Advertisement

Bulletin of Experimental Biology and Medicine

, Volume 166, Issue 5, pp 617–621 | Cite as

Contribution of Fetal Programming in the Formation of Cognitive Impairments Induced by Lead Poisoning in White Rats

  • L. M. SosedovaEmail author
  • V. A. Vokina
  • E. A. Kapustina
PHARMACOLOGY AND TOXICOLOGY
  • 3 Downloads

The contribution of prenatal hypoxic damage to the CNS to the formation of high sensitivity of the body to lead acetate was studied. Prenatal fetal hypoxia was modeled by the administration of sodium nitrite in doses of 5, 25, and 50 mg/kg to pregnant female rats. Cognitive capacities of mature offspring were evaluated in the radial maze test and Morris water maze test. After attaining learning criterion in the radial maze, lead acetate in a dose of 80 mg/kg was added to the drinking water of all animals over 2 weeks. Testing was performed during the exposure to the agent until disruption of the conditioned behavior. It was found that severe prenatal hypoxia (induced by the administration of 50 mg/kg sodium nitrite) impaired spatial memory, increased latency of funding the platform in Morris water maze test, and serves as a factor contributing to earlier manifestations of the neurotoxic effects of lead acetate.

Key Words

white rats prenatal hypoxia lead cognitive abilities 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Badalyan BYu, Sarkisyan DzhS, Khudaverdyuan AD, Ambratsymyan GR, Saroyan MYu, Khudaverdyuan DN. Prenatal stress as a factor of morphofunctional disorders of CNS during pre- and postnatal ontogeny. Vopr. Ter. Klin. Med (Erevan). 2012;15(3):7-19. Russian.Google Scholar
  2. 2.
    Vataeva LA, Tyul’kova EI, Khozhai LI, Samoilov MO, Otellin VA. Training in the Morris water maze of female and male rats exposed to hypoxia at various periods of prenatal development. J. Evol. Biochem. Physiol. 2005;41(6):660-664.CrossRefGoogle Scholar
  3. 3.
    Vokina VA, Sosedova LM, Rukavishnikov VS, Yakimova NL, Lizarev AV. Neurotoxic effect of toluene on background of prenatal hypoxic brain damage to white rats. Med. Truda Prom. Ekol. 2014;(4):30-34. Russian.Google Scholar
  4. 4.
    Gamma TV, Katyushina OV, Korenyuk II, Khusainov DR, Kolotilova OI, Chertaev IV. Modification of rat behavior during intoxication with heavy metals. Tavrich. Med.-Biol. Vestn. 2012;15(1):341-344. Russian.Google Scholar
  5. 5.
    Grjibovski AM, Bygren LO, Tedder YuR. Intrauterine programming of adult diseases. Ekol. Chel. 2003;(5):14-22. Russian.Google Scholar
  6. 6.
    Dubrovskaya NM, Zhuravin IA. Ontogenetic peculiarities of the behavior in rats subjected to hypoxia on embryonic days 14 or 18. Zh. Vyssh. Nervn. Deyat. 2008;28(6):718-727. Russian.Google Scholar
  7. 7.
    Otellin VA, Khozhai LI, Gilerovich EG, Korzhevskii DE, Kostkin VB, Belostotskaya GB. Damaging effects in critical periods of prenatal ontogeny as a factor modifying structural development and behavioral reactions after birth. Vestn. Ross. Akad. Med. Nauk. 2002;(12):32-35. Russian.Google Scholar
  8. 8.
    Sosedova LM, Vokina VA, Rukavishnikov VS. Patent RU No. 2497202. Method for simulating prenatal hypoxic encephalopathy in small laboratory animals. Bull. No. 30. Published October 27, 2013.Google Scholar
  9. 9.
    Yaverbaum PM. General Aspects of Lead Toxicity. Irkutsk, 2006. Russian.Google Scholar
  10. 10.
    Dong Y, Yu Z, Sun Y, Zhou H, Stites J, Newell K, Weiner CP. Chronic fetal hypoxia produces selective brain injury associated with altered nitric oxide synthases. Am. J. Obstet. Gynecol. 2011;204(3):254.e16-28. doi:  https://doi.org/10.1016/j.ajog.2010.11.032.CrossRefGoogle Scholar
  11. 11.
    Gómez-González B, Escobar A. Prenatal stress alters microglial development and distribution in postnatal rat brain. Acta Neuropathol. 2010;119(3):303-315.CrossRefGoogle Scholar
  12. 12.
    Gunn AJ, Bennet L. Fetal hypoxia insults and patterns of brain injury: insights from animal models. Clin. Perinatol. 2009; 36(3):579-593.CrossRefGoogle Scholar
  13. 13.
    Lucassen PJ, Bosch OJ, Jousma E, Krömer SA, Andrew R, Seckl JR, Neumann ID. Prenatal stress reduces postnatal neurogenesis in rats selectively bred for high, but not low, anxiety: possible key role of placental 11beta-hydroxysteroid dehydrogenase type 2. Eur. J. Neurosci. 2009;29(1):97-103.CrossRefGoogle Scholar
  14. 14.
    Morton JS, Rueda-Clausen CF, Davidge ST. Mechanisms of endothelium-dependent vasodilation in male and female, young and aged offspring born growth restricted. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2010;298(4):R930-R938.CrossRefGoogle Scholar
  15. 15.
    Nesterenko TH, Aly H. Fetal and neonatal programming: evidence and clinical implications. Am. J. Perinatol. 2009; 26(3): 191-198.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • L. M. Sosedova
    • 1
    Email author
  • V. A. Vokina
    • 1
  • E. A. Kapustina
    • 1
  1. 1.East Siberian Institute of Medical and Ecological ResearchAngarskRussia

Personalised recommendations