Neonatal exposure to estradiol-17β modulates tumour necrosis factor alpha and cyclooxygenase-2 expression in brain and also in ovaries of adult female rats

2016 ◽  
Vol 25 (2) ◽  
Author(s):  
Radhika Nagamangalam Shridharan ◽  
Harshini Krishnagiri ◽  
Vijayakumar Govindaraj ◽  
SitiKantha Sarangi ◽  
Addicam Jagannadha Rao
Keyword(s):  
Recent Observation ◽  
Endocrine Disrupting Compounds ◽  
Perinatal Period ◽  
Female Rats ◽  
Neonatal Exposure ◽  
Sexually Dimorphic ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
And Behavior ◽  
Estradiol 17Β

AbstractThe sexually dimorphic organization in perinatal rat brain is influenced by steroid hormones. Exposure to high levels of estrogen or endocrine-disrupting compounds during perinatal period may perturb this process, resulting in compromised reproductive physiology and behavior as observed in adult In our recent observation neonatal exposure of the female rats to estradiol-17β resulted in down-regulation of

Proteomic identification of non-erythrocytic alpha-spectrin-1 down-regulation in the pre-optic area of neonatally estradiol-17β treated female adult rats

2016 ◽  
Vol 26 (3) ◽  
Author(s):  
Vijayakumar Govindaraj ◽  
Addicam Jagannadha Rao
Keyword(s):  
Adult Stage ◽  
Interaction Analysis ◽  
Recent Observation ◽  
Protein Profile ◽  
Strong Association ◽  
Sexually Dimorphic ◽  
Female Rat ◽  
Down Regulation ◽  
Adult Rats ◽  
Estradiol 17Β

AbstractIt is well established that sexually dimorphic brain regions, which are critical for reproductive physiology and behavior, are organized by steroid hormones during the first 2 weeks after birth in the rodents. In our recent observation, neonatal exposure to estradiol-17β (E2) in the female rat revealed increase in cyclooxygenase 2 (COX-2) level, sexually dimorphic nucleus (SDN)-pre-optic area (POA) size and down-regulation of synaptogenesis related genes in POA in the adult stage. In the present study, using the same animal model, the protein profile of control and neonatally E2-treated POA was compared by 1D-SDS-PAGE, and the protein that shows a change in abundance was identified by LC-MS/MS analysis. Results indicated that there was a single protein band, which was down-regulation in E2-treated POA and it was identified as spectrin alpha chain, non-erythrocytic 1 (SPTAN1). Consistently, the down-regulation of SPTAN1 expression was also confirmed by reverse transcription polymerase chain reaction (RT-PCR) and Western blot analysis. The SPTAN1 was identified as a cytoskeletal protein that is involved in stabilization of the plasma membrane and organizes intracellular organelles, and it has been implicated in cellular functions including DNA repair and cell cycle regulation. The evidence shows that any mutation in spectrins causes impairment of synaptogenesis and other neurological disorders. Also, protein-protein interaction analysis of SPTAN1 revealed a strong association with proteins such as kirrel, actinin, alpha 4 (ACTN4) and vinculin (VCL) which are implicated in sexual behavior, masculinization and defeminization. Our results indicate that SPTAN1 expression in the developing rat brain is sexually dimorphic, and we suggest that this gene may mediate E2-17β-induced masculinization and defeminization, and disrupted reproductive function in the adult stage.

Sexual Behavior: From Hormonal Regulation to Endocrine Disruption

2018 ◽  
Vol 107 (4) ◽  
pp. 400-416 ◽  
Author(s):  
Sakina Mhaouty-Kodja ◽  
Lydie Naulé ◽  
Daphné Capela
Keyword(s):  
Sexual Behavior ◽  
Hormonal Regulation ◽  
Experimental Studies ◽  
Endocrine Disrupting Compounds ◽  
Perinatal Period ◽  
Sexually Dimorphic ◽  
Hormonal Changes ◽  
Exogenous Factors ◽  
Underlying Mechanisms ◽  
A Chain

Sexual behavior constitutes a chain of behavioral responses beginning with courtship and leading to copulation. These responses, which are exhibited in a sexually dimorphic manner by the two partners, are tightly regulated by sex steroid hormones as early as the perinatal period. Hormonal changes or exposure to exogenous factors exhibiting hormone-mimetic activities, such as endocrine disrupting compounds (EDC), can therefore interfere with their expression. Here we review the experimental studies in rodents performed to address the potential effects of exposure to EDC on sexual behavior and underlying mechanisms, with particular attention to molecules with estrogenic and/or anti-androgenic activities.

scholarly journals Fluctuation of Serum Apelin Level during Pregnancy

2019 ◽  
pp. 1-9
Author(s):  
Sherif Wagih Mansour ◽  
Ali Khalil Asalah ◽  
Kamelia Ibrahim Attia ◽  
Somya E. l. Sayed Mohammed ◽  
Ahmad Desoky
Keyword(s):  
Serum Levels ◽  
Female Rats ◽  
Albino Rats ◽  
Pregnant Rats ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Apelin Receptor ◽  
Factor Alpha ◽  
G Protein Coupled ◽  
Necrosis Factor

Background: Apelin is an endogenous ligand for the G protein-coupled receptor Apelin receptor (APJ), The expression of both apelin and APJ has been detected in a variety of tissues including  heart, brain ,ovary , placenta and uterus. Aim of the Study: This study was designed to examine the circulating levels of apelin, estradiol, progesterone, glucose, insulin and Tumor necrosis Factor alpha (TNF α)  in non-pregnant, pregnant rats at different stages of  pregnancy. Materials and Methods: Sixty adult albino rats (48 females and 12 males). Female rats were randomly divided into (non -pregnant rats, early pregnant rats on day 6 of gestation, mid pregnant rats on day 12 of gestation and rats late pregnant rats on day 19 of gestation. The blood samples were obtained from the orbital venous plexus of animals and serum was separated from each blood sample and kept deep frozen until analysed. Results: The present study revealed that the serum levels of apelin were progressively  and significantly increased from early (day 6) to mid-pregnancy (day 12) of gestation when compared to non- pregnant rats then showed a marked decrease on day 19 when compared to pregnant rats on day 12 of gestation. Conclusion: The fluctuations in serum apelin levels during pregnancy may be attributed to changes in serum levels of multiple interrelated factors such as insulin, insulin resistance, pro inflammatory cytokines such as TNF α and other factors such as changes in fat mass, the  expression of angiotensin converting enzyme related carboxy peptidase-2 (ACE 2) and hormonal levels during pregnancy.

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