Post on 04-Nov-2015
227 Views
Preview:
DESCRIPTION
TRANSCRIPT
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
160
IMPACT OF SLEEP DEPRIVATION AND SLEEP RECOVERY
ON REPRODUCTIVE HORMONES AND TESTICULAR
OXIDATIVE STRESS IN ADULT MALE RATS
Ebtihal A. Abd El-Aziz And Dalia G. Mostafa
Department.of Physiology, faculty of Medicine, Assiut University
ABSTRACT
Objectives: sleep deprivation is a significant problem among adult men. It
is considered to be a risk factor that contributes to several disease. It has been
proposed that reactive oxygen species and the resulting oxidative stress may be
responsible for some of the effects of sleep deprivation. The present study was
performed to determine the impact of sleep deprivation for different periods on
serum testosterone, luteinizing hormone, corticosterone and whether sleep
deprivation causes oxidative stress indicated by measuring malondialdehyde
(MDA) level in testicular tissue as a direct evidence of cellular damage and
measuring glutathione (GSH) in testicular tissue to determine possibility of
reversible nature of oxidative stress by scavenger antioxidant system. We
studied also if sleep recovery after sleep loss could relieve these effects or not.
Material and methods: 42 adult male albino rats aged 12 weeks weighing about
200-250 gm were used in this study. They were divided into seven groups, six
animals in each group, a control group and six experimental groups. Three
experimental groups were used as sleep deprivation (SD) groups and another
three experimental groups were used as sleep recovery (SR) groups. The SR
groups were also sleep deprived and then returned to home-cages and were
allowed to undisturbed and spontaneous sleep. Group I: served as a control
group. Group II: rats were subjected to sleep deprivation for one day. Group
III: rats were subjected to sleep deprivation for three days. Group IV: rats were
subjected to sleep deprivation for five days. Group V: rats were subjected to
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
161
sleep deprivation for three days followed by a period of sleep recovery for one
day. Group VI: rats were subjected to sleep deprivation for three days followed
by a period of sleep recovery for three days. Group VII: rats were subjected to
sleep deprivation for three days followed by a period of sleep recovery for five
days. After each planned SD and SR period, blood samples were collected for
hormonal assay. The rats were decapitated and the testes were dissected out
and used for the study of malondialdehyde and glutathione. The parameters
were measured then analyzed by using Student's t-test. Results: serum
testosterone level and luteinizing hormone (LH) showed significant decrease
after three days of deprivation. Serum corticosterone level increased
significantly from the first day of deprivation in comparison with the control
group. After five days of sleep recovery, serum testosterone level and
corticosterone returned to the level of the control group. Serum LH level
improved after three days of sleep recovery. Sleep deprivation increased the
testicular tissue MDA significantly and GSH was significantly decreased after
three day of sleep deprivation when comparing with the control. Sleep recovery
decreased testicular tissue MDA significantly and significant increase in GSH
after the fifth day as non-significant change noticed on comparing their levels
on that day with the control. Conclusions: The present study demonstrated the
sleep deprivation effects on testosterone, luteinizing hormone, corticosterone
levels in serum, malondialdehyde and glutathione in testicular tissue of rat.
Sleep recovery was associated with restoration of the serum hormone levels.
Also with sleep recovery MDA level was decreased and GSH content was
improved in testicular tissue.
Key words: sleep deprivation, sleep recovery, testosterone hormone ,
luteinizing hormone, corticosterone hormone , malondialdehyde and
glutathione
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
162
INTRODUCTION
Sleep deprivation is a significant problem among adult men (Andersen et
al., 2005 and Andersen & Tufik, 2008). It is considered to be a risk factor that
contributes to several disease processes (Wu et al., 2011) via its ability to alter
behavioral (Andersen et al., 2000 & 2003), hormonal (Andersen et al., 2004 &
2005) and neurochemical pathways (Martins et al., 2004 and Pedrazzoli et al.,
2004). Sleep deprivation is one of the consequences of the pressure from society
on individuals, impacting their health and wellbeing (Tufik et al., 2009).
In rodents, sleep interference causes alterations in several aspects of
physiological and behavioral functioning, such as sexual behavior (Alvarenga et
al., 2009 and Andersen et al., 2009), memory (Alvarenga et al., 2008), anxiety
(Suchecki et al., 2002), attention (Godoi et al., 2005), hormonal changes
(Antunes et al., 2006), and damage to the immune system (Zager et al., 2009).
Several studies have shown that sleep deprivation reduces circulating
androgens in healthy men including testosterone (Eacker et al., 2008 and Maia
et al., 2011). Decreased testosterone levels can impair gonadal and sexual
functions, and potentially result in decreased fertility (Luboshitzky et al., 2002).
Circulating testosterone levels are known to increase during sleep (Corts-
Gallegos et al., 1983).
The control of androgen production from the Leydig cell is dependent
upon the episodic secretion of LH hormone, which is released in pulses from the
anterior pituitary gland (Dufau et al., 1984).
Sleep deprivation involves some degree of stress which results in
stimulation of hypothalamicpituitaryadrenal axis (HPA axis). This stimulation
can result in an increase in the plasma level of corticosterone and a concomitant
change in testosterone (Suchecki and Tufik, 2000), mediated by a change in LH
(Demura et al., 1989).
Sleep deprivation per se causes changes in lipid peroxidation or in
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
163
antioxidant defenses. Oxidative stress is a condition associated with an
increased rate of cellular damage induced by oxygen derived oxidants
commonly known as reactive oxygen species (ROS). ROS are reported to
damage almost all macromolecules of the cell, including polyunsaturated fatty
acids of membranes, thus causing impairment of cellular functions (Halliwell,
1996). Testicular membranes are extremely rich in polyunsaturated fatty acids
therefore; the organ is highly susceptible to oxidative stress (Manna et al.,
2003). Sleep after sleep deprivation is widely considered to have restorative
properties; free radicals accumulate during wakefulness and are removed during
sleep (Everson et al., 2005).
AIM OF THE STUDY
The present study was designed to determine the impact of sleep
deprivation for different periods on serum testosterone, luteinizing hormone,
corticosterone and whether sleep deprivation causes oxidative stress indicated
by measuring MDA level in testicular tissue as a direct evidence of cellular
damage and measuring GSH in testicular tissue to determine the possibility of
reversible nature of oxidative stress by scavenger antioxidant system and
whether sleep recovery after sleep loss could relieve these effects or not.
MATERIAL AND METHODS
Animals and groups:
42 adult male albino rats aged 12 weeks weighing about 200-250 gm were
used in this study. The rats were housed in animal house of Assiut University in
standard cages in normal room temperature with normal lightdark cycle. Food
and water were provided ad libitum. They were divided into seven groups, six
animals in each group, a control group and six experimental groups. The control
group was allowed to undisturbed, spontaneous sleep.
Rats were subjected to sleep deprivation according to Bergmann et al.
(1989) with slight modification by placing the animal on the top of a bottle
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
164
filled with water, the diameter of which is small relative to the animal's size.
The bottle is placed in a large tanks filled with water to be 5 cm less than the top
of the bottle. The animal is able to rest on the top of a bottle and if it began to
sleep, muscular relaxation occurred which result in either fall into the water
and clamber back to its site on the top of the bottle or get its nose wet enough to
awaken it. The water in the tanks was changed daily, throughout the SD period.
So the groups are classified as follows:
Group I: served a control group.
Group II: subjected to sleep deprivation for one day.
Group III: subjected to sleep deprivation for three days.
Group IV: subjected to sleep deprivation for five days.
Group V: subjected to sleep deprivation for three days then followed by a
period of sleep recovery for one day.
Group VI: subjected to sleep deprivation for three days then followed by a
period of sleep recovery for three days.
Group VII: subjected to sleep deprivation for three days then followed by a
period of sleep recovery for five days.
Blood sampling and hormone determination:
After each planned SD and SR period, blood samples were collected from
the retro-orbital venous plexus before sacrifice. The whole blood was incubated
to clot for 30 minutes and serum was separated by centrifugation. The separated
serum was stored frozen at -20 oC until use. Samples were assayed for
testosterone, luteinizing hormone and corticosterone by ELISA method using
available Kits according to manufacture. Testosterone hormone levels in serum
were determined using ELISA kit Coate A count kit from diagnostic product
corporation Los Anglos (A 90045 5597 USA). Luteinizing hormone levels in
serum were determined using rat ELISA kit cattalloge No.E0830Rb according
to manufacture. Corticosterone hormone in serum was determined using Assay
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
165
Max Corticosterone ELISA kit Catalloge No EC3001- 1 according to
manufacture.
Testicular tissue Collection
After each planned SD and SR period, the rats were decapitated; the testes
were dissected out and used for the study of lipid peroxidation and glutathione.
The tissues of testes of different groups were homogenized in ice-cold 100 mM
phosphate buffer (pH7.4). The obtained supernatants were used for estimation
of lipid peroxidation (malondialdehyde) and GSH. MDA was estimated by
method according to (El-Shahat et al., 2009). GSH was measured by following
the standard method (Ellman, 1959).
Statistical analysis
Data were expressed as mean SD for all parameters then analyzed using
Student's t-test. P values less than 0.05 were considered significant.
RESULTS
Serum testosterone (table 1 & 2, Fig. 1 & 2)
Serum testosterone level showed non-significant decrease after one day of
sleep deprivation (5.5 0.7 ng/ml) in comparing with the control (5.9 0.8
ng/ml). The level decreased significantly after three (4.6 0.5 ng/ml) and five
(2.9 0.7 ng/ml) days of deprivation.
After one day of sleep recovery, serum testosterone level (4.7 0.4 ng/ml)
still significantly lower than that of the control group (5.9 0.8 ng/ml) but non-
significant changes were noticed in comparison with the three days deprivation
(4.6 0.5 ng/ml) group.
After three days of sleep recovery, serum testosterone level (4.8 0.6
ng/ml) was still significantly lower than that of the control group (5.9 0.8
ng/ml) but non-significantly changed in comparison with the three days of sleep
deprivation (4.6 0.5 ng/ml) group.
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
166
After five days of sleep recovery, serum testosterone level (5.8 0.9
ng/ml) returned to the control group (5.9 0.8 ng/ml) and non-significantly
changed on comparing both. There was significant increase on comparing them
with the three days of deprivation (4.6 0.5 ng/ml).
Serum luteinizing hormone (table 1&2, Fig. 3&4)
Serum luteinizing hormone levels after sleep deprivation for one, three and
five days were 6.03 0.3 ng/ml, 4.2 0.5 ng/ml and 2.8 0.3 ng/ml,
respectively. The effect of sleep deprivation on serum luteinizing hormone
started from the third day onward. Significant decrease was reported on
comparing three and five days sleep deprivation with the control (6.5 0.5
ng/ml).
Serum luteinizing hormone level improved earlier from the third day of
recovery. After one day of sleep recovery, serum luteinizing hormone level (3.1
0.1 ng/ml) was non-significantly lower than that of three days sleep
deprivation (4.2 0.5 ng/ml), but significantly lower than that of the control
group (6.5 0.5 ng/ml).
After three days of sleep recovery, serum luteinizing hormone level (6.3
0.7 ng/ml) was significantly higher than that of the three days sleep deprivation
(4.2 0.5 ng/ml) but no significant changes in comparison with the control
group (6.5 0.5 ng/ml).
After five days of sleep recovery, serum luteinizing hormone level (6.8
0.7 ng/ml) was significantly higher than that of the three days sleep deprivation
(4.2 0.5 ng/ml) but no significant changes on comparing with the control
group (6.5 0.5 ng/ml).
Serum corticosterone (table 1&2, Fig. 5&6)
Sleep deprivation increased the serum corticosterone from the first day,
significant increase was reported on comparing the sleep deprivation groups of
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
167
the three periods with that of the control (137.3 8.2 ng/ml) vs (147.5 5.3
ng/ml, 168.2 9.4 ng/ml and 192.4 6.1 ng/ml) respectively.
Serum corticosterone of the animals that underwent sleep recovery for one
day (158.0 8.6 ng/ml), three days (150.3 5.1 ng/ml) and five days (138.5
2.0 ng/ml). Non-significant change was noticed only on comparing the five days
recovery with the control group (137.3 8.2 ng/ml). Highly significant decrease
in serum corticosterone level of the three and five days recovery groups on
comparing with the three days sleep deprivation group (168.2 9.4 ng/ml).
Testicular tissue MDA (table 3, Fig. 7)
Sleep deprivation increased the testicular tissue MDA from the first day.
Significant increase was reported after three and five day of sleep deprivation on
comparing with that of the control (8.62 0.7 mole/g tissue). One day sleep
deprivation was (8.97 0.8 mole/g tissue), three days sleep deprivation (9.55
0.8 mole/g tissue) and five days sleep deprivation (11.96 0.9 mole/g tissue).
Sleep recovery improved testicular tissue MDA after the fifth day as non-
significant change noticed on comparing its level with the control. One day
sleep recovery was (9.82 0.7 mole/g tissue), three days sleep deprivation
(9.59 0.5 mole/g tissue) and five days sleep deprivation (8.79 0.9 mole/g
tissue).
Testicular tissue glutathione (table 3, Fig. 8)
Sleep deprivation decreased the testicular tissue glutathione from the first
day. Significant decrease was reported after three and five days of sleep
deprivation on comparing with that of the control (310.0 13.2 nmol/mg
protein). One day sleep deprivation was (304.0 10.4 nmol/mg protein), three
days sleep deprivation (284.0 13.8 nmol/mg protein) and five days sleep
deprivation (270.0 17.1 nmol/mg protein). On the fifth day, sleep recovery
returned testicular tissue glutathione to control level as non-significant change
noticed on comparison with the control. One day sleep recovery was (285.0
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
168
20.6 nmol/mg protein), three days sleep deprivation (287.0 9.5 nmol/mg
protein) and five days sleep deprivation (305.0 19.4 nmol/mg protein).
Table (1): Serum testosterone, luteinizing hormone and corticosterone
concentrations of rats that underwent sleep deprivation (SD) for different
durations.
Testosterone
(ng/ml) P
(SDvC)
Luteinizing
hormone
(ng/ml)
P
(SDvC)
Corticosterone
(ng/ml) P
(SDvC)
Control 5.9 + 0.8 6.5+ 0.5 137.3+ 8.2
SD1 5.5 + 0.7 0.4ns 6.03+ 0.3 0.1ns 147.5+ 5.3 0.03*
SD3 4.6 + 0.5 0.02* 4.2+ 0.5 0.002** 168.2+ 9.4 0.002**
SD5 2.9 + 0.7 0.0001*** 2.8+ 0.3
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
169
Table (3): Testicular Malondialdehyde level (MDA) and glutathione of rats
that underwent sleep deprivation (SD) and sleep recovery (SR) for different
durations.
MDA(moles/g
tissue) P
Glutathione
(nmol/mg protein) P
Control 8.62+ 0.7 310.0+ 13.2
SD1 8.97+ 0.8 (SD1vC) 0.1 ns 304.0+ 10.4 (SD1vC)0.2 ns
SD3 9.55+ 0.8 (SD3vC)0.03* 284.0+ 13.8 (SD3vC)0.02*
SD5 11.96+ 0.9 (SD5vC)0.002** 270.0+ 17.1 (SD5vC)0.006**
SR1 9.82+ 0.7 (SR1vC)0.04* 285.0+ 20.6 (SR1vC)0.03*
SR3 9.59+ 0.5 (SR3vC)0.03* 287.0+ 9.5 (SR3vC)0.03*
SR5 8.79+ 0.9 (SR5vC)0.8ns 305.0+ 19.4 (SR5vC)0.6ns
-
1-lppuS ,2102 ,peS ,3 .N ,01 .loV ,JMAA
071
-
AFATSOM .G AILAD dna ZIZA-LE DBA .A LAHITBE
171
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
172
DISCUSSION
Sleep deprivation is a known physiological stressor and considered as a
major problem for in males (Wu et al., 2011 and Meerlo et al., 2008). The
activation of hypothalamo-pituitary-adrenocortical system and the sympatho-
adrenomedullary system was considered to be the main regulators of the stress
response (Reeder and Kramer, 2005, Joels et al., 2007 and McEwen et al.,
2007). So, the current study tried to focus on the effects of sleep deprivation and
recovery of different durations on changes of male reproductive hormones;
serum testosterone, luteinizing hormone and corticosterone levels in adult male
rats.
Our model for sleep deprivation was described as a good physiological
stressor as it produces alterations in almost all studied hormones (Knutson et al.,
2007). We compared our results of sleep recovery with sleep deprivation of the
third day because at that day we get establish socially stable group animals,
thereby obviating other possible stress variables (Suchecki & Tufik, 2000 and
Suchecki et al., 2002).
We studied the effect of SD from the 1st day up to the 5th day as Andersen
et al. (2002 & 2004), Andersen and Tufik (2008) and Eacker et al. (2008)
reported that testosterone concentrations were decreased following one to four
days of SD and this reduction was further enhanced with longer durations of
SD.
The present study estimated the serum levels of testosterone, luteinizing
hormone and corticosterone after recovery period from the 1st day up to the 5th
day trying to estimate the time elapsed to return to the resting level.
Our study revealed reduction in serum testosterone levels after SD and the
level decreased significantly after three to five days of deprivation. The same
results were reported by Amikishieva et al., 2001 and Dong et al., 2004 (for
mice), Almedia et al., 2000 and Manna et al., 2004 (for rats), and Oltmanns et
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
173
al., 2005 (humans). The reduction was explained according to Rajaratnam &
Arendt (2001) and Mazaro & Lamano-Carvalho (2006) by stress. The synthesis
of testosterone is dependent on endocrine (Rajaratnam & Arendt, 2001) and
neuronal (Roman et al. 2006) signals which in turn are influenced by
physiological conditions such as stress. Stress in fact results in secretion of
several hormones such as, CRH (Rivest and Rivier, 1991), ACTH (Ishikawa et
al., 1992 and Monder et al., 1994), and corticosterone (Suchecki & Tufik, 2000
and Machado et al., 2010) on HPG axis function. Although the mechanism(s)
for these effects on reproductive function are not fully elucidated, possible sites
of action include: (1) a centrally mediated inhibition of gonadotropin releasing
hormone (GnRH) release by CRH, opioids and glucocorticoids (MacLusky et
al., 1988; ); (2) glucocorticoid-induced tissue resistance to gonadal sex steroids
(Rabin et al., 1990), decreasing the sensitivity of Leydig cells to LH, or
decreasing testicular receptors to this hormone (Payne & Youngblood, 1995);
(3) direct gonadal effects of glucocorticoids with subsequent alterations in sex
steroid output (Hardy and Ganjam, 1997), corticosterone reduce testosterone
production in Leydig cells and to induce apoptosis in these cells (Gao et al.,
2002, Retana-Mrquez et al., 2003 and) (4) a glucocorticoid-mediated decrease
in pituitary responsiveness to GnRH, resulting in decreased LH secretion
(Chichinadze & Chichinadze, 2008).
The decreased testosterone levels associated with SD may be in part due to
serotonin-related inhibition of testosterone production (Gao et al., 2002 and
Meerlo et al., 2008). In addition, both serotonin and serotonin receptors have
been localized in Leydig cells isolated from the testes of golden hamsters and
serotonin has also been demonstrated to inhibit testosterone production
(Frungieri et al., 2002).
Kraut et al. (2004), Hones & Marin, (2006) and McEwen (2007) explained
the decrease in testosterone level during SD by decrease in the blood flow to
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
174
the testicles (less vital organs) leading to suppression of its activity during stress
in order to maximally increase the resources supplied to organs critically
important for adaptation.
In our study we observed that a decrease of LH levels were associated with
a decrease of testosterone levels in SD. This was in agreement with Almeida et
al., 2000 and Manna et al., 2004 (in rat), Stackpole et al., 2003 & Wingfield &
Sapolsky, 2003 (in farm animals) and Oltmanns et al., 2005 (humans). Rivest &
Rivier (1995) explained that by inhibiting LHRH synthesis and release from the
hypothalamus.
We found an increase of corticosterone levels during SD from the first day
to the fifth day which was associated with decreased levels of testosterone.
These findings are confirmed by the previous studies in rats and men. In rats
Gonzlez-Quijano et al., 1991 (stress by immobilization), Watanabe et al., 1991
(stress by prolonged exercise), Ishikawa et al., 1992 (stress by intermittent
electric foot shocks), Bidzinska et al., 1993 (stress by forced swimming in cold
water), Novati et al., 2008; Tiba et al., 2008; Tartar et al., 2009 (stress by
plateform). In men Opstad, 1994 (prolonged physical stress due to military
training).
In the present study, there was an increased level of testicular MDA level
(the product of lipid peroxidation) significantly after three to five days of
deprivation. These findings are confirmed by Ramanathan et al (2002) who
found that with sleep deprivation there was increase in lipid peroxidation in the
hippocampal region of the brain in wistar rats. Sleep deprivation could enhance
metabolic rate and in turn increase oxidative stress. An increase in MDA level is
related to an increase in the levels of lipid peroxidation in cell membrane. ROS
can cause cytotoxicity, one of the manifestations of which can be observed
through lipid peroxidations (Jana and Samanta, 2006).
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
175
The current study revealed a decrease of GSH level in testicular tissue
during SD, the level decreased significantly after three to five days of
deprivation. This was in agreement with Everson et al (2005) who found a
decrease in glutathione activity in liver after 5 days of sleep deprivation and this
decrease was sustained or worsened by prolongation of sleep deprivation. GSH
plays multiple roles as a cellular antioxidant defense because its main function
is to remove hydrogen peroxide and organic peroxides (Chainy et al., 1997).
Therefore, any decline in the level of GSH indicates the increased production of
free radicals (Debnath and Mandal., 2000). In contrast, Singh et al (2008)
noticed that sleep deprivation did not affect oxidative stress parameters in the
striatum; and the activity of glutathione peroxidase was not affected in any of
the studied brain regions.
During the recovery period, the preset study showed that the testosterone
and corticosterone reached the control level at the fifth day of recovery. While
the LH level reached the control level at the third day of recovery. This is may
be due to the ability of the rats in recovery period to accommodate the HPA axis
derangements that accompany SD and allowing them to return to a normally
functioning HPA axis during periods of SR.
The present results of corticosterone were in agreement with that reported
by Leenaars et al. (2011). In contrast, Andersen et al. (2005) found that
testosterone did not return to basal values during the recovery periods after 96 h
of SD and they suggested that long periods of SD lead to long-term effects that
may become harmful.
During the recovery period, we found that the level of MDA decreased and
level of glutathione increased and reached the basal level at the fifth day of
recovery. The decrease in lipid peroxidation following restorative sleep
indicates that there is decrease in free radical production. The other possibility is
that the free radicals are scavenged by the antioxidant mechanism. This is well
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
176
correlated by increase in glutathione level following restorative sleep. These
results were in accordance with the results of Mallik et al. (1995). The present
study provides evidence that sleep recovery restores or accentuates antioxidants
and antioxidant activities in the testes. Sleep recovery resulted in dramatic
returns toward normal testicular glutathione(Everson et al., 2005).
In conclusion, the present study demonstrates that sleep deprivation is a
type of stress induces changes in testosterone, luteinizing hormone and
corticosterone levels in serum and biochemical effects in rat testes. The
increased oxidative stress resulted from SD in testicular tissue might be
responsible, at least in part, for the changes occurred. SR had restoration effect
evidenced by reduction of MDA and increase of GSH in testicular tissue.
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
177
REFERENCES
1. Almeida AS, Petenusci SO, France JA, Rosa-e-Silva AAM, Carvalho TLL.
Chronic immobilization-induced stress increases plasma testosterone and
delays testicular maturation in pubertal rats. Andrologia 2000;32:711.
2. Alvarenga TA, Andersen ML, Velzquez-Moctezuma J, Tufik S. Food
restriction or sleep deprivation: which exerts a greater influence on the
sexual behaviour of male rats? Behav Brain Res 2009;202:26671.
3. Alvarenga TA, Patti CL, Andersen ML, Silva RH, Calzavara MB, Lopez
GB, et al. Paradoxical sleep deprivation impairs acquisition, consolidation,
and retrieval of a discriminative avoidance task in rats. Neurobiol Learn
Mem 2008;90:62432.
4. Amikishieva AV, Avgustinovich DF, Koryakina LA. Buspirone prevents
sexual motivation in depressed male mice from reduction. Eur
Neuropsychopharmacol 2001;11(3):3145.
5. Andersen ML, Tufik S. The effects of testosterone on sleep and sleep
disordered breathing in men: its bidirectional interaction with erectile
function. Sleep Med. Rev 2008;12:36579.
6. Andersen ML, Alvarenga TA, Guindalini C, Perry JC, Silva A, Zager A, et
al. Paradoxical sleep deprivation influences sexual behavior in female rats. J
Sex Med 2009;6:216272.
7. Andersen ML, Bignotto M, Machado RB, Tufik S. Different stress
modalities result in distinct steroid hormone responses by male rats. Braz
JMed Biol Res 2004;37:7917.
8. Andersen ML, Bignotto M, Machado RB, Tufik S. Does paradoxical sleep
deprivation and cocaine induce penile erection and ejaculation in old rats?
Addict Biol 2002;7:28590.
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
178
9. Andersen ML, Martins PJ, Almeida V D, Bignotto, Tufik S.
Endocrinological and catecholaminergic alterations during sleep deprivation
and recovery in male rats. J Sleep Res 2005;14:83-90.
10. Andersen ML, Bignotto M, Tufik S. Cocaine-induced genital reflexes
during paradoxical sleep deprivation and recovery. Physiol Behav
2003;78:2559.
11. Andersen ML, Bignotto M, Machado RB, Tufik S. Effects of chronic stress
on steroid hormones secretion in male rats. Braz J Med Biol Res
2004;37:7917.
12. Andersen ML, Palma BD, Rueda AD, Tufik S. The effects of acute cocaine
administration in paradoxical sleep-deprived rats. Addiction Biol
2000;5:41720.
13. Antunes IB, Ansersen ML, Baracat EC, Tufik S. The effects of paradoxical
sleep deprivation on estrous cycles of the female rats. Horm Behav
2006;49:43340.
14. Bergmann BM, Kushida CA, Everson CA, Gilliland MA, Obermeyer
W,Rechtschaffen A. Sleep deprivation in the rat: II. Methodology.
Sleep.1989 Feb;12(1):5-12.
15. Bidzinska B, Petraglia F, Angioni S, Genazzani AD, Riscuolo M, Ficarra G,
et al. Effect of different chronic intermittent stressors and acetyl-I-carnitine
on hypothalamic beta-endorphin and GnRH and on plasma testosterone
levels in male rats. Neuroendocrinology 1993;57:98590.
16. Chainy GBN, Samantaray S, Samanta L. Testosterone-induced changes in
testicular antioxidant system. Andrologia 1997; 29: 343349.
17. Chichinadze K, Chichinadze N. Stress-induced increase of testosterone:
contributions of social status and sympathetic reactivity. Physiol Behav
2008;Jul94(4):595-603.
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
179
18. Corts-Gallegos V, Castaeda G, Alonso R, Sojo I, Carranco A, Cervantes
C. Sleep deprivation reduces circulating androgens in healthy men. Arch
Androl 1983;10:3337.
19. Debnath D, Mandal TK. Study of quinalphos (an envioronmental
oestrogenic insecticide) formulation (Ekalux 25 E. C.) induced damage of
the testicular tissues and antioxidant defense systems in Sprague-Dawley
albino rats. J Appl Toxicol 2000; 20: 19704.
20. Demura H. Effect of immobilization stress on testosterone and inhibit in
male rats. J Androl 1989;10:2103.
21. Demura R, Suzuki T, Nakamura S, Komatsu H, Odagiri E, Dufau ML.
Hormonal regulation of androgen production by the Leydig cell. J Steroid
Biochem 1984;Jan20(1):161-73.
22. Demura R, Suzuki T, Nakamura S, Komatsu H, Odagiri E, Demura H.
Effect of immobilization stress on testosterone and inhibit in male rats. J
Androl 1989;10:2103.
23. Dong Q, Salva A, Sottas CM, Niu E, Holmes M, Hardy MP. Rapid
glucocorticoid mediation of suppressed testosterone biosynthesis in male
mice subjected to immobilization stress. J Androl 2004;25(6):97381.
24. Eacker SM, Agrawal N, Qian K, Dichek HL, Gong EY, Lee K. Hormonal
regulation of testicular steroid and cholesterol homeostasis. Mol Endocrinol
2008;22:62335.
25. Ellman GL. Tissue sulfhydryl groups. Arch Biochem Biophys 1959; 82: 70
77.
26. El-Shahat AER, Gabr A, Meki AR and Mehana ES. Altered testicular
morphology and oxidative stress induced by cadmium in experimental rats
and protective effect of simultaneous green tea extract. Int. J.
Mrophol.2009;27: 757-64.
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
180
27. Everson CA, Laatsch CD, Hogg N. Antioxidant defense responses to sleep
loss and sleep recovery. Am J Physiol Regul Integr Comp Physiol. 2005
Feb;288(2):R374-83.
28. Fernandez-Garcia B, Lucia A, Hoyos J, Chicharro JL, Rodriguez-Alonso M,
Bandres F, et al. The response of sexual and stress hormones of male pro-
cyclists during continuous intense competition. Int J Sports Med
2002;23(8):55560.
29. Frias J, Rodriguez R, Torres J, Ruiz E, Ortega E. Effects of acute alcohol
intoxication on pituitary gonadal axis hormones, pituitary adrenal axis
hormones, -endorphin and prolactin in human adolescents of both sexes.
Life Sci 2000;67:10816.
30. Frungieri MB, Zitta K, Pignataro OP, Gonzalez-Calvar SI, Calandra RS.
Interactions between testicular serotoninergic, catecholaminergic, and
corticotropin-releasing hormone systems modulating cAMP and
testosterone production in the golden hamster. Neuroendocrinology
2002;76:3546.
31. Gao HB, Tong MH, Hu YQ, Guo QS, Ge R, Hardy MP. Glucocorticoid
induces apoptosis in rat Leydig cells, Endocrinology 2001;143:1308.
32. Godoi FR, Oliveira MG, Tufik S. Effects of paradoxal sleep deprivation on
the performance of rats in a model of visual attention. Behav Brain Res
2005;165:13845.
33. Gonzlez-Quijano M, Ariznavarreta C, Martin A, Tresguerres J, Lpez-
Caldern A. Naltrexone does not reverse the inhibitory effect of chronic
restraint on gonadotropin secretion in the intact male rat.
Neuroendocrinology 1991;54:44753.
34. Halliwell B, Vitamin C. antioxidant or pro-oxidant in vivo? Free Rad Res
1996; 25: 439454.
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
181
35. Hardy MP, Gao HB, Dong Q, Ge R, Wang Q, Chai WR, et al. Stress
hormone and male reproductive function. Cell Tissue Res 2005;322(1):147
53.
36. Hardy MP, Sottas CM, Ge R, McKittrick CR, Tamashiro KL, McEwen BS,
et al. Trends of reproductive hormones in male rats during psychosocial
stress: role of glucocorticoid metabolism in behavioral dominance. Biol
Reprod 2002;67(6):17505.
37. Hardy MP, Ganjam VK. Stress, 11_-HSD, and Leydig cell function. J
Androl 1997;18:4759.
38. Hjollund NHI, Bonde JPE, Henriksen TB, Giwercman A, Olsen J.
Reproductive effects of male psychologic stress. Epidemiology 2004;15:21
7.
39. Hones PE, Marin CM. Behavioral and physiological aspects of stress and
aggression in nonhuman primates. Neurosci Biobehav Rev 2006;30:390
412.
40. Ishikawa M, Hara Ch, Ohdo S, Ogawa N. Plasma corticosterone response of
rats with sociopsychological stress in the communication box. Physiol
Behav 1992;52:47580.
41. Jana K, Samanta PK. Evaluation of single intratesticular injection of
calcium chloride for non-surgical sterilization in adult albino rats.
Contraception 2006; 73: 289300.
42. Joels M, Karst H, Krugers J, Lucassen PJ. Chronic stress: implications for
neuronal morphology, function and neurogenesis. Front Neuroendocrinol
2007;28:7296.
43. Knutson KL, Spiegel K, Penev P, Van Cauter E. The metabolic
consequences of sleep deprivation. Sleep Medicine Reviews 2007;
jun11(3):16378.
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
182
44. Kraut A, Barbiro-Michaely E, Mayevsky A. Differential effects of
norepinephrine on brain and other less vital organs detected by a multisite
multiparametric monitoring system. Med Sci Monit 2004;10(7):BR21520.
45. Leenaars CH, Dematteis M, Joostena RN, Eggelsa L, Sandberga H, Schirris
M, et al. A new automated method for rat sleep deprivation with minimal
confounding effects on corticosterone and locomotor activity. Journal of
Neuroscience Methods 2011;196:10717
46. Luboshitzky R, Aviv A, Hefetz A, Herer P, Shen-Orr Z, Lavie L. Decreased
pituitary-gonadal secretion in men with obstructive sleep apnea. J Clin
Endocrinol Metab 2002;87:33948.
47. Machado, RB., Tufik, S. and Suchecki, D. (2010): Modulation of Sleep
Homeostasis by Corticotropin Releasing Hormone in REM Sleep-Deprived
Rats. International Journal of Endocrinology Volume. Article ID 326151,
12 pages
48. MacLusky, N., Naftolin, F., Leranth, C., (1988): Immunocytochemical
evidence for direct synaptic connections between corticotrophin-releasing
factor (CRF) and gonadotrophin releasing hormone (GnRH)-containing
neurons in the preoptic area of the rat. Brain Res. 439, 391395.
49. Maia LO, Jnior WD, Carvalho LS, Jesus LR, Paiva GD, Araujo P, Costa
MF, Andersen ML, Tufik S, Mazaro-Costa R (2011): Association of
methamidophos and sleep loss on reproductive toxicity of male mice.
Environ Toxico Pharmacol. 32, 155161
50. Manna I, Jana K, Samanta PK. Effect of intensive exercise induced
testicular gametogenic and steroidogenic disorders in mature male Wister
strain rats: a correlative approach to oxidative stress. Acta Physiol Scand
2003; 178: 3340.
51. Manna I, Jana K, Samanta PK (2004): Effect of different intensities of
swimming exercise on testicular oxidative stress and reproductive
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
183
dysfunction in mature male albino Wistar rats. Indian J Exp Biol.
42(8):81622.
52. Manna I, Jana K, Samanta PK (2004): Intensive swimming exercise-induced
oxidative stress and reproductive dysfunction in male Wistar rats: protective
role of alphatocopherol succinate. Can J Appl Physiol. 29(2):17285.
53. Martins PJ, DAlmeida V, Pedrazzoli M, Lin L and Mignot E (2004):
Increased hypocretin-1 (orexin-a) levels in cerebrospinal fluid of rats after
short-term forced activity. Regul Pept; 117: 1558.
54. Mazaro, R., Lamano-Carvalho, T.L., (2006): Prolonged deleterious effects
of neonatal handling on reproductive parameters of pubertal male rats.
Reprod. Fertil. Dev. 18, 497500.
55. McEwen BS (2007): Physiology and neurobiology of stress and adaptation:
central role of the brain. Physiol Rev. 87, 873904.
56. Meerlo P, Sgoifo A, Suchecki D, (2008): Restricted and disrupted sleep:
effects on autonomic function, neuroendocrine stress systems and stress
responsivity,Sleep Med. Rev. 12, 197210.
57. Monder C, Sakai RR, Miroff Y, Blanchard DC, Blanchard RJ (1994):
Reciprocal changes in plasma corticosterone and testosterone in stressed
male rats maintained in a visible burrow system: evidence for a mediating
role of testicular 11 beta-hydroxysteroid dehydrogenase. Endocrinology.
Mar;134(3):1193-8.
58. Novati A, Roman V, Cetin T, Hagewoud R, den Boer JA, Luiten PG, et al.
(2008): Chronically restricted sleep leads to depression-like changes in
neurotransmitter receptor sensitivity and neuroendocrine stress reactivity in
rats. Sleep. 31, 157985.
59. Oltmanns KM, Peters A, KernW, Fehm HL, Born J, Schultes B (2005):
Preserved inhibitory effect of recurrent hypoglycaemia on the male
gonadotrophic axis. Clin Endocrinol (Oxf). 62(2):21722.
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
184
60. Opstad, P.K., (1994): Circadian rhythm of hormones is extinguished during
prolonged physical stress, sleep and energy deficiency in young men. Eur. J.
Endocrinol. 131, 5666.
61. Park S.P, F. Lopez-Rodriguez, C.L. Wilson, N. Maidment, Y. Matsumoto, J.
Engel Jr, (1999): In vivo microdialysis measures of extracellular serotonin
in the rat hippocampus during sleepwakefulness, Brain Res. 833, 291296.
62. Payne, A.H., Youngblood, G.L., (1995): Regulation of expression of
steroidogenic enzymes in Leydig cells. Biol Reprod. 52, 217225.
63. Pedrazzoli M, DAlmeida V, Martins PJF, Machado RB, Lin L, Nishino S,
Tufik S and Mignot E (2004): Increased hypocretin-1 levels in cerebrospinal
fluid after REM sleep deprivation. Brain Res. 995, 16.
64. Rabin, D., Johnson, E.O., Brandon, D.D., Liapi, C., Ghrousos, G.P., (1990):
Glucocorticoids inhibit estradiol-mediated uterine growth: Possible role of
the uterine estradiol receptor. Biol. Reprod. 42, 7480.
65. Rajaratnam S.M. & Arendt J, (2001): Health in a 24-h society, Lancet
358, 9991005.
66. Ramanathan L, Gulyani S, Nienhuis R, et al. Sleep deprivation decreases
superoxide dismutase activity in rat hippocampus and brain
stem.Neuroreport 2002; 13(11): 13871390.
67. Reeder DM, Kramer KM (2005): Stress in free-ranging mammals:
integrating physiology, ecology, and natural history. J Mammal. 86(2):225
35.
68. Retana-Mrquez, S, Bonilla-Jaime, H., Vzquez-Palacios, G., Martnez-
Garca, R. and Velzquez-Moctezuma, J (2003): Changes in masculine
sexual behavior, corticosterone and testosterone in response to acute and
chronic stress in male rats. Hormones and Behavior. 44, 327337.
-
EBTIHAL A. ABD EL-AZIZ and DALIA G. MOSTAFA
185
69. Rivest S, Rivier C (1995): The role of corticotropin-releasing factor and
interleukin-1 in the regulation of neurons controlling reproductive functions.
Endocr Rev. 16, 17799.
70. Rivest, S., Rivier, C., (1991): Influence of the paraventricular nucleus of the
hypothalamus in the alteration of neuroendocrine functions induced by
intermittent foot shock or interleukin. Endocrinology. 129, 20492057.
71. Roman, V., Hagewoud, R., Luiten, P.G., Meerlo, P.,(2006): Differential
effects of chronic partial sleep deprivation and stress on serotonin-1A and
muscarinic acetylcholine receptor sensitivity. J. Sleep Res. 15, 386394.
72. Singh R, Kiloung J, Singh S, Sharma D. Effect of paradoxical sleep
deprivation on oxidative stress parameters in brain regions of adult and old
rats.Biogerontology. 2008 Jun;9(3):153-62
73. Stackpole CA, Turner AI, Clarke IJ, Lambert GW, Tilbrook AJ (2003):
Seasonal differences in the effect of isolation and restraint stress on the
luteinizing hormone response to gonadotropin-releasing hormone in
hypothalamopituitary disconnected gonadectomized rams and ewes. Biol
Reprod. 69, 115864.
74. Suchecki D, Tiba PA and Tufik S (2002): Hormonal and behavioral
responses of paradoxical sleep-deprived rats to the elevated plus maze. J.
Neuroendocrinol. 14, 549554.
75. Suchecki D, Tufik S(2000);: Social stability attenuates the stress in the
modified multiple platform method for paradoxical sleep deprivation in the
rat. Physiol Behav. 68, 30916.
76. Tartar JL, Ward CP, Cordeira JW, Legare SL, Blanchette AJ, McCarley
RW, et al. (2009): Experimental sleep fragmentation and sleep deprivation
in rats increases exploration in an open field test of anxiety while increasing
plasma corticosterone levels. Behav Brain Res. 197, 4503.
-
AAMJ, Vol. 10, N. 3, Sep, 2012, Suppl-1
186
77. Tiba PA, Oliveira MG, Rossi VC, Tufik S, Suchecki D (2008):
Glucocorticoids are not responsible for paradoxical sleep deprivation-
induced memory impairments. Sleep. 31, 50515.
78. Tufik S, Andersen ML, Bittencourt LR and Mello MT (2009): Paradoxical
sleep deprivation: neurochemical, hormonal and behavioral alterations.
Evidence from 30 years of research. An. Acad. Bras. Cienc. 81, 521538.
79. Watanabe, T., Morimoto, A., Sakata, Y., Wada, M., Murakami, N., (1991):
The effect of chronic exercise on the pituitary-adrenocortical response in
conscious rats. J. Physiol. 439, 691699.
80. Wingfield JC, Sapolsky RM (2003): Reproduction and resistance to stress:
when and how. J Neuroendocrinol. 15, 71124.
81. Wu JL, Wu RS, Yang JG, Huang CC, Chen KB, Fang KH, Tsai HD (2011):
Effects of sleep deprivation on serum testosterone concentrations in the rat.
Neuroscience Letters. Apr 494, 124129.
82. Zager A, Andersen ML, Lima MM, Reksidler AB, Machado RB and Tufik
S (2009): Modulation of sickness behavior by sleep: the role of
neurochemical and neuroinflammatory pathways in mice. Eur.
Neuropsychopharmacol. 19, 589602.
-
AFATSOM .G AILAD dna ZIZA-LE DBA .A LAHITBE
781
:
.
.
.
.
.
:
.
.
-
1-lppuS ,2102 ,peS ,3 .N ,01 .loV ,JMAA
881
- -
:
. .
.
.
.
24 :
. 052-002 21
: . : .
. : .
: . :
: .
: .
.
.
.
top related