UDC 577.1
DOI: 10.36871/vet.zoo.bio.202205005
Authors
Milyausha Ya. Ibragimova,
Russian Institute for Advanced Study (RIAS), Moscow State Pedagogical University, Moscow, Russia; Institute of Fundamental Medicine and Biology of the Kazan (Volga region) Federal University, Kazan, Russia
Sergei Y. Zaitsev,
Federal Research Center for Animal Husbandry named after
Academy Member L. K. Ernst, Dubrovitsy, Russia
Valeriy V Semenov,
Kazan State Medical University, Kazan, Russia
Abstract
The aim of this study was to evaluate the genetic activity of a number of medicinal drugs on a
model of mice peripheral blood erythrocytes.
In our work, we studied the ability of adrenergic agonists and adrenergic blockers – lipid metabolism
modulators – to induce two opposite effects in the cell: mutagenesis and antimutagenesis.
The method, we used for the analysis of chromosomal mutations after the administration of the
analyzed drugs in the mice peripheral blood erythrocytes made it possible to obtain a visual and
detailed idea of the genetic effects of ligands involved in lipid metabolism.
It is shown that genome instability, expressed in the formation of micronuclei in the mice peripheral
blood erythrocytes as a result of a single action of the cyclophosphamide mutagen (at a dose of
30 mg/kg) is significantly reduced by lipid metabolism modulators (both stimulants and blockers of
α- and β-adrenergic receptors).
The α-adrenergic receptor ligands – phenylephrine (stimulant) and proroxan (blocker), as well as
the β-adrenergic receptor ligands – orciprenaline (stimulant) and propranolol (blocker) – have an antimutagenic
effect. The maximum antimutagenic effect of phenylephrine is at doses of 1 and 10 mg/
kg, of proroxan – 1 mg/kg, orciprenaline – at a dose of 0,5 mg/kg, propranolol – 1×10–3 and 1 mg/kg.
Keywords
cyclophosphamide, adrenoreceptor ligands, antimutagenesis, lipid metabolism.
