Influence of GABA derivatives on the DNA damage of placenta and fetuses’s brain at experimental preeclampsia

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Abstract

Gestosis is a complication of the normal course of the gestational process that occurs during pregnancy, childbirth and in the first days of the postpartum period, characterized by a deep disorder of the functions of vital organs and systems. Preeclampsia (PE), as a form of gestosis, is an important health and social problem worldwide, remaining one of the main causes of perinatal and maternal morbidity and mortality. The aim of the study was to evaluate the effects of GABA derivatives on the genome integrity of placental cells of female rats with experimental PE and the state of DNA of brain cells of the offspring of these animals. Material and methods: the experiment was carried out on white nonlinear pregnant rats at the age of3 months weighing 210-230 g. After fertilization, pregnant females were moved to individual maintenance cells and an EP model was reproduced on them by replacing drinking water with 1.8% sodium chloride solution from the 1st to the 20h day of pregnancy. Increased blood pressure and registered proteinuria in the daily urine on the 1st and 20th days of gestation were considered to be signs of PE in pregnant female rats. The assessment of DNA damage was investigated by the DNA comet method. The results of the study showed a 3 and 2.6-fold increase in DNA in comet tails respectively. In animals treated with salifen (an adduct of phenibut and salicylic acid in a molar ratio of 2:1) at a dose of 15 mg/ kg once, intragastrically during pregnancy, the level of DNA damage in the corresponding organs was 3.0 and 1.4 times lower than in the group with EP. Phenibut (y-amino-ß-phenylbutyric acid hydrochloride) at a dose of 50 mg/kg and succicard (an adduct of phenotropil and succinic acid) at a dose of 44 mg/kg once, intragastrically, did not affect the level of genome damage in placenta and fetal brain cells.

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About the authors

Anna Gragatovna Sirekanyan

Volgograd State Medical University

Author for correspondence.
Email: annart888@yandex.ru
assistant of the department of Theoretical Biochemistry with a Course in Clinical Biochemistry Pavshikh Bortsov Sq. 1, Volgograd, 400131, Russian Federation

Olga Vladimirovna Verle

Volgograd State Medical University

Email: verle_olga@mail.ru
assistant of the department of Theoretical Biochemistry with a Course in Clinical Biochemistry Pavshikh Bortsov Sq. 1, Volgograd, 400131, Russian Federation

Galina Petrovna Dudchenko

Volgograd State Medical University

Email: dgalina@mail.ru
Professor of the department of Theoretical Biochemistry with a Course in Clinical Biochemistry; Doctor of Biological Sciences, Professor. Pavshikh Bortsov Sq. 1, Volgograd, 400131, Russian Federation

Valentina Nikolaevna Perfilova

Volgograd State Medical University

Email: vnperfilova@mail.ru
Professor of the Department of Pharmacology and Pharmacy of the NYMPH Institute; Doctor of Biological Sciences, Professor. Novorossiyskaya Sq. 39, Volgograd, 400087, Russian Federation

Valerian Evgenevich Verovskiy

Volgograd State Medical University

Email: veverovsky@gmail.com
Docent of the department of Theoretical Biochemistry with a Course in Clinical Biochemistry; Candidate of Chemical Sciences. Pavshikh Bortsov Sq. 1, Volgograd, 400131, Russian Federation

Oleg Vladimirovich Ostrovsky

Volgograd State Medical University

Email: ol.ostr@gmail.com
The Head of the chair of the department of Theoretical Biochemistry with a Course in Clinical Biochemistry; Doctor of medical sciences, Professor. Pavshikh Bortsov Sq. 1, Volgograd, 400131, Russian Federation

Ivan Nikolaevich Tyurenkov

Volgograd State Medical University

Email: fibfuv@mail.ru
The Head of the chair of the department of Pharmacology and Pharmacy of the NYMPH Institute; Doctor of medical sciences, Professor, corresponding member of RAS. Novorossiyskaya Sq. 39, Volgograd, 400087, Russian Federation

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Supplementary files

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2. Fig. 1. Cells with intact DNA

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3. Fig. 2. Cells with damaged DNA

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4. Fig. 3. Dependence of % DNA damage in the embryo’s brain on the daily excretion of protein in the urine

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