals born to mothers of two age groups with fetoplacental insufficiency. Pharmaceutical composition contributed to normal physiological sexual development in males born to mothers of mature reproductive age with fetoplacental insufficiency, in young females, pharmaceutical composition did not show any corrective effect on offspring as well as the comparison drug – Dipyridamole. Conclusions and prospects of further developments. Fetoplacental insufficiency affects the somato-sexual development of male offspring born to mothers of different reproductive ages, which is manifested in delayed puberty and imbalance of sex hormones (decreased testosterone in all animals and increased estrogen levels only in offspring born to reproductively young). Which in the future can lead to problems with the functioning of the reproductive system. In the application of the new pharmaceutical composition which is administered to correct abnormal condition of pregnancy and observed high levels of testosterone but not estradiol levels decrease high only in offspring born to young females, which subsequently led to the normal sexual development of males. The comparison drug Dipyridamole did not show a corrective effect in pubertal males. The prospect of further development is to study the effects of fetoplacental insufficiency on the reproductive system of mature male rats of offspring born to mothers of different reproductive ages. It is possible to develop specific approaches to the prevention of detected pathology.

Added: 14.05.2020

Keywords: fetoplacental insufficiency, pharmaceutical composition, Dipyridamole, offspring, reproductive system

Full text: PDF (Ukr) 556K

References
  1. 1. Burton GJ, Fowden AL, Thornburg KL. Placental Origins of Chronic Disease. Physiol Rev. 2016;96(4):1509-65. doi.org/10.1152/physrev.00029.2015
  2. 2. Rodríguez-Rodríguez P, Ramiro-Cortijo D, Reyes-Hernández CG, López de Pablo AL, González MC, Arribas SM. Implication of Oxidative Stress in Fetal Programming of Cardiovas- cular Disease. Front Physiol. 2018;9:602. doi.org/10.3389/fphys.2018.00602
  3. 3. Simmons RA. Developmental origins of diabetes: The role of oxidative stress. Best Pract Res Clin Endocrinol Metab. 2012;26(5):701-8. doi.org/10.1016/j.beem.2012.03.012
  4. 4. Guarner-Lans V, Ramírez-Higuera A, Rubio-Ruiz ME, Castrejón-Téllez V, Soto ME, Pérez-Torres I. Early Programming of Adult Systemic Essential Hypertension. Int J Mol Sci. 2020;21(4):1203. doi.org/10.3390/ijms21041203
  5. 5. Burren CP, Caswell R, Castle B, Welch CR, Hilliard TN, Smithson SF, Ellard S. TRPV6 compound heterozygous variants result in impaired placental calcium transport and severe under- mineralization and dysplasia of the fetal skeleton. Am J Med Genet A. 2018 Sep;176(9):1950-5. doi.org/10.1002/ajmg.a.40484
  6. 6. Shallie PD, Naicker T. The placenta as a window to the brain: A review on the role of pla- cental markers in prenatal programming of neurodevelopment. Int J Dev Neurosci. 2019;73:41-9.
  7. 7. Saveleva GM, Fedorova MV, Klymenko PA, Sychynava LG. Platsentarnaya nedostatochnost. M.: Medytsyna, 1991. 272 s. doi.org/10.1016/j.ijdevneu.2019.01.003
  8. 8. Botting KJ, McMillen IC, Forbes H, Nyengaard JR, Morrison JL Chronic hypoxemia in late gestation decreases cardiomyocyte number but does not change expression of hypoxia- responsive genes. J Am Heart Assoc. 2014;Jul 28;3(4). doi.org/10.1161/JAHA.113.000531
  9. 9. Luyckx VA, Brenner BM. Birth weight, malnutrition and kidney-associated outcomes--a global concern. Nat Rev Nephrol. 2015;Mar 11(3):135-49. doi.org/10.1038/nrneph.2014.251
  10. 10. Yalovchuk AV. Viddaleni rezultaty porushen nervovoyi systemy u nemovlyat, narodzhenykh vid materiv z uskladnenym perebigom vagitnosti. Bukovynskyy medychnyy visnyk. 2006:10(2);83-6.
  11. 11. Bekmukhambetov Y, Mamyrbayev A, Dzharkenov T, Kravtsova N, Utesheva Z, Tusupkaliev A et al. Metabolic and immunologic aspects of fetoplacental insufficiency. Am J Reprod Immunol. 2016;Oct;76(4):299-306. doi.org/10.1111/aji.12544
  12. 12. Kupryyanova LS. Patomorfologycheskye osobennosty stroenyya yaychnykov plodov ot materey, beremennost u kotorykh protekala na fone platsentarnoy dysfunktsyy. Zaporizkyy med. zhur. 2014;5(86):78-81.
  13. 13. Verkhovna Rada Ukrayiny. Yevropeyska konventsiya pro zakhyst khrebetnykh tvaryn, shcho vykorystovuyutsya dlya doslidzhennya abo inshchykh naukovykh tsiley vid 18.03.1986.
  14. 14. Nakaz No 1287 vid 19.11.2012. Polozhennya pro komytet z pytan etyky (byoetyky) http activity/63/64/ normativno-pravova-baza.
  15. 15. Yakovlyeva LV, Zaychenko GV, Tsypkun AG, Lar'yanovska YuB, Butenko IG, Deyeva TV et al. Doklinichne vyvchennya likarskykh zasobiv, pryznachenykh dlya likuvannya platsentarnoyi dysfunktsiyi [Tekst] : metod. rekomendatsiyi / DFTs MOZ Ukrayiny; K., 2009, 62 s.
  16. 16. Pampanini V, Germani D, Puglianiello A, Stukenborg JB, Reda A, Savchuk I et al. Impact of uteroplacental insufficiency on postnatal rat male gonad. J Endocrinol. 2017 Feb;232(2):247-57. doi.org/10.1530/JOE-16-0418
  17. 17. Ghazarian AA, Trabert B, BI Graubard BI, Longnecker MP, Klebanoff MA, McGlynn KA. Placental Weight and Risk of Cryptorchidism and Hypospadias in the Collaborative Perinatal Project. American Journal of Epidemiology, 2018;187(7):1354-61. doi.org/10.1093/aje/kwy005
  18. 18. GurneyJK, McGlynn KA, Stanley J, Merriman T, Signal V, Shaw C et al. Risk factors for cryptorchidism. Nat Rev Urol. 2017 Sep;14(9):534-48. doi.org/10.1038/nrurol.2017.90
  19. 19. Mavrogenis S, Urbán R, Czeizel AE. Characteristics of boys with the so-called true undescended testis diagnosed at the third postnatal month - A population-based case-control study. Journal of Maternal-Fetal and Neonatal Medicine. 2015;28:1152-7. doi.org/10.3109/14767058.2014.947569
  20. 20. Csermely G, Susánszky É, Czeizel AE. Association of young and advanced age of pregnant women with the risk of isolated congenital abnormalities in Hungary - A population-based case-matched control study. Journal of Maternal-Fetal and Neonatal Medicine. 2015;28:436-42.doi.org/10.3109/14767058.2014.918946
  21. 21. Flück CE, Meyer-Böni M, Pandey AV, Kempná P, Miller WL, Schoenle EJ et al. Why boys will be boys: two pathways of fetal testicular androgen biosynthesis are needed for male sexual differentiation. Am J Hum Genet. 2011 Aug 12;89(2):201-18. doi.org/10.1016/j.ajhg.2011.06.009
  22. 22. Ross A, Bhasin S. Hypogonadism: Its Prevalence and Diagnosis. Urol Clin North Am. 2016;May;43(2):163-76. doi.org/10.1016/j.ucl.2016.01.002
  23. 23. Salonia A, Rastrelli G, Hackett G, Seminara SB, Huhtaniemi T, Rey RA et al. Paediatric and adult-onset male hypogonadism. Nat Rev Dis Primers. 2019;May30;5(1):38. doi.org/10.1038/s41572-019-0087-y
  24. 24. Goncharova OA. Osoblyvosti avtoimunnoyi patologiyi na tli vikovoyi involyutsiyi tymusa i gipoestrogeniyi. Problemy endokrynnoyi patologiyi 2014;1:72-9. doi.org/10.21856/j-PEP.2014.1.09
  25. 25. Chedane C, Puissant H, Weil D, Rouleau S, Coutant R. Association between altered placental human chorionic gonadotrophin (hCG) production and the occurrence of cryptorchidism: a retrospective study. BMC Pediatr. 2014;Jul 26;14:191. doi.org/10.1186/1471-2431-14-191
  26. 26. Scott HM, Mason JI, Sharpe RM. Steroidogenesis in the fetal testis and its susceptibility to disruption by exogenous compounds. Endocr Rev. 2009,Dec;30(7):883-925. doi.org/10.1210/er.2009-0016
  27. 27. Seliukova NYu, Misyura KV. Osoblyvosti endokrynnoyi funktsiyi platsenty samyts riznogo viku z fetoplatsentarnoyu nedostatnistyu (oglyad literatury ta vlasni doslidzhennya). Probl. endokryn. patologiyi. 2019;4:128-39.


Програмування - Roman.im