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2017 | 77 | Suppl.1 |
Tytuł artykułu

Rats redox status changes to low ethanol (hormetic) dose exposure

Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
INTRODUCTION: In the aspect of the hormesis concept, ethanol is considered to be a classic example, as the consumption of low or moderate doses of ethanol is associated with positive phenomena. Alcohol consumption by women during pregnancy leads to the formation of Fetal Alcohol Syndrome (FAS), that causes the violation of the basic processes of neurogenesis. Under the conditions of hormesis the stimulation of cell endogenous protective mechanisms causes the neuroprotective effect of low doses of toxic substances and allows the therapeutic use of hormesis. Therefore, it is important research of alcohol hormetic effect on the nervous system. AIM(S): The aim of this study was to determine the neuroprotective effect of hormetic dose of ethanol in the offspring of female white rats during pregnancy intraperitoneally treated with ethanol at low doses. METHOD(S): We studied free radicals signal intensity in cerebral cortex and hippocampus of 60-day-old offspring of female white rats, treated hormetic dose (0.25 g/kg) of ethanol during pregnancy. The intensity of free radicals by electron paramagnetic resonance (EPR) method was determined with use of spin‑trap α‑phenyl‑tertbutilnitron (PBN) for lipoperoxide radicals (LOO∙) and the free nitric oxide (NO) for sodium diethil-ditio-carbomate (DEDTC). RESULTS: The significant changes in EPR signals of spin‑trapped LOO∙ in the cortex and hippocampus samples of experimental group rats were not detected. The intensity of NO EPR signal was statistically reliably increased in the cortex and was not changed in the hippocampus. A number of studies show the increase in iNOS and nNOS protein synthesis and the activity under the influence of alcohol. Probably the low (hormetic) dose of alcohol induces only slight activation of NO-synthase, resulted in 7% increase of free NO content in the cortex. CONCLUSIONS: In the present series of experiments was not observed intensification of free radical oxidation in brain tissues. FINANCIAL SUPPORT: The study was supported by the Sh. Rustaveli National Science Foundation of Georgia.
Słowa kluczowe
Wydawca
-
Rocznik
Tom
77
Numer
Opis fizyczny
p.49
Twórcy
autor
  • I. Beritashvili Center of Experimental Biomedicine, Departement of Neurotoxicology, Tbilisi, Georgia
autor
  • I. Beritashvili Center of Experimental Biomedicine, Departement of Neurotoxicology, Tbilisi, Georgia
autor
  • I. Beritashvili Center of Experimental Biomedicine, Departement of Neurotoxicology, Tbilisi, Georgia
autor
  • I. Beritashvili Center of Experimental Biomedicine, Departement of Neurotoxicology, Tbilisi, Georgia
autor
  • I. Beritashvili Center of Experimental Biomedicine, Departement of Neurotoxicology, Tbilisi, Georgia
autor
  • I. Beritashvili Center of Experimental Biomedicine, Departement of Neurotoxicology, Tbilisi, Georgia
Bibliografia
Typ dokumentu
Bibliografia
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