Assessment of aggression, sexual behavior and fertility in adult male rat following long-term ingestion of four industrial metals salts

1998 ◽  
Vol 17 (10) ◽  
pp. 570-576 ◽  
Author(s):  
H. Bataineh ◽  
M.H. Al-Hamood ◽  
A.M. Elbetieha
2005 ◽  
Vol 30 (12) ◽  
pp. 2192-2204 ◽  
Author(s):  
Paul M Plotsky ◽  
K V Thrivikraman ◽  
Charles B Nemeroff ◽  
Christian Caldji ◽  
Shakti Sharma ◽  
...  

1997 ◽  
Vol 20 (3) ◽  
pp. 133-149 ◽  
Author(s):  
H. Bataineh ◽  
M. H. Al-Hamood ◽  
A. Elbetieha ◽  
I. Bani Hani

1983 ◽  
Vol 97 (3) ◽  
pp. 401-407 ◽  
Author(s):  
A. S. McNeilly ◽  
D. W. Lincoln

To investigate the role of the pineal gland in the long-term suppression of gonadotrophin secretion induced by prolactin, the effects of pinealectomy were studied in adult male rats with hyperprolactinaemia produced by the transplantation of two pituitary glands under the kidney capsule. Pinealectomy had no effect on basal levels of LH, FSH or prolactin. The presence of pituitary transplants induced a significant twofold increase in prolactin levels and a prolonged suppression in both LH and FSH. These changes were not affected by pinealectomy. Castration resulted in a similar rise in plasma levels of LH and FSH in rats with and without pituitary transplants. In control rats this rise in LH and FSH was reduced by testosterone-containing silicone elastomer implants (s.c) of 10 mm in length and delayed by implants of 30 mm. These rises in LH and FSH were significantly delayed (10-mm implant) or abolished (30-mm implant) in rats with pituitary transplants indicating an increase in sensitivity of the hypothalamic-pituitary axis to the negative feedback effects of testosterone in these animals compared to controls. These responses were not affected by pinealectomy. These results suggest that the pineal gland is not involved in the mechanism whereby pituitary grafts, possibly through their secretion of prolactin, cause long-term suppression of gonadotrophin secretion.


2012 ◽  
Vol 23 (7) ◽  
pp. 703-709 ◽  
Author(s):  
Maria M. Bernardi ◽  
Thiago B. Kirsten ◽  
Elizabeth Teodorov ◽  
Ana C.Z. Baso ◽  
Fabio C. Prosdocimi ◽  
...  

2020 ◽  
Vol 26 (3) ◽  
pp. 509-523 ◽  
Author(s):  
Amany Mohamed Shalaby ◽  
Adel Mohamed Aboregela ◽  
Mohamed Ali Alabiad ◽  
Dina Fouad El Shaer

AbstractTramadol is a centrally acting analgesic drug, used for the management of moderate to severe pain in a variety of diseases. The long-term use of tramadol can induce endocrinopathy. This study aimed to evaluate the effect of tramadol dependence on the adrenal cortex and the effect of its withdrawal. Thirty adult male rats were divided into three experimental groups: the control group, the tramadol-dependent group that received increasing therapeutic doses of tramadol orally for 1 month, and the recovery group that received tramadol in a dose and duration similar to the previous group followed by a withdrawal period for another month. Specimens from the adrenal cortex were processed for histological, immunohistochemical, enzyme assay, and quantitative real-time PCR (RT-qPCR) studies. Tramadol induced a significant increase in malondialdehyde level and a significant decrease in the levels of glutathione peroxidase and superoxide dismutase. A significant decrease in the levels of adrenocorticotrophic hormones, aldosterone, cortisol, corticosterone, and dehydroepiandrosterone sulfate was also detected. Severe histopathological changes in the adrenal cortex were demonstrated in the form of disturbed architecture, swollen cells, and shrunken cells with pyknotic nuclei. Inflammatory cellular infiltration and variable-sized homogenized areas were also detected. A significant increase in P53 and Bax immunoreaction was detected and confirmed by RT-qPCR. The ultrastructural examination showed irregular, shrunken adrenocorticocytes with dense nuclei. Dilated smooth endoplasmic reticulum, mitochondria with disrupted cristae, and numerous coalesced lipid droplets were also demonstrated. All these changes started to return to normal after the withdrawal of tramadol. Thus, it was confirmed that the long-term use of tramadol can induce severe adrenal changes with subsequent insufficiency.


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