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Bulletin of Experimental Biology and Medicine, Vol. 154, No.

6, April, 2013 GENERAL PATHOLOGY AND PATHOPHYSIOLOGY 731

Antioxidant Potential of the Blood in Men


with Obstructive Sleep Breathing Disorders
L. I. Kolesnikova, I. M. Madaeva, N. V. Semenova, B. Ya. Vlasov,
L. A. Grebenkina, M. A. Darenskaya, and M. I. Dolgikh
Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 154, No. 12, pp. 695-697, December, 2012
Original article submitted January 30, 2012

We studied the state of the LPO–antioxidant defense system in men aged from 46 to 55 years.
The main group included patients with obstructive sleep breathing disorders. The state of the
antioxidant defense system was assessed by measuring the blood levels of LPO substrates
with conjugated double bonds, conjugated dienes, ketodienes and conjugated trienes, MDA,
retinol, α-tocopherol, reduced and oxidized glutathione, SOD activity, and the level of total
antioxidant activity of blood. Calculation of antioxidant potential helps to identify the pro-
cesses of “oxidative stress” in the main group, which is a pathogenetic substantiation for
including antioxidant drugs in the complex therapy of patients with OSBD.

Key Words: antioxidant potential; sleep-related obstructive breathing disorders

Activation of LPO reactions in vivo is closely asso- MATERIALS AND METHODS


ciated with oxygen transport and utilization system.
This is of particular importance for human adapta- The study involved 51 men aged 46-55 years. The
tion to hypoxia arising in obstructive sleep breath- inclusion criteria were snoring for 6 or more months,
ing disorders (OSBD), when the probability of such morning headache, predominant increase in blood
activation increases dramatically and leads to the pressure in the morning, daytime sleepiness, unrefresh-
development of pathology depending on a number ing sleep, poor concentration and memory, decreased
of conditions [1,9]. OSBD-related disorders of gas libido, and nocturnal diuresis. Exclusion criteria were
exchange result in changes of free radical homeosta- the absence of acute pathologies and exacerbation of
sis, manifested in reactive oxygen species and LPO chronic diseases. All participants were included in the
activation [5,8,14]. However, most researchers point study after signing informed consent in accordance
out that integral indices are more sensitive for assess- with the Declaration of Helsinki (2000). After a night
ment of the balance between LPO and the antioxidant of adaptation in a specially equipped sleep laboratory
defense system (AOS) than comparison of selected under conditions close to home, all persons were sub-
indicators. jected to polysomnographic monitoring using GRASS-
In this paper, we applied the methodology for TELEFACTOR Twin PSG system (Comet) with an As
evaluation of antioxidant potential (AOP), which 40 amplifier and integrated module for sleep. Applica-
was used as an integral parameter characterizing tion of electrodes and sensors, installation and physi-
LPO—AOS imbalance disorders. ological calibration, eliminating of possible artifacts,
Here we estimated AOS in men with OSBD. and identification and assessment of sleep stages were
conducted in accordance with international recommen-
Research Center of Family Health Protection and Human Reproduc-
dations and criteria of American experts [13]. After
tion Problems, Siberian Division of Russian Academy of Medical Sci- the study, the patients were divided into two groups.
ences, Irkutsk, Russia. Address for correspondence: natkor_84@ Group of patients with OSBD duration of 10.5±1.5
mail.ru. N. V. Semenova years (mean age 53.16±3.45 years, BMI 33.19±5.76

0007-4888/13/15460731 © 2013 Springer Science+Business Media New York


732 Bulletin of Experimental Biology and Medicine, Vol. 154, No. 6, April, 2013 GENERAL PATHOLOGY AND PATHOPHYSIOLOGY

kg/m2) consisted of 37 persons. Control group included


14 men (mean age 50.38±2.63 years, BMI 34.27±3.48
kg/m2) without obstructive sleep breathing disorders.
The intensity of LPO and AOS was assessed by
the levels of their individual components in blood se-
rum and hemolisate as well as by the values of total
antioxidant activity [4]. The levels of substrates and
products of LPO, compounds with conjugated double
bonds, conjugated dienes, ketodienes and conjugated
trienes were determined spectrophotometrically [3].
The content of LPO end-product MDA was deter-
mined fluorometrically by the reaction with TBA [2].
Activity of AOS was evaluated also by the levels of
α-tocopherol and retinol [10], reduced and oxidized
glutathione (GSH and GSSG) [11], SOD activity, and
Fig. 1. Relative values of the indicators of lipid peroxidation in men
by the dynamics of epinephrine autoxidation [12]. The with OSBD (control as 0%). CD, conjugated dienes; DB, double
measurements were performed on a Shimadzu RF- bonds; KD and CT, ketodienes, and conjugated trienes.
1501 spectrofluorometer.
For statistical analysis of the data, Statistica 6.1
software was used (Stat Soft Inc.; license owner Re-
search Center of Family Health Protection and Human
Reproduction Problems, Siberian Division of Russian
Academy of Medical Sciences). Intergroup differences
for independent samples were analyzed with paramet-
ric Student’s t test and nonparametric Mann–Whitney
test. The differences were significant at p<0.05.

RESULTS
The results of LPO and AOS evaluation in men with
OSBD are presented in Figs. 1 and 2. The study of all
LPO processes revealed a tendency to increase in blood
levels of the substrates with conjugated double bonds
(DB), ketodienes and conjugated trienes (KD and CT)
and final LPO product MDA in patients with OSBD.
The content of primary LPO products, conjugated dienes Fig. 2. Relative values of ADS in men with OSBD (control taken as
(CD), in men of the main group was lower than in the 0%). АОА, antioxidant activity.
control group. Assessing the state of AOS, we observed a
decrease in SOD activity, and blood levels of antioxidants oxidant and prooxidant elements; value less than 1,
retinol and GSH and an increased in total antioxidant ac- the shift toward prooxidant activity; greater than 1,
tivity (AOA) in the serum of patients with OSBD. sufficient AOS. Index AOP in men with OSBD was
For better understanding of LPO and AOS in men 0.75. This indicates a marked imbalance in LPO–
with OSBD, we calculated AOP values. To this end, AOS system towards prooxidant activity. The shift of
we used the principle proposed by A. S. Losev and A. prooxidant-antioxidant balance in favor of prooxidant
F. Fesyuk in 2000. [7]. In this paper, all the indicators factors is “oxidative stress” and can cause potential
were divided into two groups. The first group included cell damage [6]. Given the duration of the disease in
parameters characterizing AOS and the other group these patients, which corresponds to severe OSBD,
characterized prooxidants. Then, the integral paramer we can assume that prolonged and severe hypoxia
was calculated by the formula: with aggravation of the characteristic signs of sleep
АОА+GSH+SOD+retinol+α-tocopherol disorders during a number of years causes a depletion
AOP= . of function. This results in the disorders in the self-
MDA+CD+KD-CT+DB+GSSG regulation mechanisms and failure of compensatory-
In this case, their relative values were used. The adaptive mechanisms, which leads to the disintegra-
resulting value was compared with the control taken tion and transformation of the physiological system
as 1. Value closer to 1 suggest the balance between into pathological one.
L. I. Kolesnikova, I. M. Madaeva, et al. 733

7. Patent No. 2194984. Way of Estimating Anti-and Pro-Oxi-


In conclusion, it should be noted that the obtained dant Status of the Body by Determining Antioxidant Poten-
results are pathogenetic substantiation for including tial / A. S. Losev, V. I. Petrov, and A. F. Fesyuk, Published
drugs that inhibit the activation of LPO, in the com- 16.10.2000.
plex therapy of patients with OSBD. 8. Yu. V. Smolyaninova, L. I. Kolesnikova, I. M. Madaeva, et al.,
Byul. VSNTS SO RAMN, No. 1, 239-240 (2007).
9. I. E. Chazova and A. Yu. Litvin, Sistemnyye Gipertenzii, No.
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