Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation
We investigated the effects of vitamin E supplementation on neurobehavioral alterations induced by chronic ingestion of lead acetate in mice. The animals were divided into three main groups, group 1 (control) given with normal saline (10 ml/kg) and groups 2 and 3 given with 3000 mg/kg lead acetat...
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| Опубліковано в: : | Нейрофизиология |
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| Дата: | 2015 |
| Автори: | , |
| Формат: | Стаття |
| Мова: | Англійська |
| Опубліковано: |
Інститут фізіології ім. О.О. Богомольця НАН України
2015
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| Назва журналу: | Digital Library of Periodicals of National Academy of Sciences of Ukraine |
| Цитувати: | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation / G.F. Ibironke, S.T. Adu // Нейрофизиология. — 2015. — Т. 47, № 3. — С. 295-299. — Бібліогр.: 12 назв. — англ. |
Репозитарії
Digital Library of Periodicals of National Academy of Sciences of Ukraine| _version_ | 1859654058338418688 |
|---|---|
| author | Ibironke, G.F. Adu, S.T. |
| author_facet | Ibironke, G.F. Adu, S.T. |
| citation_txt | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation / G.F. Ibironke, S.T. Adu // Нейрофизиология. — 2015. — Т. 47, № 3. — С. 295-299. — Бібліогр.: 12 назв. — англ. |
| collection | DSpace DC |
| container_title | Нейрофизиология |
| description | We investigated the effects of vitamin E supplementation on neurobehavioral alterations induced
by chronic ingestion of lead acetate in mice. The animals were divided into three main groups,
group 1 (control) given with normal saline (10 ml/kg) and groups 2 and 3 given with 3000 mg/kg
lead acetate alone and in combination with 13 IU of vitamin E, respectively, for a period of
90 days. Lead intoxication resulted in significant (P < 0.05) reduction of the number of head dips
in the hole-board test and the time spent in the open arm of the elevated plus maze test, compared
with the control. Intoxication also induced increased pain sensitivity, as shown by significant
(P < 0.05) reduction in the tail flick latency and increase in the frequency of abdominal
constrictions in the writhing test. The periods of immobility in both tail suspension and
forced swimming tests in intoxicated animals were greater, as compared with the control.
Co-administration of vitamin E with lead in group 3 significantly (P < 0.05) reversed all the
mentioned shifts (increased the number of head dips and time spent in the maze open arm,
increased the tail flick latency, decreased the frequency of writhings, and decreased the periods
of immobility in the forced swimming and tail suspension tests). Thus, vitamin E treatment
is capable of effectively attenuating the negative neurobehavioral consequences of lead
intoxication.
Ми досліджували зміни нейроповедінкових показників у
мишей, викликані хронічним пероральним уведенням ацетату свинцю, та корекцію цих змін за допомогою вітаміну
Е. Тварини були поділені на три групи: контрольну групу 1,
що отримувала фізіологічний розчин (10 мл/кг), та групи
2 і 3, котрим протягом 90 діб уводили 3000 мг/кг ацетату
свинцю ізольовано або в комбінації з 13 М.О. вітаміну Е
відповідно. Свинцева інтоксикація зумовлювала істотне
(P < 0.05) зменшення кількості зазирань в отвори під час
проходження тесту «отвори в дошці» та часу, проведеного
у відкритих рукавах «підвищеного» лабіринту. Інтоксикація також призводила до підвищення чутливості до болю,
про що свідчили істотні скорочення латентного періоду відсмикування хвоста та збільшення кількості «корчів», індукованих уведенням оцтової кислоти, у відповідних тестах.
Періоди нерухомості у тестах підвішування за хвіст та примусового плавання в інтоксикованих тварин були довшими, ніж у контролі. Паралельне уведення вітаміну Е тваринам групи 3 істотно (P < 0.05) нейтралізувало вказані
негативні зрушення. Ставали більшими число зазирань в
отвори та час, проведений у відкритих рукавах лабіринту;
латентний період відсмикування хвоста подовжувався, а
число «корчів» зменшувалося; періоди імобілізації у згаданих вище тестах скорочувалися. Отже, вітамін Е, будучи
потужним антиоксидантом, ефективно згладжує негативні
нейроповедінкові наслідки свинцевої інтоксикації.
|
| first_indexed | 2025-12-07T13:37:25Z |
| format | Article |
| fulltext |
NEUROPHYSIOLOGY / НЕЙРОФИЗИОЛОГИЯ.—2015.—T. 47, № 3 295
UDC 615.099.092:577.161.3
G. F. IBIRONKE1 and S. T. ADU1
NEUROBEHAVIORAL CONSEQUENCES OF CHRONIC LEAD INTOXICATION:
EFFECTS OF VITAMIN E SUPPLEMENTATION
Received February 5, 2014
We investigated the effects of vitamin E supplementation on neurobehavioral alterations induced
by chronic ingestion of lead acetate in mice. The animals were divided into three main groups,
group 1 (control) given with normal saline (10 ml/kg) and groups 2 and 3 given with 3000 mg/kg
lead acetate alone and in combination with 13 IU of vitamin E, respectively, for a period of
90 days. Lead intoxication resulted in significant (P < 0.05) reduction of the number of head dips
in the holeboard test and the time spent in the open arm of the elevated plus maze test, compared
with the control. Intoxication also induced increased pain sensitivity, as shown by significant
(P < 0.05) reduction in the tail flick latency and increase in the frequency of abdominal
constrictions in the writhing test. The periods of immobility in both tail suspension and
forced swimming tests in intoxicated animals were greater, as compared with the control.
Coadministration of vitamin E with lead in group 3 significantly (P < 0.05) reversed all the
mentioned shifts (increased the number of head dips and time spent in the maze open arm,
increased the tail flick latency, decreased the frequency of writhings, and decreased the periods
of immobility in the forced swimming and tail suspension tests). Thus, vitamin E treatment
is capable of effectively attenuating the negative neurobehavioral consequences of lead
intoxication.
Keywords: lead intoxication, vitamin E, neurobehavioral indices, anxiety, pain,
depression.
1 Department of Physiology, College of Medicine, University of Ibadan,
Ibadan, Nigeria.
Correspondence should be addressed to G. F. Ibironke
(e mail: gibironk@yahoo.com).
INTRODUCTION
Heavy metals, in particular lead, are extensively used
in industry, building, and everyday life; they represent
important factors in contemporary contamination
of the environment. Most heavy metals do not play
known physiological roles in the organism, but their
harmful effects are obvious.
Lead intoxication strongly influences negatively
a variety of biological process in many organs and
tissues; its effects on the nervous system are especially
significant [1�. Although the use of lead in various
spheres has at present been minimized, exposure to
this factor still creates strong biological risks due to
its stable presence in the environment.
Common sources of lead include some paints,
contaminated dust, and drinking water [2�; ingestion,
inhalation, and dermal contacts are common routes
of exposure [3�. Children are more vulnerable to lead
exposure due, in part, to a high rate of absorption
after ingestion [4�; in this part of the population, lead
intoxication induces irreversible learning and behavioral
deficits. Thus, a search for ways of ameliorating the
negative effects of chronic lead exposure is urgent.
Various food supplements were proposed for this
purpose. Among them, there is βtocopherol, a form of
vitamin E characterized by very high antioxidant activity.
Vitamin E is a fatsoluble vitamin found in significant
amounts in vegetable oils, cereals, meat, poultry eggs,
fruits, and some vegetables. This vitamin may exert some
positive effects in diabetes [6�. A number of clinical trials
and a smaller number of supplementation studies were
carried out to investigate the effects of βtocopherol
in cardiovascular diseases, but with largely negative
results [7�. Information on the effects of βtocopherol in
the case of lead toxicity is very scarce. We attempted
to test the usefulness of vitamin E supplementation
on neurobehavioral alterations in mice induced by
experimental chronic lead intoxication.
METHODS
Animals. Male albino Swiss mice (2030 g) were used
in the study. The animals were housed and bred in the
NEUROPHYSIOLOGY / НЕЙРОФИЗИОЛОГИЯ.—2014.—T. 47, № 3296
G. F. IBIRONKE and S. T. ADU
preclinical animal house of the College of Medicine,
University of Ibadan, Nigeria. They were kept under
standard vivarium conditions (room temperature and
12/12 h lightdark cycle), fed with standard mouse
cubes (Ladokun Feeds, Nigeria), and provided with
water ad libitum.
The animals were randomly divided into three
groups with six mice in each. Within the exposure
period (90 days), mice of group I (control) received
perorally (p.o.) normal saline (10 ml/kg), group II
received also p.o. 3000 mg/kg of lead acetate, and
group III received a combination of 3000 mg/kg
of lead acetate and 13 IU vitamin E. Lead acetate
trihydrate (Oxford Laboratory, India) was dissolved in
drinking water. Vitamin E was obtained from a local
pharmaceutical outfit (Ibadan, Nigeria).
Hole Board Test. The standard test was carried out
on a wooden board (40 × 40 cm) with 16 evenly spaced
holes, as previously described [8�. The number of head
dips into holes within a 5minlong observation period
was counted.
Elevated Plus Maze Test. The standard version of
the test was used. The time spent by an animal during
the observation period in the open arm of the maze
characterized the level of anxiety.
In all the above experiments, the arenas were
cleaned after each test with 70% alcohol to eliminate
olfactory bias.
Tail Withdrawal Test. A modification of the
original tail flick test was used [10�. The animal was
gently handheld with a piece of towel, and a terminal
3cmlong segment of the tail was immersed in a water
bath maintained at 52 ± 0.2°C. The time taken for the
animal to flick its tail out of water was taken as the tail
withdrawal latency.
Acetic Acid Writhing Test. The test was carried out
as previously described [9�. Acetic acid (0.2 ml, 3%)
was injected i.p. to induce the characteristic writhings.
The number of the latter occurring between the 5th and
10th min post injection was measured.
Tail Suspension Test. The tail suspension test (TST)
was performed according to the method described
earlier [11�. Mice were individually suspended 60
cm above the surface of a table with an adhesive
tape placed 1 cm away from the tip of the tail. The
immobility duration was recorded within the last 5 min
during 6 min of observation. Mice were considered
immobile only when they hung passively and were
completely motionless.
Forced Swimming Test. A standard variant of this
test was used. Mice were put into cold water (10 °C),
and the period of immobility before attempts to swim
was measured.
RESULTS
Effects of Lead Intoxication and Its Treatment
With Vitamin E on the Level of Anxiety. Chronic
intoxication with lead (group 2) induced significant
(P < 0.05) reductions in the frequency of head dips
in the holeboard test and the duration of stay of the
tested mice in the open arm of the elevated plus maze,
as compared with the control group 1. In the former
test, the difference from the control values (decrement)
was about 47%, while in the latter test it was about
24% (Fig. 1A, B). When peroral introduction of lead
acetate was combined with administration of vitamin
E (group 3, lead + vitamin E), these negative effects
were neutralized, and the respective indices (numbers
of head dips and time spent for exploration of the
open arm) even somewhat (insignificantly, P > 0.05)
exceeded the control data. At the same time, these
values in group 3 significantly (P < 0.05) exceeded the
respective values in group 2 (lead alone) (Fig. 1A, B).
40
35
30
25
20
15
10
5
0
*
#
A
B120 sec
100
80
60
40
20
*
#
0
F i g. 1. Effects of lead and vitamin E on the indices characterizing
the anxiety level. A) Number of head dips in the holeboard test;
B) time, sec, spent in the open arm of the elevated plus maze. Groups
13 are the control, treated with lead acetate alone, and treated with
lead acetate + vitamin E, respectively. Means ± s.e.m are shown,
n = 6 in each group. *P < 0.05 compared with the control (group 1);
#P < 0.05 compared with group 2.
Р и с. 1. Впливи свинцю та вітаміну Е на показники, що харак
теризують рівень тривожності.
NEUROPHYSIOLOGY / НЕЙРОФИЗИОЛОГИЯ.—2015.—T. 47, № 3 297
NEUROBEHAVIORAL CONSEQUENCES OF CHRONIC LEAD INTOXICATION
Effects of lead intoxication and its treatment
with vitamin E on the results of the open field
test. Chronic lead intoxication noticeably suppressed
locomotion activities (mean number of crossed
squares) in the above test; the respective index in
group 2 was only 76% of that in the control group 1.
The treatment with vitamin E neutralized this negative
shift, and locomotor activity in group 3 was even more
intense than in the control (Fig. 2). Lead intoxication
also significantly suppressed orientation/research
activity of mice (number of stands) and grooming
activity. The treatment with vitamin E in group 3
provided considerable correction effects on the
respective indices.
Effects of lead intoxication and its treatment
with vitamin E on the pain sensitivity. Lead
intoxicated mice demonstrated increased sensitivity
to thermal pain stimulation in the tailflick test. The
mean latency of the tailflick reaction in group 2 was
equal to 47% of that in the control group (P < 0.05,
Fig. 3A). The sensitivity of animals with respect to
chemically induced visceral pain in the writhing test
was also significantly higher than that in the control;
the increment in the mean number of writhings was
about 31% (P < 0.05, Fig. 3B). Parallel treatment
of intoxicated mice with vitamin E completely
neutralized negative consequences of lead intoxication
(in comparison of group 3 with group 2, P < 0.05 in
both tests) and even provided rather intense analgesic
effects, as compared with the control group 1
(Fig. 3A, B).
*
#
250
200
150
100
50
0
F i g. 2. Mean values of the locomotion activities observed in the
open field test in the control and treated groups. Designations are
the same as in Fig. 1.
Р и с. 2. Середні індекси локомоторної активності в тесті від
кри того поля у мишей контрольної та експериментальної груп.
100
90
80
70
60
50
40
30
20
10
0
*
#
B
A
Effects of lead intoxication and its treatment
with vitamin E on the depression-related indices.
In group 2 (administration of lead acetate alone), the
average period of immobility in the tail suspension
test was 16% longer than that in the control group 1
(P < 0.05). The treatment of leadintoxicated mice with
vitamin E (group 3) significantly (P < 0.05) decreased
F i g. 3. Effects of lead and vitamin E on the sensitivity to pain. A)
Tail flick latency, sec; B) number of writhings within the observation
period. Designations are the same as in Figs. 1 and 2.
Р и с. 3. Впливи свинцю та вітаміну Е на чутливість до болю.
120
100
80
60
40
20
*
*
0
F i g. 4. Effects of lead and vitamin E on the indices characterizing
the level of depression. A) Period of immobility, sec, in the
tail suspension test, sec; B) that in the forced swimming test.
Designations are the same as in Figs. 13.
Р и с. 4. Впливи свинцю та вітаміну Е на показники, що
характеризують рівень депресії.
A
3.0
sec
sec
2.5
2.0
1.5
1.0
0.5
*
#
0
40
35
30
25
20
15
10
5
*
#
0
B
NEUROPHYSIOLOGY / НЕЙРОФИЗИОЛОГИЯ.—2014.—T. 47, № 3298
G. F. IBIRONKE and S. T. ADU
the respective time interval, as compared with that
in group 2 (Fig. 4A). Nearly the same situation was
observed in the force swimming test. The mean period
of immobility in group2 mice exceeded by 32%
the corresponding index in control mice (group 1).
A quite comparable decrease in this index related to
introduction of vitamin E was observed in group 3
compared with group 2 (Fig. 4B).
DISCUSSION
In our study, we examined the effects of chronic
lead intoxication (peroral introduction) on a few
neurobehavioral indices in mice and the effects of
treatment with vitamin E on the respective alterations.
The results obtained demonstrated a clear ability of
vitamin E (in the doses tested) to reverse negative
behavioral changes induced by chronic lead ingestion.
Lead intoxication resulted in a clear increase in
the level of anxiety in tested animals. Manifestations
of orientation/research activity (characterized by the
number of muzzle dips in the openings of the hole
board plate and time spent in the open arm of the
elevated plus maze) in leadintoxicated mice were
noticeably smaller than the respective values in the
control. These shifts toward greater values of anxiety
in group2 mice were effectively neutralized by
accompanying treatment with vitamin E in group 3.
Ingestion of large amounts of lead also resulted
in the development of noticeable hyperalgesia in
experimental mice of group 2. This was demonstrated
by an about twofold drop of the tail flick latency
(thermally evoked somatic pain) and a noticeable
increase in the intensity of writhings in the respective
test (chemically induced visceral pain). These negative
shifts were removed by the treatment with vitamin E,
and even relative hypoalgesia was observed in group3
mice in both abovementioned tests.
Quite comparable results were obtained in the tail
suspension and forced swimming tests. In both tests,
the initial periods of immobility (which is usually
interpreted as an index of the depression level) were
in leadintoxicated mice noticeably longer than those
in the control. Again, these negative shifts could be
effectively removed by the E vitamin treatment.
Thus, chronic lead intoxication provides clear
anxiogenic and depressive effects and increases in
the sensitivity to somatic and visceral pain. Co
administration of vitamin E effectively removed the
negative effects of lead. The orientation/research
activity of the intoxicated mice is intensified,
locomotor activity in the open field test increased, and
hyperalgesia in group2 mice is replaced by relative
hypoalgesia in group3 animals. In other words,
vitamin E is a rather effective means for amelioration
of negative behavioral effects of lead intoxication.
Antioxidants, in general, have been shown to inhibit
apoptosis [2�, a mechanism supposed to contribute to
the development of lead neurotoxicity. Since vitamin
E is a powerful antioxidant, this mechanism might in
part be responsible for amelioration of the respective
neurotoxic effect.
Oxidative damage was shown to be associated with
the molecular mechanism of lead poisoning [12�.
Lead is capable of easily penetrating the bloodbrain
barrier, thereby making the brain easily susceptible
to freeradical damage and, hence, oxidative
stress. Our data convincingly demonstrate that lead
neurotoxicity is due, to a considerable extent, to
the development of such stress because vitamin E,
as a powerful antioxidant, effectively removes the
respective negative neurobehavioral shifts. No doubt,
other mechanisms of lead intoxication and effects
counteracting this intoxication cannot be ruled out and
should be examined in the future.
In conclusion, our study demonstrated that
vitamin E, when coadministered with lead acetate,
significantly reversed negative neurobehavioral
alterations induced by chronic lead ingestion. This
vitamin, therefore, might be of clinical importance in
the management of lead poisoning.
All experimental protocols were in agreement with the
internationally accepted ethical norms and with the guidelines
of the Ethics Committe of the College of Medicine, University
of Ibadan, Nigeria.
The authors of this study, G. F. Ibironke and S. T. Adu, confirm
that the research and publication of the results were not
associated with any conflicts regarding commercial or financial
relations, relations with organizations and/or individuals who
may have been related to the study, and interrelations of co
authors of the article.
NEUROPHYSIOLOGY / НЕЙРОФИЗИОЛОГИЯ.—2015.—T. 47, № 3 299
NEUROBEHAVIORAL CONSEQUENCES OF CHRONIC LEAD INTOXICATION
Г. Ф. Ібіронке1, С. Т. Аду1
НЕЙРОПОВЕДІНКОВІ НАСЛІДКИ ХРОНІЧНОГО
ОТРУЄННЯ СВИНЦЕМ: КОРЕКЦІЙНІ ВПЛИВИ
ВІТАМІНУ Е
1Медичний коледж Ібаданського університету, Ібадан
(Нігерія).
Р е з ю м е
Ми досліджували зміни нейроповедінкових показників у
мишей, викликані хронічним пероральним уведенням аце
тату свинцю, та корекцію цих змін за допомогою вітаміну
Е. Тварини були поділені на три групи: контрольну групу 1,
що отримувала фізіологічний розчин (10 мл/кг), та групи
2 і 3, котрим протягом 90 діб уводили 3000 мг/кг ацетату
свинцю ізольовано або в комбінації з 13 М.О. вітаміну Е
відповідно. Свинцева інтоксикація зумовлювала істотне
(P < 0.05) зменшення кількості зазирань в отвори під час
проходження тесту «отвори в дошці» та часу, проведеного
у відкритих рукавах «підвищеного» лабіринту. Інтоксика
ція також призводила до підвищення чутливості до болю,
про що свідчили істотні скорочення латентного періоду від
смикування хвоста та збільшення кількості «корчів», інду
кованих уведенням оцтової кислоти, у відповідних тестах.
Періоди нерухомості у тестах підвішування за хвіст та при
мусового плавання в інтоксикованих тварин були довши
ми, ніж у контролі. Паралельне уведення вітаміну Е тва
ринам групи 3 істотно (P < 0.05) нейтралізувало вказані
негативні зрушення. Ставали більшими число зазирань в
отвори та час, проведений у відкритих рукавах лабіринту;
латентний період відсмикування хвоста подовжувався, а
число «корчів» зменшувалося; періоди імобілізації у зга
даних вище тестах скорочувалися. Отже, вітамін Е, будучи
потужним антиоксидантом, ефективно згладжує негативні
нейроповедінкові наслідки свинцевої інтоксикації.
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|
| id | nasplib_isofts_kiev_ua-123456789-148196 |
| institution | Digital Library of Periodicals of National Academy of Sciences of Ukraine |
| issn | 0028-2561 |
| language | English |
| last_indexed | 2025-12-07T13:37:25Z |
| publishDate | 2015 |
| publisher | Інститут фізіології ім. О.О. Богомольця НАН України |
| record_format | dspace |
| spelling | Ibironke, G.F. Adu, S.T. 2019-02-17T17:09:20Z 2019-02-17T17:09:20Z 2015 Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation / G.F. Ibironke, S.T. Adu // Нейрофизиология. — 2015. — Т. 47, № 3. — С. 295-299. — Бібліогр.: 12 назв. — англ. 0028-2561 https://nasplib.isofts.kiev.ua/handle/123456789/148196 615.099.092:577.161.3 We investigated the effects of vitamin E supplementation on neurobehavioral alterations induced by chronic ingestion of lead acetate in mice. The animals were divided into three main groups, group 1 (control) given with normal saline (10 ml/kg) and groups 2 and 3 given with 3000 mg/kg lead acetate alone and in combination with 13 IU of vitamin E, respectively, for a period of 90 days. Lead intoxication resulted in significant (P < 0.05) reduction of the number of head dips in the hole-board test and the time spent in the open arm of the elevated plus maze test, compared with the control. Intoxication also induced increased pain sensitivity, as shown by significant (P < 0.05) reduction in the tail flick latency and increase in the frequency of abdominal constrictions in the writhing test. The periods of immobility in both tail suspension and forced swimming tests in intoxicated animals were greater, as compared with the control. Co-administration of vitamin E with lead in group 3 significantly (P < 0.05) reversed all the mentioned shifts (increased the number of head dips and time spent in the maze open arm, increased the tail flick latency, decreased the frequency of writhings, and decreased the periods of immobility in the forced swimming and tail suspension tests). Thus, vitamin E treatment is capable of effectively attenuating the negative neurobehavioral consequences of lead intoxication. Ми досліджували зміни нейроповедінкових показників у мишей, викликані хронічним пероральним уведенням ацетату свинцю, та корекцію цих змін за допомогою вітаміну Е. Тварини були поділені на три групи: контрольну групу 1, що отримувала фізіологічний розчин (10 мл/кг), та групи 2 і 3, котрим протягом 90 діб уводили 3000 мг/кг ацетату свинцю ізольовано або в комбінації з 13 М.О. вітаміну Е відповідно. Свинцева інтоксикація зумовлювала істотне (P < 0.05) зменшення кількості зазирань в отвори під час проходження тесту «отвори в дошці» та часу, проведеного у відкритих рукавах «підвищеного» лабіринту. Інтоксикація також призводила до підвищення чутливості до болю, про що свідчили істотні скорочення латентного періоду відсмикування хвоста та збільшення кількості «корчів», індукованих уведенням оцтової кислоти, у відповідних тестах. Періоди нерухомості у тестах підвішування за хвіст та примусового плавання в інтоксикованих тварин були довшими, ніж у контролі. Паралельне уведення вітаміну Е тваринам групи 3 істотно (P < 0.05) нейтралізувало вказані негативні зрушення. Ставали більшими число зазирань в отвори та час, проведений у відкритих рукавах лабіринту; латентний період відсмикування хвоста подовжувався, а число «корчів» зменшувалося; періоди імобілізації у згаданих вище тестах скорочувалися. Отже, вітамін Е, будучи потужним антиоксидантом, ефективно згладжує негативні нейроповедінкові наслідки свинцевої інтоксикації. en Інститут фізіології ім. О.О. Богомольця НАН України Нейрофизиология Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation Нейроповедінкові наслідки хронічного отруєння свинцем: корекційні впливи вітаміну Е Article published earlier |
| spellingShingle | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation Ibironke, G.F. Adu, S.T. |
| title | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation |
| title_alt | Нейроповедінкові наслідки хронічного отруєння свинцем: корекційні впливи вітаміну Е |
| title_full | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation |
| title_fullStr | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation |
| title_full_unstemmed | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation |
| title_short | Neurobehavioral Consequences of Chronic Lead Intoxication: Effects of Vitamin E Supplementation |
| title_sort | neurobehavioral consequences of chronic lead intoxication: effects of vitamin e supplementation |
| url | https://nasplib.isofts.kiev.ua/handle/123456789/148196 |
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