DOI: 10.36871/vet.zoo.bio.202102001
UDC 577.1
Authors
M. Ya. Ibragimova
Candidate of Biological Sciences, Associate Professor of the Department
of Biochemistry, Russian Institute for Advanced Study RIAS,
Moscow State Pedagogical University, Biotechnology and Pharmacology
of the Institute of Fundamental Medicine and Biology
of the Kazan (Volga region) Federal University, Russian Federation
S. Yu. Zaytsev
Doctor of Biological Sciences, Doctor of Chemistry, Professor, Leading
Researcher at the Department of Physiology and Biochemistry,
All-Russia research institute of animal husbandry
named after academy member L. K. Ernst,
Dubrovitsy, Russian Federation
V. V. Semenov
Doctor of Medical Sciences, Professor, Kazan State Medical University,
Kazan, Russian Federation
Abstract
The aim of the study was to evaluate the genetic activity of erythrocytes in peripheral on the model of peripheral blood erythrocytes in mice. The studies were carried out on mice (males) of the C XNUMXBXNUMX/XNUMX line weighing XNUMX g (XNUMX–XNUMX months of age). For each experimental and control variant, six males were taken. The animals were kept in vivarium conditions according to international criteria for rinofix bedding, food and water ad libitum. When determining the genetic effects, the adrenergic receptor ligand was injected subcutaneously once. After XNUMX hours, a mutation inducer, an alkylating drug, cyclophosphamide, was injected intraperitoneally at a dose of XNUMX mg/kg. Before the end of the experiment in XNUMX hour, mice were injected intraperitoneally with XNUMX mg/kg of colchicine. XNUMX hours after injection, the animals were euthanized by delongation. The number of erythrocytes with micronuclei was counted from XNUMX analyzed cells. The greatest antimutagenic effect (XNUMX%) of epinephrine hydrotartrate, a stimulator of α- and β-adrenergic receptors, was found at doses of XNUMX and XNUMX mg/kg.
Keywords
cyclophosphamide, adrenoreceptor ligands, mutagenesis, antimutagenesis, lipid metabolism, laboratory animals.
