Contribution of fetal programming in the formation of cognitive impairments induced by lead poisoning in white rats

Sosedova, LM; Vokina, VA; Kapustina, EA

HERO ID

7091634

Reference Type

Journal Article

Year

2019

Language

English

PMID

30903499

HERO ID 7091634
In Press No
Year 2019
Title Contribution of fetal programming in the formation of cognitive impairments induced by lead poisoning in white rats
Authors Sosedova, LM; Vokina, VA; Kapustina, EA
Journal Bulletin of Experimental Biology and Medicine
Volume 166
Issue 5
Page Numbers 617-621
Abstract 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.
Doi 10.1007/s10517-019-04404-4
Pmid 30903499
Wosid WOS:000463162900007
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English