REDOX BALANCE IN UTERINE TISSUE AND BLOOD PLASMA OF RATS DURING ENDOTOXEMIA AND THE ACTION OF EXOGENOUS GLUTATHIONE
V.R. Strutynskyi1, Y.P. Korkach2, L.A. Mys3, R.I. Yanchiy4
- Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz72.02.040

Abstract
Lipopolysaccharide, as endotoxin, causes systemic inflam-
mation and oxidative stress, alters metabolism and gene
expression, disrupts the function of many organs, including
the uterus, and depresses the reproductive capacity of animals.
By maintaining redox homeostasis, glutathione reduces the
pathogenic effects of endotoxin. However, lipopolysaccha-
ride inhibits endogenous glutathione synthesis, which can
potentially increase damage. Our work aimed to determine the
impact of exogenous glutathione on markers of oxidative stress
and lipid peroxidation, nitric oxide synthases (NOS) activity,
and hydrogen sulfide content in uterine tissues and blood
plasma of rats with lipopolysaccharide-induced endotoxemia.
Lipopolysaccharide was administered intraperitoneally at a
dose of 3 mg/kg one day before removing the animals from
the experiment. Glutathione was injected intraperitoneally at
a dose of 52 mg/kg twice: one hour before lipopolysaccharide
administration and one day later. It has been shown that during
endotoxemia, markers of oxidative stress (the rate of forma-
tion of superoxide anion and hydroxyl radical, the content of
hydrogen peroxide, malondialdehyde, and diene conjugates)
significantly increased in uterine tissues and blood plasma.
An increase in the activity of inducible NO synthase was also
observed, which creates the prerequisites for the formation of
highly toxic peroxynitrite. At the same time, a decrease in the
content and activity of such metabolic regulators important
for the normal function of organs and systems, such as H
2
S
and constitutive NOS, was observed. The administration of
glutathione to animals prevented these pathogenic changes,
reducing markers of oxidative stress and the synthesis of nitric
oxide by inducible NOS, and increasing the protective activity
of constitutive NO synthase. At the same time, the content of
H
2
S in the blood plasma of animals with endotoxemia upon
administration of this antioxidant increased almost threefold,
exceeding its concentration in control animals. Thus, glutathi-
one supports redox homeostasis and optimises the organism's
protective and regulatory systems (in particular, nitric oxide
and hydrogen sulfide) and adaptive capabilities in conditions
of endotoxemia, and is an important protective factor in condi-
tions of systemic inflammation.
Keywords:
myometrium; smooth muscle; rats; inflammation; oxidative stress; oxytocin receptor; KIR channel; plasma membrane; expression; NO; glutathione; hydrogen sulfide
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