Delayed puberty and response to testosterone in a rat model of colitis

2001 ◽  
Vol 281 (5) ◽  
pp. R1483-R1491 ◽  
Author(s):  
Omiea G. Azooz ◽  
Michael J. G. Farthing ◽  
Martin O. Savage ◽  
Anne B. Ballinger
Keyword(s):  
Experimental Colitis ◽  
Male Rats ◽  
Delayed Puberty ◽  
Plasma Testosterone ◽  
Trinitrobenzenesulfonic Acid ◽  
Estrous Cycles ◽  
Testosterone Treatment ◽  
Relative Contribution ◽  
Reproductive Axis ◽  
Testosterone Administration

Delayed puberty is a frequent complication of inflammatory bowel disease. The precise etiological mechanisms are not known. In this study, we wanted to determine the relative contribution of undernutrition and inflammation to delayed puberty and the effect of inflammation on the reproductive axis. Puberty was assessed in rats with 2,4,6-trinitrobenzenesulfonic acid induced-colitis, healthy controls, and animals pair fed to match the food intake of the colitic group. The response to testosterone administration was assessed in colitic rats. We found that induction of colitis was associated with hypophagia and reduced weight gain, and undernutrition in healthy females (i.e., pair fed) resulted in a delay in the onset (by 4.8 days, P < 0.001) and progression of puberty (normal estrous cycles in 42%, P = 0.04) compared with controls. However, puberty was further delayed in the colitic group (1.4 days after pair fed) with the absence of normal estrous cycling in all rats. In males, the onset of puberty was also delayed, and weights of accessory sex organs were reduced compared with pair-fed controls. Plasma testosterone concentrations were low, and gonadotropin concentrations were normal in colitic rats. Testosterone treatment normalized puberty in male rats with colitis. In conclusion, in rats with experimental colitis, inflammation appears to potentiate the effect of undernutrition on puberty. The weights of secondary sex organs and the onset of puberty were normalized by testosterone treatment.

scholarly journals Sigma-1 Receptor Engages an Anti-Inflammatory and Antioxidant Feedback Loop Mediated by Peroxiredoxin in Experimental Colitis

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1081
Author(s):  
Nikoletta Almási ◽  
Szilvia Török ◽  
Zsuzsanna Valkusz ◽  
Máté Tajti ◽  
Ákos Csonka ◽  
...  
Keyword(s):  
Experimental Colitis ◽  
The Body ◽  
Male Rats ◽  
Trinitrobenzenesulfonic Acid ◽  
Simultaneous Treatment ◽  
Sigma 1 Receptor ◽  
Beneficial Effects ◽  
Chronic Inflammatory Condition ◽  
Sigma 1 ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition of the gastrointestinal tract. Since the treatment of IBD is still an unresolved issue, we designed our study to investigate the effect of a novel therapeutic target, sigma-1 receptor (σ1R), considering its ability to activate antioxidant molecules. As a model, 2,4,6-trinitrobenzenesulfonic acid (TNBS) was used to induce colitis in Wistar–Harlan male rats. To test the beneficial effects of σ1R, animals were treated intracolonically (i.c.): (1) separately with an agonist (fluvoxamine (FLV)), (2) with an antagonist of the receptor (BD1063), or (3) as a co-treatment. Our results showed that FLV significantly decreased the severity of inflammation and increased the body weight of the animals. On the contrary, simultaneous treatment of FLV with BD1063 diminished the beneficial effects of FLV. Furthermore, FLV significantly enhanced the levels of glutathione (GSH) and peroxiredoxin 1 (PRDX1) and caused a significant reduction in 3-nitrotyrosine (3-NT) levels, the effects of which were abolished by co-treatment with BD1063. Taken together, our results suggest that the activation of σ1R in TNBS-induced colitis through FLV may be a promising therapeutic strategy, and its protective effect seems to involve the antioxidant pathway system.

Prenatal BPA and its analogs BPB, BPF, and BPS exposure and reproductive axis function in the male offspring of Sprague Dawley rats

2019 ◽  
Vol 38 (12) ◽  
pp. 1344-1365 ◽  
Author(s):  
A Ullah ◽  
M Pirzada ◽  
S Jahan ◽  
H Ullah ◽  
S Razak ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Male Offspring ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Sprague Dawley ◽  
Bisphenol S ◽  
Histological Changes ◽  
Reproductive Tissues ◽  
Reproductive Axis

Research in the past has indicated associated long-term and low levels of exposure of bisphenol A (BPA) in early life and neuroendocrine disorders, such as obesity, precocious puberty, diabetes, and hypertension. BPA and its analogs bisphenol B (BPB), bisphenol F (BPF), and bisphenol S (BPS) have been reported to have similar or even more toxic effect as compared to BPA. Exposure of rats to BPA and its analogs BPB, BPF, and BPS resulted in decreased sperm production, testosterone secretion, and histological changes in the reproductive tissues of male rats. In the present study, BPA, BPB, BPF, and BPS were administered in drinking water at concentrations of (5, 25, and 50 μg/L) from pregnancy day (PD) 1 to PD 21. Body weight (BW), hormonal concentrations, antioxidant enzymes, and histological changes were determined in the reproductive tissues. BPA and its analogs prenatal exposure to female rats induced significant statistical difference in the antioxidant enzymes, plasma testosterone, and estrogen concentrations in the male offspring when compared with the control. Histological parameters of both testis and epididymis revealed prominent changes in the reproductive tissues. The present study suggests that BPA and its analogs BPB, BPF, and BPS different concentrations led to marked alterations in the development of the male reproductive system.

scholarly journals Investigation of H2S Donor Treatment on Neutrophil Extracellular Traps in Experimental Colitis

2021 ◽  
Vol 22 (23) ◽  
pp. 12729
Author(s):  
Szilvia Török ◽  
Nikoletta Almási ◽  
Zsuzsanna Valkusz ◽  
Anikó Pósa ◽  
Csaba Varga ◽  
...  
Keyword(s):  
High Mobility ◽  
Experimental Colitis ◽  
Neutrophil Extracellular Traps ◽  
Treated Group ◽  
Arginine Deiminase ◽  
Male Rats ◽  
Trinitrobenzenesulfonic Acid ◽  
Extracellular Traps ◽  
Bowel Diseases ◽  
Anti Inflammatory

Inflammatory bowel diseases (IBD) are chronic, immune-mediated disorders, which affect the gastrointestinal tract with intermittent ulceration. It is increasingly clear that neutrophil extracellular traps (NETs) seem to have a role in IBD; however, the associated pathogenesis is still not known. Furthermore, several conventional therapies are available against IBD, although these might have side effects. Our current study aimed to investigate the effects of hydrogen sulfide (H2S) treatment on NETs formation and on the expression of inflammatory mediators in experimental rat colitis. To model IBD, 2,4,6-trinitrobenzenesulfonic acid (TNBS) was administered intracolonically (i.c.) to Wistar–Harlan male rats. Animals were treated (2 times/day) with H2S donor Lawesson’s reagent per os. Our results showed that H2S treatment significantly decreased the extent of colonic lesions. Furthermore, the expression of members of NETs formation: peptidyl arginine deiminase 4 (PAD4), citrullinated histone H3 (citH3), myeloperoxidase (MPO) and inflammatory regulators, such as nuclear transcription factor-kappa B (NF-κB) and high-mobility group box 1 (HMGB1) were reduced in H2S treated group compared to TNBS. Additionally, H2S donor administration elevated the expression of ubiquitin C-terminal hydroxylase L1 (UCHL-1), a potential anti-inflammatory mediator. Taken together, our results showed that H2S may exert anti-inflammatory effect through the inhibition of NETs formation, which suggests a new therapeutic approach against IBD.

Effects of oestradiol benzoate (OeB) and human chorionic gonadotrophin (hCG) on the testes and accessory sex glands of the rat

1981 ◽  
Vol 96 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Mridula Chowdhury ◽  
Robert Tcholakian ◽  
Emil Steinberger
Keyword(s):  
Treated Group ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Control Group ◽  
Intact Male ◽  
Intact Control ◽  
Testosterone Levels ◽  
Oestradiol Benzoate ◽  
Direct Inhibitory Effect

Abstract. It has been suggested that treatment of intact male rats with oestradiol benzoate (OeB) causes an interference with testosterone (T) production by the testes by a direct inhibitory effect on steroidogenesis. To test this hypothesis, different doses (5, 10 or 25 IU) of hCG were administered concomitantly with 50 μg of OeB to adult intact or hypophysectomized male rats. The testicular and plasma testosterone, and serum hCG levels were determined. The sex accessory weights were recorded. In the intact OeB-treated group of animals, hCG stimulated both the secondary sex organs and plasma testosterone levels above the intact control group. However, in hypophysectomized animals, although plasma testosterone levels increased above that of intact controls, their secondary sex organ weights did not. Moreover, inspite of high circulating hCG levels, the testicular testosterone content and concentration remained suppressed in OeB-treated animals. The reason for such dichotomy of hCG action on OeB-treated animals is not clear at present.

scholarly journals Low-dose testosterone protects against renal ischemia-reperfusion injury by increasing renal IL-10-to-TNF-α ratio and attenuating T-cell infiltration

2016 ◽  
Vol 311 (2) ◽  
pp. F395-F403 ◽  
Author(s):  
Chetan N. Patil ◽  
Kedra Wallace ◽  
Babbette D. LaMarca ◽  
Mohadetheh Moulana ◽  
Arnaldo Lopez-Ruiz ◽  
...  
Keyword(s):  
T Cell ◽  
Low Dose ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Male Rats ◽  
Plasma Creatinine ◽  
Cell Infiltration ◽  
Plasma Testosterone ◽  
T Cell Infiltration ◽  
Tnf Α

Renal ischemia-reperfusion (I/R) in male rats causes reductions in plasma testosterone, and infusion of testosterone 3 h postreperfusion is protective. We tested the hypotheses that acute high doses of testosterone promote renal injury after I/R, and that acute low-dose testosterone is protective by the following: 1) increasing renal IL-10 and reducing TNF-α; 2) its effects on nitric oxide; and 3) reducing intrarenal T-cell infiltration. Rats were subjected to renal I/R, followed by intravenous infusion of vehicle or testosterone (20, 50, or 100 μg/kg) 3 h postreperfusion. Low-dose testosterone (20 μg/kg) reduced plasma creatinine, increased nitrate/nitrite excretion, increased intrarenal IL-10, and reduced intrarenal TNF-α, whereas 50 μg/kg testosterone failed to reduce plasma creatinine, increased IL-10, but failed to reduce TNF-α. A higher dose of testosterone (100 mg/kg) not only failed to reduce plasma creatinine, but significantly increased both IL-10 and TNF-α compared with other groups. Low-dose nitro-l-arginine methyl ester (1 mg·kg−1·day−1), given 2 days before I/R, prevented low-dose testosterone (20 μg/kg) from protecting against I/R injury, and was associated with lack of increase in intrarenal IL-10. Intrarenal CD4+ and CD8+ T cells were significantly increased with I/R, but were attenuated with low-dose testosterone, as were effector T helper 17 cells. The present studies suggest that acute, low-dose testosterone is protective against I/R AKI in males due to its effects on inflammation by reducing renal T-cell infiltration and by shifting the balance to favor anti-inflammatory cytokine production rather than proinflammatory cytokines.

scholarly journals The effect of testosterone on the rate of oxygen consumption by prostate tissue

2018 ◽  
Vol 99 (5) ◽  
pp. 775-778
Author(s):  
A O Lobkarev ◽  
R Kh Khafiz’yanova ◽  
O A Lobkarev
Keyword(s):  
Oxygen Consumption ◽  
Chronic Prostatitis ◽  
Clinical Effectiveness ◽  
Prostatic Hyperplasia ◽  
Prostate Tissue ◽  
Male Rats ◽  
Rate Of Oxygen Consumption ◽  
Testosterone Administration ◽  
Air Tightness ◽  
Increasing Demand

Aim. To study the effect of testosterone on the rate of oxygen consumption by rodent prostate homogenate. Methods. The study included 30 healthy old white outbred male rats divided into two groups with 15 animals in each group. The rats of the first group were administered the application of 1 % testosterone-containing gel Androgel before the operation. The rats of the second group received no testosterone. Under anesthesia prostatectomy was performed. Homogenate was immediately prepared from each prostate. Further every homogenate was placed into 250 ml vial to determine the rate of oxygen consumption. Then the device measuring the concentration of oxygen dissolved in water was placed into the vial, and the air-tightness was created. Each vial was put into the thermostat for 30 minutes at 36.6 ˚C. Then the measurement of the concentration of O2 dissolved in the water was performed. Results. Application of transdermal gel with 1 % testosterone was found to cause increase of oxygen consumption by prostate tissue. This fact can explain why the clinical effectiveness of testosterone is individual to each patient with benign prostatic hyperplasia (BPH) and chronic prostatitis (CP): oxygen supply to the prostate is different in each patient with BPH and CP. So not in every patient the oxygen-transporting system is capable of supplying prostate tissues with the amount of oxygen according to increasing demand of the organ on testosterone administration. Conclusion. Testosterone increases the rate of oxygen consumption by prostate tissue.

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