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PubMed1979

LH and testosterone release in developing bulls following LH-RH treatment. Effect of gonadectomy and chronic testosterone propionate pre-treatment.

LH and testosterone release after LH-RH treatment was studied in male calves from 1 week to 8 months of age. Total LH release, LH peak values and duration of the discharge increased from 1 week to 4 months of age by 406, 453 and 110%, respectively. Significant decreases of 54, 48 and 24% were observed at 6 months of age compared to 4 months of age. This was followed by steep increases in those variables of 344, 129 and 69% at 8 months compared to 4 months. A testosterone response following an LH increase was first seen at 4 months of age when a weak discharge occurred in 2 out of 5 calves. In older calves strong and LH-correlated testosterone responses were always observed. In a second experiment the LH response to LH-RH was studied in 6 months old calves castrated 2 months previously. The total LH response was 61% greater than in intact controls. When animals were castrated and pre-treated briefly with testosterone propionate the response was increased by 183% and the time to reach the LH peak was increased by 360%. From these and other results a synthesis of endocrine events during the first year of life is proposed. In particular it seems that the period between 4 and 8 months of age is crucial since interactions between steroid feedback and pituitary sensitivity to LH-RH change and eventually reach an equilibrium.

Age Factors↗
PubMed1976

Solubilities of testosterone propionate and related esters in organic solvents.

The solubility parameters of a range of saturated hydrocarbons were calculated from vapor pressures and heats of vaporization. Solubilities of testosterone propionate were determined in these solvents at 25 degrees and yielded solute solubility parameters which varied from solvent to solvent. The solubility parameter of testosterone propionate was determined by several other methods, and support was found for the previously published figure of 9.5 cal(1/2) cm(-3/2). The geometric mean coefficient (l(12)) in saturated hydrocarbons was found to be a rectilinear function of the branching ratio (r). The mean l(12) of androstanolone and testosterone propionates was used to calculate the solubilities of other esters, giving good agreement with experimental results. IR data, presented as the sum of the shifts of the 3-keto and 17-ester carbonyl stretching frequencies in polar solvents, correlated rectilinearly with the geometric mean coefficients and the plot extrapolated to the l(12) value of n-hexane, calculated from the branching ratio plot. Attempts to predict solubilities of other esters in polar solvents using l(12) values achieved only limited success.

Chemical Phenomena↗
PubMed1999

Strength training does not alter the effects of testosterone propionate injections on high-density lipoprotein cholesterol concentrations.

The purpose of the study was to examine the long-term effects of a high-volume strength training program (vertical ladder climbing) and testosterone propionate injections (intraperitoneal) on serum lipid and lipoprotein concentrations in male Sprague-Dawley rats. The animals were randomly divided into a testosterone (T)-treated group (dose per injection, 2.5 mg/kg testosterone propionate solubilized in 1 mL safflower oil) and a control (C) group (injected with an isovolumic amount of safflower oil alone). Animals were further divided into a strength-trained group (E) and a sedentary group (S). The 10-week resistance training program consisted of weights (100% of body mass) appended to the tail as the animal climbed an 85-cm ladder to volitional fatigue. Following 10 weeks of strength training and testosterone injections, body weight was not significantly different between the main effects of strength training exercise (TE + CE v TS + CS) and testosterone injections (TE + TS v CE + CS) or between groups. Testicular mass (mean +/- SE) was measured as a relative indicator of testosterone effects. Both TE and TS had significantly reduced testicular mass (2.56 +/- 0.04 and 2.38 +/- 0.03 g, respectively) compared with CE and CS (3.49 +/- 0.03 and 3.49 +/- 0.04 g, respectively). No significant differences were observed between groups for total serum cholesterol, serum triglycerides, or serum low-density lipoprotein cholesterol (LDL-C). In contrast, significant decreases in high-density lipoprotein cholesterol (HDL-C) were observed for both TE (26.7 +/- 1.6 mg/dL) and TS (27.5 +/- 1.3 mg/dL) compared with CE (48.7 +/- 2.9 mg/dL) and CS (43.5 +/- 2.6 mg/dL). As a result, the total cholesterol to HDL-C ratio was significantly greater for TS + TE (4.7 +/- 0.1) compared with CS + CE (2.9 +/- 0.2). These observations suggest that in animals, a 10-week program of high-volume strength training does not elicit any beneficial effect on the lipid or lipoprotein status, nor does it attenuate the altered lipoprotein profile induced by testosterone propionate injections.

Animals↗
PubMed1990

Blockade of lordosis by androst-1,4,6-triene-3,17-dione (ATD) and tamoxifen in female hamsters primed with testosterone propionate.

Normal female hamsters display lordosis after testosterone propionate (TP) plus progesterone (P) treatments. Such effect is probably mediated through aromatization of testosterone (T) into estradiol. If so, then an aromatase inhibitor (ATD) or an estrogen antagonist (tamoxifen, TAM) should be able to block the activational effect of T on lordosis. To test this hypothesis, 48 ovariectomized female hamsters were assigned into six groups which, according to treatments received, were ATD + TP, TAM + TP, OIL + TP, ATD + EB (estradiol benzoate), TAM + EB, and OIL + EB groups. The groups received assigned treatments for 2 days and were injected with P on the third day. Five minutes of behavior test was conducted 4 hr after P injection. The OIL + TP, OIL + EB, and ATD + EB groups all had averaged total lordosis duration (TLD) longer than 200 sec. The TLD of the TAM + EB group was only 117 sec. The ATD + TP and TAM + TP groups showed almost no lordosis. The results showed that the estrogen antagonist (TAM) impaired lordosis no matter whether the animals were primed with TP or EB, but the aromatase inhibitor (ATD) blocked lordosis only in TP primed females. It is concluded that the aromatization of T to estrogen is required for testosterone activation of lordosis in female hamsters.

Androstatrienes↗
PubMed1975

Effects of diethylstilbestrol and testosterone propionate implanted in the hypothalamus on spermatogenesis in rats.

Small quantities of diethylstilbestrol and testosterone proprionate were implanted into the hypothalamic arcuate nucleus of male rats of the Wistar-Imamichi strain at 43 days of age. The animals were sacrificed at 64 or 76 days of age. Diethylstilbestrol suppressed the development of all genital organs and disturbed spermatogenesis. The damage was found to have recovered slightly in rats sacrificed at 76 days of age. Testosterone propionate was also effective for the atrophy of some genital organs. Its influence was not so severe as that of diethylstilbestrol. It extinguished almost completely 33 days after implantation. On the contrary, the numbers of spermatogonia and spermatocytes per cross section of the seminiferous tubule were smaller at 76 days than at 64 days of age. The diameter of the seminiferous tubule in the rat implanted with testosterone propionate was longer at 76 days than at 64 days of age. Therefore, the tubular diameter did not always represent the quantity or quality of spermatogenesis. The results also suggested that spermatogenesis might have been disturbed in some of the rats in which androgen was considered to be secreted almost normally.

Animals↗
PubMed1998

Effect of oil on the level of solubilization of testosterone propionate into nonionic oil-in-water microemulsions.

The level of solubilization of the drug testosterone propionate into 2% w/w oil-in-water (o/w) microemulsions, stabilized by the nonionic surfactant polyoxyethylene 10-oleyl ether (Brij 96) and containing a range of oils, has been determined. Although testosterone propionate was readily soluble in the ethyl esters ethyl oleate, ethyl caprylate, and ethyl butyrate, and the triglycerides soybean oil, Miglyol 812, and tributryin, and the alkene 1-heptene, only microemulsions containing the ethyl esters and the triglyceride oils exhibited a significant increase in solubilization over the corresponding micellar solution (i.e., surfactant solution in the absence of oil). Furthermore, the increase in drug solubility observed in the microemulsion systems was not related to the solubility of the drug in the bulk oil. That is, while the smaller molecular volume oils, such as ethyl butyrate, exhibited a greater capacity for the drug, microemulsions containing these oils were only marginally better at solubilizing the drug than the corresponding micellar solution. In contrast, microemulsions containing the larger molecular volume oil, Miglyol 812, gave levels of drug solubilization almost three times those containing ethyl butyrate, yet the bulk capacity for drug in this oil was less than half that of ethyl butyrate. Light scattering and phase inversion temperature studies suggested that the structure of the microemulsion was sensitive to the oil being used, in that, at the low oil concentrations used in this study, the smaller molecular volume oils generally penetrated the interfacial surfactant monolayer in much the same way as a cosurfactant, causing an alteration, presumably a dilution, of the relatively concentrated polyoxyethylene region close to the hydrophobic core, thereby destroying one of the main loci of drug solubilization and counteracting any advantages encountered due to the high solubility of the drug in the bulk oil.

Emulsions↗
PubMed2005

[Effect of testosterone propionate on the distribution pattern of calcitonin gene-related peptide in different motoneuron pools].

OBJECTIVE: To study the effect of testosterone propionate (TP) on the distribution pattern of calcitonin gene-related peptide (CGRP) in two types of motoneuron (Mn) pools in rats. METHOD: The double labeling of cholera toxin B subunit coupled with colloidal gold (CB-Au) retrograde identification combining with immunocytochemistry was mainly used to reveal the distribution pattern of CGRP-like immunoreactivity (CGRP-LI) and its changes in the motoneuron pools labeled by CB-Au. RESULT: TP injected intramuscularly 28 days later significantly decreased CGRP expression in Mn pool innervating extensor digitorum longus (EDL, fast-twitch), comparing with corresponding control and castration group respectively (P < 0.001), while no significant effect on Mn pools innervating soleus (SOL, slow-twitch, P > 0.05) was observed. CONCLUSION: EDL-Mn pool is more sensitive to testosterone propionate than SOL-Mn pool in regulating CGRP expression.

Animals↗
PubMed1989

Endogenous and exogenous testosterone levels after administration of deuterium-labelled testosterone propionate in hypogonadotropic hypogonadism.

A gas chromatography-mass spectrometry-selected ion monitoring technique was employed to determine simultaneously the plasma concentrations of endogenous and exogenous testosterone in three patients with hypogonadotropic hypogonadism after a single i.m. dose of testosterone propionate-19,19,19-d3. The plasma levels of testosterone-19,19,19-d3 derived from testosterone propionate-19,19,19-d3 were maintained above the normal testosterone levels (greater than 4 ng/ml) for 48 h, while the plasma levels of endogenous testosterone changed little.

Adult↗
PubMed1978

Age difference in the response to synthetic luteinizing hormone-releasing hormone (LHRH) in androgenized rats with special reference to the dose of testosterone propionate for androgenization.

Five-day-old female rats were androgenized with 1,000 or 100 microgram testosterone propionate and were examined regarding the response to LHRH at 4, 7 and 12 weeks of age by measuring peripheral LH concentrations. The order of magnitude in LH release was 7 greater than 4 greater than 12 weeks old, whereas in normal rats, 4 greater than 12 greater than 7 weeks old. LH release in 4- and 7-week-old rats was higher than that in normal controls at the respective age, but was much lower than that in normal controls 12 weeks old. The LH release by Des-Gly10-(D-Ala6)-LHRH-ethylamide (TAP127) was greater than that by natural LHRH both in normal and androgenized rats at 7 or 12 weeks old. The results indicate that the pituitary gland in androgenized rats responds to LHRH to a much larger extent during the premature period and its responsiveness declines during the course of maturation. A marked hypersensitivity was observed in 7-week-old rats androgenized with 100 microgram testosterone propionate. The process of androgenization may include the induction of alterations in the sensitivity of the pituitary to LHRH and probably in the LH synthesizing ability of the pituitary.

Aging↗
PubMed1981

Some solute-solvent complexes involving testosterone and testosterone propionate.

Solute-solvent interactions have been studied by observing the influences of carbon tetrachloride, carbon disulphide, ethyl oleate, isopropyl myristate and octanol on the solubilities of testosterone and testosterone propionate in an inert solvent (cyclohexane). Complexation with testosterone was detected, but there was no evidence of complexation between testosterone propionate and these solvents. The solvent-induced infrared shifts were due to non-specific solvent effects. The existence of solute-solvent complexes between the two solutes and chloroform, previously detected by infrared absorption, was confirmed. The solubility technique, which has previously only been used with solid complexing agents, is adaptable to liquid complexing agents, but has limitations.

Solubility↗
PubMed1987

Influence of solvent on the availability of testosterone propionate from oily, intramuscular injections in the rat.

The suggestion that the biological response to an oily intramuscular injection of testosterone ester is regulated by rapid accumulation of the steroid in body fat, followed by a slow release, has been tested by comparing the release rates of 14C-labelled testosterone propionate from different solvents following intramuscular injection into rats. Disappearance from the injection site was rectilinearly related to in-vitro partition coefficients, but elimination of radioactivity in urine and faeces was significantly longer, and the same for all four solvents. Testosterone and testosterone propionate were found in equal concentration in body fat, 2 and 3 days after injection, but their concentrations were too low to form an effective depot. It is suggested that the delay in release, and the independence of the delay on the nature of the solvent is a consequence of biliary recycling of testosterone.

Adipose Tissue↗
PubMed1980

Synergism between bovine seminal plasma extract and testosterone propionate in suppressing serum concentrations of gonadotrophins in acutely castrated rats: a role for inhibin.

The rise in concentrations of FSH and LH in serum seen 24 h after castration was suppressed by the administration of an extract of bull seminal plasma or testosterone propionate at the time of castration. Whereas testosterone propionate preferentially suppressed LH, the seminal plasma extract suppressed FSH and LH equally. Small doses of bull seminal plasma extract and testosterone, that had little effect separately, acted synergistically to supress levels of FSH and LH to those found in intact animals, while combinations of larger doses had little further effect. This selective interaction suggests how inhibin and testosterone might together regulate concentrations of FSH and LH in the blood of the male rat.

Animals↗
PubMed1980

The B-cell development independent of the bursa of Fabricius but dependent upon the thymus in chickens treated with testosterone propionate.

Spleen cells taken from chickens treated with testosterone propionate, surgically bursectomized and immunized, were treated with anti-bursa-cell antiserum in the presence of complement, and transferred together with the mixed antigens into immunodeficient chickens. The recipient chickens showed restored capacity for antibody response to sheep red blood cells. In contrast, adoptive immune responses by spleen cells from normal chickens were abolished by treating with anti-bursa-cell antiserum in the presence of complement. These findings indicate that antibody-forming cells in TP-treated chickens do not bear cell-surface antigens specific for bursa cells; Testosterone-treated chickens were thymectomized at 7 days of age and immunized with the mixed antigens; the chickens thus treated were not able to produce antibodies. Thymocytes and thymus-derived cells taken from normal chickens were transferred into the testosterone-treated and surgically thymectomized chickens; but the antibody responses were not restored, indicating that absence of antibody formation in testosterone-treated, thymectomized birds is not due to lack of T cells as such. This result was confirmed by using adoptive transfer of B cells taken from testosterone-treated chickens together with T cells.

Animals↗
PubMed1983

Prenatal testosterone propionate and postnatal ovarian activity in the rat.

Testosterone propionate (TP) was given to rats on days 16 through 20 of pregnancy (2 mg/day). Female young had masculinized external genitalia. Sexual maturity was accelerated in TP females, despite lower weights and shorter lengths of body and tail. Placental and body weights were lower in TP females and males than in controls. The inhibiting effect of TP on postnatal growth is probably mediated by its effect on birth weight through placental damage. Ovarian cyclicity occurred upon reaching sexual maturity. In one experiment TP females were ovariectomized at 6 weeks, and given ovarian and vaginal grafts. Most of these animals showed regular cyclicity in vaginal smears between 74-100 days. Thus neither the 'early', nor the 'delayed early androgen syndrome' occurred in these experiments. This absence of effect of prenatal TP on ovarian cyclicity is attributable to a placental barrier for testosterone. When maternal plasma testosterone was raised 20-fold by exogenous TP, foetal testosterone levels remained unchanged. More detailed information was obtained when labelled testosterone was infused into a pregnant rat. Testosterone did not reach the foetus as such, but mainly as androsterone, which cannot be converted into oestrogens. This explains why prenatal TP can cause masculinization of genitalia, without 'masculinizing' the gonadotrophin secretion pattern in female rats. The latter process would presumably require oestrogenic compounds.

Animals↗
PubMed1982

Studies on hemopoietic stem cells in mice treated with testosterone propionate and anticancer drugs.

The alleged possibility that testosterone propionate (TP) has a protective effect on hemopoietic cells submitted to the damaging effect of antitumoral drugs was studied. The bone marrow content and the proliferating fraction of CFUs were determined following a single dose on 450 mg/kg of TP. At selected times after TP injection (2 and 4 days), TP-treated mice received a single dose of azathioprine, hydroxyurea, vinblastine, cyclophosphamide, BCNU and doxorubicin. The bone marrow of CFUs were determined 24 h after drug administration. The CFUs-surviving fraction in all cases appeared similar to or lower than that found in controls not treated with TP. It seems therefore that in this experimental setting TP does not reduce the toxic effect of anticancer drugs on hemopoietic pluripotent stem cells. However, this finding does not exclude a possible protective effect of TP at different levels of hemopoiesis or when the steroid is administered with a different schedule.

Animals↗
PubMed1985

Testosterone propionate treatment of an XY gonadal dysgenetic chacma baboon.

Behavioral studies of an XY gonadal dysgenetic chacma baboon prior to and during testosterone propionate treatment were carried out. The orchidectomized dysgenetic individual, two intact males, a castrate male, and two ovariectomized females were pair-tested with a group of eight ovariectomized stimulus females prior to and during their treatment with estradiol benzoate. Three test series were carried out. One series occurred prior to any treatment of the agonadal focal subject animals. During this series it was only the intact males who showed behavior change during their testing with the estrogen treated females. A second test series occurred after a month of daily testosterone propionate injections (1 mg/kg/day) had been given to the four agonadal subjects. During this test series the castrate male ejaculated once with one of the estrogen-treated females. All of the treated subjects showed increases in their frequency of yawning. Upon completion of this test series the androgen dosage was increased (2 mg/kg/day) and 2 weeks later a third test series was carried out. During this series the castrate male ejaculated with five of his eight estrogen-treated partners. The yawning of all the treated subjects continued. As had been the case in the second series the XY gonadal dysgenetic individual continued to behave as did the ovariectomized females. None of these animals showed any increase in any measure of male sexual behavior. This study establishes the fact that a genetic male primate deprived of in utero exposure to testicular hormones will go on to develop as a normal genetic female and will fail to exhibit increased levels of male sexual behavior during androgen treatment.

Animals↗