Sexual behavior attenuates the effects of chronic stress in body weight, testes, sexual accessory glands, and plasma testosterone in male rats

Retana‐Márquez, Socorro; Vigueras-Villaseñor, Rosa María; Juárez‐Rojas, Lizbeth; Martínez, Andrés; Torres, Gabriela Reyes

doi:10.1016/j.yhbeh.2014.09.002

Cited by 31 publications

(23 citation statements)

References 73 publications

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“…lumen diameter and cellular area were decreased that might be the result of an impairment in the division and conversion of the spermatogonia to the spermatozoa. Consistent with our findings, Retana-Márquez et al (2014) observed that epithelial surface area decreased in testis of male rats stressed for 20 days. In addition, Nirupama et al (2013) reported that following restraint stress, the seminiferous tubules of rats were shrunken and contained less spermatozoa.…”

Section: Discussionsupporting

confidence: 93%

Effects of antiglucocorticoid pretreatment on testes in chronically stressed adult rats – a histomorphometric study

Kheirabad¹,

Jahromi²,

Rahmanifar³

et al. 2016

BJVM

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Male fertility and reproduction can be affected by stress. The aim of the present study was histomorphometric evaluation of the role of glucocorticoids during chronic restraint stress on spermatogenesis. Twenty four male adult Sprague-Dawley rats were allocated randomly to four equal groups; stress group, mifepristone (RU486)-treated group, stress/RU486 and control groups. In stress group, the rats were restrained 1 h/day for 12 days. In RU486 group, the rats were injected RU486 at a dose of 2.5 mg/kg for 12 days. In stress/RU486 group, the rats were injected RU486 1 h before the stress process for 12 days. The testes of the all groups were removed and on 10 circular transverse sections of tubules stained with hematoxylin-eosin, histomorphometric parameters including cellular (germinal epithelium) diameter and area of the seminiferous tubules, total diameter and cross sectional area, number of seminiferous tubules per unit area, and numerical density of the tubules of the seminiferous tubules were measured. Restraint stress reduced lumen diameter, thickness of germinal epithelium and numerical density of seminiferous tubules (P<0.05). This reduction was reversed by subcutaneous injection of the anti-glucocorticoid, RU486 prior to stress session (P<0.05). In conclusion, chronic stress acts on testicular tissue via glucocorticoid receptors to suppress spermatogenesis in male rats.

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Section: Discussionsupporting

confidence: 93%

Effects of antiglucocorticoid pretreatment on testes in chronically stressed adult rats – a histomorphometric study

Kheirabad¹,

Jahromi²,

Rahmanifar³

et al. 2016

BJVM

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“…There are currently animal models that are used to study the effect of stress, such as immobilization [41], unpredictable chronic stress [10], cold water immersion [42] or hot stress [43], applied in rats. These types of stressors trigger the activation of the HHA axis stimulating glucocorticoid secretion from the adrenal cortex, into the systemic circulation.…”

Section: Stress Causes Testicular Cells Deathmentioning

confidence: 99%

“…Activation of the caspase cascade indicates that both signaling pathways (extrinsic and intrinsic) could probably be involved in the activation of apoptosis of Germ cells [47]. In recent years, the effect of chronic cold-water immersion stress on various aspects of male reproductive function, such as sexual behavior, testosterone secretion and spermatogenesis [42] has been investigated in the male rat [42].…”

Section: Cell Death Activation By Stress In Testicular Germ Cellsmentioning

confidence: 99%

“…It has been shown that this stressor has a profound inhibitory effect on testosterone plasma concentration, which significantly decreases, and at the same time causes a significant increase in plasma corticosterone concentration [42]. Cold water immersion stress (15°C for 15 min) applied to rats for 1, 20, 40 and 50 consecutive days has been shown to increase the percentage of seminiferous tubules containing apoptotic germ cells positive for TUNEL (Terminal deoxynucleotidetransferase).…”

Section: Cell Death Activation By Stress In Testicular Germ Cellsmentioning

confidence: 99%

“…However, spermatogonia, primary spermatocytes and round and elongated spermatids appear to be the most affected. Chronic exposure to stress causes alterations in the progression of spermatogenesis and decreases male fertility, as chronic exposure to water by immersion in cold water, for 20 or 50 consecutive days, causes loss of germ cells, causing a decrease in the seminiferous epithelium are and fertility, with a decrease in the number of offspring in females copulating with chronically stressed males [42]. In rats exposed to chronic stress by immobilization (1 hour) followed by forced swimming (15 min daily for 60 consecutive days), an increase was observed in the apoptosis of germ cells, mainly in type A spermatogonia, in primary spermatocytes in pachytene and in round spermatids, located in stage VII of the cycle of seminiferous epithelium.…”

Section: Effect Of Stress and Apoptosis On Male Fertilitymentioning

confidence: 99%

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Stress and Cell Death in Testicular Cells

Juárez-Rojas¹,

Lizbeth²,

Casillas³

et al. 2017

Andrology

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The success of male reproduction requires the production of a large number of spermatozoa by a unique process known as spermatogenesis. Spermatogenesis is carried out in close association with the Sertoli cells, the only somatic cells of the seminiferous epithelium which are responsible for providing structural, nutritional and endocrine support to the developing germ cells. The seminiferous epithelium of the testes is a rapid proliferation tissue, where the germinal cells, through a large number of mitotic and meiotic divisions prior to their differentiation culminate with the structural and functional formation of spermatozoa. The number of germ cells that Sertoli cells can sustain is maintained by apoptosis, which fulfills the elimination of germ cells with genetic errors, damage to DNA or excess cell production. Apoptosis can also be activated by external factors such as stress, causing alterations in spermatogenesis and testicular involution, which compromises fertility. However, death in testicular cells is not attributed only to apoptosis, as cells use different mechanisms to activate their self-elimination, such as anoikis and autophagy. All of these mechanisms are discussed.

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Stress Response to Physical Exercise in Rats with Alimentary Obesity

2018

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Stress response to physical exercise was studied in rats with alimentary obesity with and without caloric diet restriction. Daily excretion of corticosterone, progesterone, and testosterone, weights of internal organs, and serum levels of glucose, free fatty acids, triglycerides, corticosterone, and testosterone were estimated. Stress response to moderate exercise in rats with alimentary obesity was associated with predominance of anabolic influence of testosterone over the catabolic effects of corticosterone, which promoted the increase in the weight of reproductive organs. Exposure to physical loads against the background of restricted ration potentiated the response of the adrenocortical system and reduced the concentration and anabolic effects of testosterone.

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Sexual behavior attenuates the effects of chronic stress in body weight, testes, sexual accessory glands, and plasma testosterone in male rats

Cited by 31 publications

References 73 publications

Effects of antiglucocorticoid pretreatment on testes in chronically stressed adult rats – a histomorphometric study

Effects of antiglucocorticoid pretreatment on testes in chronically stressed adult rats – a histomorphometric study

Stress and Cell Death in Testicular Cells

Stress Response to Physical Exercise in Rats with Alimentary Obesity

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