Studies on the effect of prolactin treatment on testicular steroidogenesis and gametogenesis in lithium-treated rats

1991 ◽  
Vol 125 (3) ◽  
pp. 313-318 ◽  
Author(s):  
D. Ghosh ◽  
N. M. Biswas ◽  
P. K. Ghosh
Keyword(s):  
Lithium Chloride ◽  
Lithium Treatment ◽  
Serum Levels ◽  
Hydroxysteroid Dehydrogenase ◽  
Significant Inhibition ◽  
Steroidogenic Enzymes ◽  
Subcutaneous Injections ◽  
Testicular Dysfunction ◽  
Testicular Steroidogenesis ◽  
Chloride Treatment

Abstract. The effect of PRL supplementation in lithium-treated rats on spermatogenesis, testicular Δ5-3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase activities, and serum levels of FSH, LH, PRL and testosterone were studied on the 22nd day of the experiment. Subcutaneous injections of lithium chloride at a dose of 2.0 mg·kg−1·day−1 for 21 days resulted in a significant inhibition of spermatogenesis at stage VII of the seminiferous epithelial cycle, along with remarkable diminution of serum levels of the above hormones and suppression of the activities of the above two testicular steroidogenic enzymes. Administration of bovine PRL at a dose of 0.25 mg·kg−1·day−1 plus lithium treatment resulted in a remarkable protection of spermatogenic and steroidogenic activities of the testes, along with restoration of serum levels of FSH and testosterone. It is concluded that PRL can markedly protect the testicular dysfunction induced by lithium chloride treatment in rats.

Effect of lithium chloride on testicular steroidogenesis and gametogenesis in immature male rats

1991 ◽  
Vol 124 (1) ◽  
pp. 76-82 ◽  
Author(s):  
P. K. Ghosh ◽  
N. M. Biswas ◽  
D. Ghosh
Keyword(s):  
Lithium Chloride ◽  
Sperm Count ◽  
Serum Levels ◽  
Hydroxysteroid Dehydrogenase ◽  
Significant Inhibition ◽  
Male Rats ◽  
Hormonal Changes ◽  
Subcutaneous Injections ◽  
Immature Male ◽  
Testicular Steroidogenesis

Abstract. The present study was performed on immature male rats aged 35 days. Subcutaneous injections of lithium chloride at a daily dose of 2.0 mg/kg for 15 days resulted in significant inhibition of spermatogenesis at stage VII of the seminiferous epithelial cycle. Spermatogonia A, preleptotene spermatocytes and step 7 spermatids were decreased in number in comparison to controls. Serum levels of FSH, LH, PRL, and testosterone were decreased. Activities of testicular Δ5-3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase were suppressed along with a low caudal epididymal sperm count in comparison with controls. When the treatment was prolonged for 20 and 25 days, it showed an additional significant diminution in accessory sex organ weights and number of midpachytene spermatocytes at stage VII in comparison to control animals of corresponding age. It is concluded that lithium has an adverse effect on testicular function in immature rats by reducing serum levels of FSH, LH, PRL, and testosterone. Furthermore, since hormonal changes and altered spermatogenic activities were evident when the serum concentration of lithium was within the therapeutic range, our data may have some potential clinical implications.

scholarly journals Selective Inhibition of Steroidogenic Enzymes by Ketoconazole in Rat Ovary Cells

2014 ◽  
Vol 8 ◽  
pp. CMRH.S14036 ◽  
Author(s):  
Michael Gal ◽  
Joseph Orly
Keyword(s):  
Selective Inhibition ◽  
Hydroxysteroid Dehydrogenase ◽  
Dependent Manner ◽  
Steroidogenic Enzymes ◽  
Ovary Cells ◽  
Estrogen Synthesis ◽  
Lyase Activity ◽  
Testicular Steroidogenesis ◽  
Rat Ovary

Objective Ketoconazole (KCZ) is an anti-fungal agent extensively used for clinical applications related to its inhibitory effects on adrenal and testicular steroidogenesis. Much less information is available on the effects of KCZ on synthesis of steroid hormones in the ovary. The present study aimed to characterize the in situ effects of KCZ on steroidogenic enzymes in primary rat ovary cells. Methods Following the induction of folliculogenesis in gonadotropin treated rats, freshly prepared ovarian cells were incubated in suspension for up to four hours while radiolabeled steroid substrates were added and time dependent generation of their metabolic products was analyzed by thin layer chromatography (TLC). Results KCZ inhibits the P450 steroidogenic enzymes in a selective and dose dependent manner, including cholesterol side-chain cleavage cytochrome P450 (CYP11A1/P450scc), the 17α-hydroxylase activity of CYP17A1/P450c17, and CYP19A1/P450arom, with IC50 values of 0.3, 1.8, and 0.3 μg/mL (0.56, 3.36, and 0.56 μM), respectively. Unaffected by KCZ, at 10 μg/mL, were the 17,20 lyase activity of CYP17A1, as well as five non-cytochrome steroidogenic enzymes including 3β-hydroxysteroid dehydrogenase-δ5-4 isomerase type 1 (3βHSD1), 5α-reductase, 20α-hydroxysteroid dehydrogenase (20α-HSD), 3α-hydroxysteroid dehydrogenase (3α-HSD), and 17β-hydroxysteroid dehydrogenase type 1 (17HSD1). Conclusion These findings map the effects of KCZ on the ovarian pathways of progestin, androgen, and estrogen synthesis. Hence, the drug may have a potential use as an acute and reversible modulator of ovarian steroidogenesis in pathological circumstances.

Changes in growth rate and thyroid- and sex-hormones blood levels in rats under sub-chronic lithium treatment

2006 ◽  
Vol 25 (5) ◽  
pp. 243-250 ◽  
Author(s):  
M S Allagui ◽  
N Hfaiedh ◽  
C Vincent ◽  
F Guermazi ◽  
J-C Murat ◽  
...  
Keyword(s):  
Growth Rate ◽  
Lithium Treatment ◽  
Lithium Carbonate ◽  
Serum Levels ◽  
Antagonistic Effect ◽  
Blood Levels ◽  
Vaginal Mucosa ◽  
Dependent Manner ◽  
Serum Concentrations ◽  
Dose Dependent

Lithium therapy, mainly used in curing some psychiatric diseases, is responsible for numerous undesirable side effects. The present study is a contribution to the understanding of the pathophysiological mechanisms underlying lithium toxicity. Male and female mature rats were divided into three batches and fed commercial pellets: one batch was the control and the second and third batches were given 2 g (Li1) and 4 g (Li2) of lithium carbonate/kg of food/day, respectively. After 7, 14, 21 and 28 days, serum levels of free tri-iodothyronine (FT3), thyroxine (FT4), testosterone and estradiol were measured. Attention was also paid to growth rate and a histological examination of testes or vaginal mucosa was carried out. In treated rats, a dose-dependent loss of appetite and a decrease in growth rate were observed, together with symptoms of polydypsia, polyuria and diarrhea. Lithium serum concentrations increased from 0.44 mM (day 7) to 1.34 mM (day 28) in Li1 rats and from 0.66 to 1.45 mM (day 14) in Li2 rats. Li2 treatment induced a high mortality after 14 days, reaching 50-60% in female and male animals. From these data, the LD50 (14 days Li2 chronic treatment) was calculated to be about 0.3 g/day per kilogram of animal, leading to Li serum concentrations of about 1.4 mM. A significant decrease of FT3 and FT4 was observed in treated rats. This effect appeared immediately for the highest dose and was more pronounced for FT3, resulting in an increase of the FT4/FT3 ratio. In males, testosterone decreased and spermatogenesis was stopped. Conversely, in females, estradiol increased in a dose-dependent manner as the animals were blocked in the diestrus phase at day 28. This finding supports a possible antagonistic effect of lithium on the estradiol receptors.

Inhibitory Effect of Tributyltin on Expression of Steroidogenic Enzymes in Mouse Testis

2008 ◽  
Vol 27 (2) ◽  
pp. 175-182 ◽  
Author(s):  
Suel-Kee Kim ◽  
Jong-Hoon Kim ◽  
Jung Ho Han ◽  
Yong-Dal Yoon
Keyword(s):  
Germ Cells ◽  
Leydig Cells ◽  
Serum Testosterone ◽  
Hydroxysteroid Dehydrogenase ◽  
Reproductive Organs ◽  
Inhibitory Effect ◽  
Testicular Development ◽  
Steroidogenic Enzymes ◽  
Hormone Production ◽  
Induced Apoptosis

Tributyltin (TBT) is known to disrupt the development of reproductive organs, thereby reducing fertility. The aim of this study was to evaluate the acute toxicity of TBT on the testicular development and steroid hormone production. Immature (3-week-old) male mice were given a single administration of 25, 50, or 100 mg/kg of TBT by oral gavage. Lumen formation in seminiferous tubule was remarkably delayed, and the number of apoptotic germ cells found inside the tubules was increased in the TBT-exposed animals, whereas no apoptotic signal was observed in interstitial Leydig cells. Reduced serum testosterone concentration and down-regulated expressions of the mRNAs for cholesterol side-chain cleavage enzyme (P450scc), 17α-hydroxylase/C17–20 lyase (P45017α), 3β-hydroxysteroid-dehydrogenase (3β-HSD), and 17β-hydroxysteroid-dehydrogenase (17β-HSD) were also observed after TBT exposure. Altogether, these findings demonstrate that exposure to TBT is associated with induced apoptosis of testicular germ cells and inhibition of steroidogenesis by reduction in the expression of steroidogenic enzymes in interstitial Leydig cells. These adverse effects of TBT would cause serious defects in testicular development and function.

scholarly journals Lithium and Renal Impairment: A Review on a Still Hot Topic

2018 ◽  
Vol 51 (05) ◽  
pp. 200-205 ◽  
Author(s):  
René Nielsen ◽  
Lars Kessing ◽  
Willem Nolen ◽  
Rasmus Licht
Keyword(s):  
Renal Impairment ◽  
Lithium Treatment ◽  
Serum Levels ◽  
Sound Studies ◽  
Renal Outcome ◽  
Unipolar Disorder ◽  
Increased Risk ◽  
The 1960S ◽  
Stage Renal Disease ◽  
End Stage

Abstract Introduction Lithium is established as an effective treatment of mania, of depression in bipolar and unipolar disorder, and in maintenance treatment of these disorders. However, due to the necessity of monitoring and concerns about irreversible adverse effects, in particular renal impairment, after long-term use, lithium might be underutilized. Methods This study reviewed 6 large observational studies addressing the risk of impaired renal function associated with lithium treatment and methodological issues impacting interpretation of results. Results An increased risk of renal impairment associated with lithium treatment is suggested. This increased risk may, at least partly, be a result of surveillance bias. Additionally, the earliest studies pointed toward an increased risk of end-stage renal disease associated with lithium treatment, whereas the later and methodologically most sound studies do not. Discussion The improved renal outcome found in the more recent lithium studies may be a result of improved monitoring and focus on recommended serum levels (preferentially 0.6–0.8 mmol/L) as compared to poorer renal outcome in studies with patients treated in the 1960s to 1980s.

Experimental pancreatic adenocarcinoma: An immunohistochemical study for CA 19-9 and its correlation with serum levels

1989 ◽  
Vol 4 (4) ◽  
pp. 229-232
Author(s):  
M. Abad ◽  
J.I. Paz ◽  
M.J. Pedraz ◽  
E. Muñoz ◽  
A. Bullón
Keyword(s):  
Tumor Marker ◽  
Pancreatic Carcinoma ◽  
Pancreatic Adenocarcinoma ◽  
Immunohistochemical Study ◽  
Serum Levels ◽  
Subcutaneous Injections ◽  
Syrian Hamsters ◽  
Important Correlation ◽  
Papillary Lesions

Experimental pancreatic carcinoma induced in Golden Syrian Hamsters by subcutaneous injections of N-nitrosobis-(2-oxopropyl) amine (BOP) was studied during the different phases of its development by determination of serum CA 19-9 levels and tissue labeling with CA 19-9 TM. Significant differences were observed in the CA 19-9 values between the controls and animals with carcinoma (p < 0.01) and between the latter and animals with cystic or cystic papillary lesions (p < 0.01). Distribution of the deposits of CA 19-9 TM was different in the initial tumoral lesions and in the longer-developed tumors. An important correlation was observed between tissue deposits and serum levels of this tumor marker.

The swelling of Na-montmorillonite due to water absorption

Soil Research ◽  
1963 ◽  
Vol 1 (2) ◽  
pp. 129 ◽  
Author(s):  
WW Emerson
Keyword(s):  
Sodium Hydroxide ◽  
Lithium Chloride ◽  
Lithium Treatment ◽  
Polarized Light ◽  
Specific Effect ◽  
Sodium Pyrophosphate ◽  
Thin Sections ◽  
Saturated Water ◽  
The Stability ◽  
Neutral Sodium

Orientated flakes of dry Na-montmorillonite were brought into equilibrium successively with relative vapour pressures of 0.92 and 0.985 and the moisture contents, (001) spacings, and swelling measured, the latter with a travelling microscope. Over saturated water vapour the clay continued to swell with time, in contrast to Ca-montmorillonite. Hysteresis in swelling was only observed at values of p/po > 0.985. The further expansion of flakes when immersed in solutions, N in Na+, of sodium chloride with dilute buffer added (from pH 4.4 to 10) or sodium hydroxide or chloride plus neutral sodium pyrophosphate was determined. The Na+ concentration was then reduced and the corresponding swelling measured, until the flake dispersed. Similar experiments were made on orientated flakes prepared from Na-montmorillonite to which 1.5% cetyltrimethylarnmonium bromide (CTAB) had been added, as well as from Na-montmorillonite which had been washed with lithium chloride and heated before reconversion to the Na form. The expansion of Li-vermiculite crystals in lithium chloride solutions was also determined. In solutions N in Na+ the swelling of Na-montmorillonite flakes was independent of pH, but for Na+ < N/2 the swelling increased sharply above pH 8.0. The swelling of Na-clay + CTAB was much less than untreated clay and was independent of pH. Na-montmorillonite which had been lithium-treated at 95�C gave a swelling pattern at pH 4.4 similar to that of Na-clay + CTAB, whereas in sodium hydroxide the pattern was similar to that of untreated clay. The specific effect of the pyrophosphate anion on the swelling of the CTAB-treated clay was slight. There was marked hysteresis in the swelling of Na-montmorillonite with respect to salt concentration, whereas the swelling of Li-vermiculite was almost reversible. Adding CTAB inhibited the intercrystalline swelling of Na-montmorillonite, the CTA+ ions forming Stern layers on the external surfaces of the crystals. A similar effect was apparently produced in the acetate buffer by aluminium ions released during the lithium treatment. The increase in the swelling of the untreated clay with pH is consistent with the removal of aluminium ions from the external surfaces of the crystals. There must be residual attractive forces between the crystal at high pH to account for the stability of the clay in dilute salt solutions. The edge to face forces linking the silicate sheets together appear to be constant above pH 4.0. Neutral sodium pyrophosphate disperses the clay at Na+ concentrations of < N Na+ by removing aluminium ions and neutralizing positive edge charges. The montmorillonite crystals are considered to be linked mainly edge to edge in a tactoid. The bands observed in thin sections of expanded gels, using polarized light, may be due to a periodicity in the stacking of the silicate sheets forming the crystals.

scholarly journals Expression of Key Androgen-Activating Enzymes in Ovarian Steroid Cell Tumor, Not Otherwise Specified

2020 ◽  
Vol 8 ◽  
pp. 232470962093341
Author(s):  
Evana Valenzuela Scheker ◽  
Amita Kathuria ◽  
Ashwini Esnakula ◽  
Hironobu Sasano ◽  
Yuto Yamazaki ◽  
...  
Keyword(s):  
Hydroxysteroid Dehydrogenase ◽  
Steroidogenic Enzymes ◽  
Androgen Excess ◽  
Ovarian Steroid ◽  
Variable Expression ◽  
Not Otherwise Specified ◽  
Chain Cleavage ◽  
Cleavage Enzyme

To characterize the expression of steroidogenic enzymes implicated in the development of ovarian steroid cell tumors, not otherwise specified (SCT-NOS). We present 4 ovarian SCT-NOS evaluated by immunohistochemical staining of steroidogenic enzymes as an approach to define this entity pathologically. All 4 ovarian SCT-NOS showed increased expression for cholesterol side-chain cleavage enzyme (CYP11A1), 17α-hydroxylase (CYP17A1), 17β-hydroxysteroid dehydrogenase 1 (HSD17B1), aldo-ketoreductase type 1 C3 (AKR1C3), 3β-hydroxysteroid dehydrogenase 2 (HSD3B2), 5α-reductase type 2 (SRD5A2), steroid sulfatase (SULT2A1), estrogen sulfotransferase (EST), and aromatase (CYP19A1). Expression was negative for 21-hydroxylase (CYP21A2) and 17β-hydroxysteroid dehydrogenase 2 (HSD17B2). 17β-hydroxysteroid dehydrogenase 3 (HSD17B3) and 5α-reductase type 1 (SRD5A1) showed variable expression. Our analysis reveals a novel finding of increased expression of AKR1C3, HSD17B1, SRD5A2, SULT2A1, and EST in ovarian SCT-NOS, which is clinically associated with androgen excess and virilization. Further studies are needed to validate these enzymes as new markers in the evaluation of hyperandrogenic ovarian conditions.

Biopotency and site of action of drugs affecting testicular steroidogenesis

1987 ◽  
Vol 113 (3) ◽  
pp. 457-461 ◽  
Author(s):  
A. Lambert ◽  
R. Mitchell ◽  
W. R. Robertson
Keyword(s):  
Cyproterone Acetate ◽  
Leydig Cells ◽  
Hydroxysteroid Dehydrogenase ◽  
Hormone Stimulation ◽  
Testosterone Secretion ◽  
Testicular Cells ◽  
Adrenal Steroidogenesis ◽  
Site Of Action ◽  
Testicular Steroidogenesis

ABSTRACT The effect of etomidate (an anaesthetic), epostane (WIN 32729; an inhibitor of ovarian and adrenal steroidogenesis) and cyproterone acetate (an antiandrogen) on testosterone secretion from mouse Leydig cells stimulated with LH (5 i.u./l) was tested. The concentration of drug which inhibited testosterone secretion by 50% was 11·5±1·1 (s.e.m.) μmol/l for cyproterone acetate, 1·2 ± 0·2 μmol/l for etomidate and 0·23 ± 0·03 μmol/l for epostane. The effect of all three drugs on testicular steroidogenesis was completely reversible. Thus testicular cells which had been washed after exposure to a >95% inhibitory dose of drug responded in a similar manner to hormone stimulation as cells similarly washed and which had not been exposed to the drug. The sites of the antisteroidogenic effect of epostane, etomidate and cyproterone acetate were established using a method based on the sequential stimulation by the exogenous precursor steroids of the various steps leading to the biosynthesis of testosterone. It was concluded that etomidate acts at the sequence between LH binding and pregnenolone production, epostane acts at 3β-hydroxysteroid dehydrogenase and cyproterone acetate inhibits 3β-hydroxysteroid dehydrogenase and C17,20-lyase. J. Endocr. (1987) 113, 457–461

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