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PubMed1995

Response to Salmonella enteritidis infection by the immunocompromised avian host.

To develop knowledge of the avian immune response and improve the ability of chickens to resist infection by Salmonella enteritidis (SE), the role of the different components of the immune response against SE infection was examined. Birds were given treatments with cyclophosphamide, cyclosporine A, or testosterone propionate to induce immunological deficiency, and experiments were performed to determine the effects of each on the immune response. Each treatment reduced hatch rate, survival rate, and rate of weight gain. As measured by flow cytometry, treatments with cyclophosphamide and testosterone propionate decreased the percentages of B cells to background levels and increased the percentages of CT8 cells significantly above controls. The intestinal shed rate of SE increased after treatment with testosterone propionate and cyclophosphamide, but dissemination to the spleen of infected birds was not different from controls for any treatment. The SE infection was also immunosuppressive as measured by the proliferative response to mitogenic stimulation. Maximum lymphocyte proliferation occurred 1 wk after infection in response to .5 micrograms concanavalin A per 10(6) cells. By the 2nd wk, proliferation dropped 10-fold to almost no response. Results showed that immunocompetence relied on interdependent functions of multiple components of the immune response, i.e., aspects of both humoral and cell-mediated immunity.

Animals↗
PubMed1989

Antiandrogenic effects of a flavonoid-rich fraction of Vitex negundo seeds: a histological and biochemical study in dogs.

The ability of the flavonoid-rich fraction (5,7,3'-trihydroxy, 6,8,4'-trimethoxy flavones) of Vitex negundo seeds to antagonize the androgen action of exogenous testosterone propionate on the male reproductive system was studied in castrated prepubertal and intact adult dog. The flavonoid-rich fraction (F) was administered 10 mg/kg i.p. every other day either alone or in combination with testosterone propionate. The duration of treatment was 30 days in castrates and 60 days in intacts. Treatment with F caused disruption of the latter stages of spermatogenesis. The epididymides were devoid of spermatozoa. Protein, sialic acid and RNA contents of the testes and epididymides were reduced significantly while testicular cholesterol and phosphatase activity in testes and epididymides were elevated. Reduced androgen production was reflected in low levels of sialic acid in testes and epididymides. Castration alone brought about reduction in size and weight of the epididymides whereas castration followed by F treatment caused a reduction in the cellular heights of epididymides. Simultaneous administration of testosterone propionate to F-treated intact adult and castrated prepubertal dogs maintained the viability of spermatozoa, kept epididymal physiology relatively normal and significantly increased the cellular heights of epididymides.

Androgen Antagonists↗
PubMed1975

Partial masculinization of rat liver enzyme activities following treatment with FSH.

The metabolism of 4-(4014C)androstene-3,17-dione and 5alpha-(4-14C)androstene-3alpha, 17beta-diol was studies in the microsomal fraction and that of 4-(4-14C) androstene-3,17-dione in the 105,000 times g supernatant fraction of livers from castrated male and female rats treated with LH and FSH. Administration of LH led to significant decreases in 17-hydroxysteroid reduction and 7alpha-hydroxylation of 4-androstene-3,17-dione in both male and female rats and in 6beta-hydroxylation of 4-androstene-3,17-dione in female rats. FSH on the other hand specifically stimulated (masculinized) the following sex-dependent hydroxylations: 16alpha-hydroxylation of 4-androstene-3,17-dione in female rats and 2alpha-, and 2beta- and 18-hydroxylation of 5alpha-androstane-3alpha,17beta-diol in male rats. The metabolism of 4-androstene-3,17-dione and 5alpha-androstane-3alpha,17beta-diol was also studied in castrated male and female rats given testosterone propionate and in castrated female rats given testosterone propionate in combination with LH or FSH. It was shown that neither LH nor FSH could compensate for the relative androgen-unresponsiveness exhibited by female as compared to male rats. It is concluded that FSH but not LH may participate in the regulation of sex-dependent hydroxylase systems in rat liver.?2,Author

17-Hydroxycorticosteroids↗
PubMed2002

Mechanism of androgen action on cell proliferation: AS3 protein as a mediator of proliferative arrest in the rat prostate.

Androgens control the proliferation of their target cells first by increasing cell proliferation and later by inhibiting the proliferation of those same cells. Recently, we reported that the AS3 protein mediates the androgen-induced quiescence in androgen-target human cell lines. Our aims were to investigate the expression of the AS3 protein in the rat prostate in situ and in human cells in culture. Adult rats were separated into four groups (intact, castrated, castrated plus 3-d testosterone propionate replacement, and castrated plus 7-d testosterone propionate replacement). S9 cells expressing a tetracycline-regulated sense AS3 were also used. AS3 was expressed in the nuclei of over 90% of the epithelial cells and about 40% of the smooth muscle cells of the intact rat prostate. AS3 was not expressed in castrated rats or during the proliferative phase of androgen-induced regeneration. It was expressed in intact and castrated animals when the prostate has reached adult organ size. The AS3 protein was not expressed in cells that incorporate bromodeoxyuridine. These data suggest that AS3 is a mediator of the proliferative arrest in the normal rat prostate in situ and human prostate cell lines and that its expression is androgen-induced.

Amino Acid Sequence↗
PubMed1987

Regulation of hepatic sulfotransferase catalyzing the activation of N-hydroxyarylamide and N-hydroxyarylamine by growth hormone.

The regulatory mechanism of hepatic sulfation of N-hydroxyarylamine and N-hydroxyarylamide by endocrine factors has been studied in rats. The cytosolic sulfations of N-hydroxy-2-acetylaminofluorene (N-hydroxy-AAF) and 2-hydroxyamino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (N-hydroxy-Glu-P-1), which were determined by the reductive formations of 2-acetylaminofluorene and Glu-P-1, were seven to nine times and three times higher, respectively, in male than female rats. Hypophysectomy of male rats decreased their activities to 23% and 41% of the levels of the untreated animals, respectively. Intermittent treatment of hypophysectomized male and female rats with human growth hormone (hGH) significantly increased their sulfating activities of both compounds. Infusion of hGH also enhanced the sulfating activity of N-hydroxy-AAF but not of N-hydroxy-Glu-P-1. The sulfating activity of N-hydroxy-AAF was also decreased by castration at neonate and was increased by the administration of testosterone propionate to gonadectomized male and female rats. Testosterone propionate and estradiol benzoate had no effect on hypophysectomized rats, but estradiol benzoate repressed the sulfating activities of N-hydroxy-AAF and N-hydroxy-Glu-P-1 in hGH-treated hypophysectomized male rats. These results indicate that sex steroids elicit their effects on the sulfations of N-hydroxyl-aryl compounds through modulating the action of growth hormone at hypothalamus-pituitary and hepatic levels in rat livers.

2-Acetylaminofluorene↗
PubMed1979

The androgenic effect on the fine structure on the Harderian gland in the male hamster.

A sexual dimorphism of the hamster Harderian gland at the ultrastructural level has been reported. The effect of testosterone on the fine structure of the gland from castrated male golden hamsters is reported here. Harderian glands from the following three groups of animals were examined at regular intervals up to 60 days after castration: (1) castrated; (2) castrated-sham-injected, receiving 0.1 ml sesame oil per day; (3) castrated-testosterone-injected, receiving 2 mg testosterone propionate in 0.1 ml sesame oil per day. In groups 1 and 2, clusters of cylindrical tubules, typical of the male gland, decreased in number and disappeared almost completely 2 wailed in these two groups throughout the remaining period of experiment. On the other hand, these changes were prevented in the group of castrated animals maintained on testosterone propionate. It is concluded that castration modified the ultrastructure of the male hamster Harderian gland toward the female type and that daily administration of testosterone propionate prevented this change.

Animals↗
PubMed1979

Altered sexual differentiation of hepatic uridine diphosphate glucuronyltransferase by neonatal hormone treatment in rats.

The hepatic microsomal enzyme UDP-glucuronyltransferase undergoes a complex developmental pattern in which enzyme activity is first detectable on the 18th day of gestation in rats. Prepubertal activities are similar for males and females. However, postpubertal sexual differentiation of enzyme activity occurs in which male activities are twice those of females. Neonatal administration of testosterone propionate or diethylstilboestrol to intact animals resulted in lowered UDP-glucuronyltransferase activity in liver microsomal fractions of adult male rats, whereas no changes were observed in the adult females and prepubertal male and female animals. Neonatal administration of testosterone propionate and diethylstilboestrol adversely affected male reproductive-tract development as evidenced by decreased weights of testes, seminal vesicles and ventral prostate. Diethylstilboestrol also markedly decreased spermatogenesis. Hypophysectomy of adult male rats resulted in negative modulation of microsomal UDP-glucuronyltransferase and prevented the sexual differentiation of enzyme activity. In contrast hypophysectomy had no effect on female UDP-glucuronyltransferase activity. A pituitary transplant under the kidney capsule was not capable of reversing the enzyme effects of hypophysectomy, therefore suggesting that the male pituitary factor(s) responsible for positive modulation of UDP-glucuronyltransferase might be under hypothalamic control in the form of a releasing factor. Neonatal testosterone propionate and diethylstilboestrol administration apparently interfered with the normal sequence of postpubertal UDP-glucuronyltransferase sexual differentiation.

Age Factors↗
PubMed1990

Neonatal hormone manipulations and the maintenance of perineal muscles and their motor neurones in Albino Swiss rats.

Newborn female Albino Swiss rats received testosterone propionate, dihydrotestosterone benzoate or oestradiol benzoate for 4 days after birth. The neonatal administration of all three hormones maintained neurones of the spinal nucleus of bulbocavernosus (SNB) complex in adulthood at levels intermediate between those found in normal females (approximately 40 neurones) and those found in normal males (approximately 220 neurones). Dihydrotestosterone benzoate was the most effective treatment. Oestradiol benzoate, while as potent as testosterone propionate in maintaining SNB neurone numbers, could not maintain the perineal muscles which are their normal target. Dihydrotestosterone benzoate and testosterone propionate maintained both neurones and muscles. Newborn male Albino Swiss rats received either the aromatase inhibitor 4-OH-androstenedione, or the 5 alpha-reductase inhibitor aza-steroid 17 beta-N,N-diethylcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one(4-MA). Only neonatal treatment with 4-MA led to reduced SNB neurone numbers in adulthood, but the reduction was modest (-16%). The results of the two experiments suggest that several hormones can maintain SNB neurone numbers in Albino Swiss rats, but that 5 alpha-reduced metabolites of testosterone may be particularly effective.

Androgen Antagonists↗
PubMed1987

Comparison of two tests to recognize or exclude 5 alpha-reductase deficiency in prepubertal children.

Plasma testosterone (T, nmol/l) and dihydrotestosterone (DTH, nmol/l) were measured in 54 children and young adults with male pseudohermaphroditism (46XY, no defect of steroid biosynthesis) 4 h after im injection of testosterone propionate (25 mg/m2, group 1, N = 18), or before and 2, 4 and 6 days after hCG (5000 IU/m2 im, group 2, N = 36). The response to hCG was also studied in 5 control children (unilateral cryptorchidism, group 3) and that to testosterone propionate in a gonadectomized child with confirmed 5 alpha-reductase deficiency. Mean T (133.1 +/- 14.0, SEM) and DHT (17.1 +/- 2.6) in group 1 were higher than in group 2 (17.3 +/- 2.1 and 2.9 +/- 0.4), but there was not significant difference in the T/DHT ratios (group 1: 10.7 +/- 2.0; group 2: 7.2 +/- 0.6). Following testosterone-propionate, there was a negative correlation of T with age (r = -0.723). After hCG, T and DHT were lower in the prepubertal children than in those under 2 or over 10 years, and the T/DHT-ratio rose with age. Two children from group 1 had a T/DHT-ratio above 18, but urinary aetiocholanolone/androsterone (Ae/A) ratios were normal. In the child with 5 alpha-reductase deficiency, the T/DHT ratio was 60, and the urinary Ae/A ratio high. We concluded that the two tests are suitable for confirming or excluding 5 alpha-reductase deficiency in prepubertal children, in whom basal DHT is too low for evaluation, but that physiological age-related changes in 5 alpha-reductase activity have to be taken into consideration.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1974

Different mechanisms of regulation of nuclear reduced nicotinamide-adenine dinucleotide phosphate-dependent 3-oxo steroid 5alpha-reductase activity in rat liver, kidney and prostate.

The regulatory mechanisms involved in the control of the nuclear NADPH-dependent 3-ketosteroid 5alpha-reductase (5alpha-reductase) activity were studied in liver, kidney and prostate. The substrate used was [1,2-(3)H]androst-4-ene-3,17-dione (androstenedione) (for liver and kidney) or [4-(14)C]androstenedione (for prostate). The hepatic nuclear 5alpha-reductase activity was greater in female than in male rats, was greater in adult than in prepubertal female rats, increased after castration of male rats, but was not affected by treatment with testosterone propionate or oestradiol benzoate. These regulatory characteristics are in part different from those previously described for the hepatic microsomal 5alpha-reductase. The renal nuclear metabolism of androstenedione, i.e. 5alpha reduction and 17beta-hydroxy steroid reduction, was relatively unaffected by sex, age, castration and treatment with testosterone propionate. However, treatment of castrated male rats with oestradiol benzoate led to a significant increase in the 5alpha-reductase activity and a significant decrease in the 17beta-hydroxy steroid reductase activity. Finally, the nuclear 5alpha-reductase activity in prostate was androgen-dependent, decreasing after castration and increasing after treatment with testosterone propionate. In conclusion, the nuclear 5alpha-reductase activities in liver, kidney and prostate seem to be under the control of distinctly different regulatory mechanisms. The hypothesis is presented that whereas the prostatic nuclear 5alpha-reductase participates in the formation of a physiologically active androgen, 5alpha-dihydrotestosterone, this may not be the true function of the nuclear 5alpha-reductase in liver and kidney. These enzymes might rather serve to protect the androgen target sites in the chromatin from active androgens (e.g. testosterone) by transforming them into less active androgens (e.g. 5alpha-androstane-3,17-dione and/or 5alpha-dihydrotestosterone).

Journal Article↗
PubMed1996

Androgens in the topical treatment of lichen sclerosus.

BACKGROUND: Testosterone propionate has been shown repeatedly to be effective in the treatment of vulvar lichen sclerosus, yet studies of androgens in serum of women with untreated vulvar lichen sclerosus suggested an abnormal activity of 5-alpha reductase in these patients. If impairment of 5-alpha reductase in women with untreated vulvar lichen sclerosus is a proximate cause of this disease, then dihydrotestosterone should be more effective than testosterone propionate in the treatment of the condition. METHODS: To test this hypothesis, five women with vulvar lichen sclerosus received topically either dihydrotestosterone or testosterone propionate in a double-blind cross-over study. RESULTS: These androgens appear to be equally effective in inducing objective improvement of the vulvar lichen sclerosus by both gross and microscopic criteria. CONCLUSIONS: Impairment of 5-alpha reductase may not be germane to the pathogenesis of vulvar lichen sclerosus.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1975

Androgen-dependent accumulation of carnitine by rat epididymis after injection of [3H]butyrobetaine in vivo.

After i.m. injection of [3H]butyrobetaine into rats, the accumulation of carnitine into the epididymis, prostate gland, seminal vesicles, testis and heart was studied. The concentration of radiolabeled carnitine into the cauda epididymis increased linearly with time up to 72 h after the injection of the precursor, while its level in the prostate and seminal vesicles decreased rapidly. Very low levels of carnitine were found in the testis. Castration reduced the carnitine accumulation by cauda epididymis to 6% of the control levels while treatment of castrated animals with testosterone propionate (500 mug/day) partly restored the carnitine uptake. Similar treatment with 17beta-oestradiol valerate or 17alpha-hydroxyprogesterone had no effect. Surprisingly, cyproterone acetate (5 mg/day) also significantly stimulated carnitine accumulation by the epididymis to a level above that of the castrated controls. Simultaneous injection of both cyproterone acetate and testosterone propionate to castrated animals caused an additive effect of these steroids. This indicated that cyproterone acetate in this system is working as a weak androgen. Treatment of rats with 17beta-oestradiol valerate also reduced carnitine accumulation by the cauda epididymis. This is due to suppression of pituiatry gonadotrophin secretion, since concommitant treatment with testosterone propionate (500 mug/day) caused a normalization of the carnitine uptake. Treatment of intact rats with cyproterone acetate significantly reduced the epididymal weight, but not the carnitine accumulation. 17alpha-Hydroxyprogesterone treatment had no effect either on the epididymal weight or the accumulation of the carnitine. Unilateral orchiectomy reduced the carnitine accumulation by the cauda epididymis to about 40% of that occurring in the non-operated control side. This indicates that the luminal contact between the testis and epididymis or the luminal content of the epididymis itself is of importance for the androgen-dependent metabolic process occurring in the cauda epididymis. Castration or hormone treatment did not change the conversion of butyrobetaine to carnitine, or the carnitine uptake by heart. Carnitine uptake by the testis after [3H]butyrobetaine injection was rather low and this would exclude the possibility of synthesis of carnitine in the testis as a source of epididymal carnitine. Carnitine only accumulated in the cauda epididymis in vivo 4 to 96 h after injection of [3H]butyrobetaine. The presence of radioactively labeled butyrobetaine or methylcholine was not detected.

Animals↗
PubMed1986

Morphological and histological study of castration-induced degeneration and androgen-induced regeneration in the mouse prostate.

Degenerative and regenerative changes in the ductal architecture of the ventral and dorsolateral prostates (VP and DLP) of the adult mouse were investigated in microdissected specimens over a time-course of 14 days following castration and subsequently during 14 days of administration of testosterone propionate. After castration, about 35% of the ductal tips and branch-points were lost in distal regions (usually near the capsule) in both prostatic lobes. By contrast, in more proximal regions of the prostate (closer to the urethra), the ducts survived in an atrophic condition. The ductal morphology that had been lost in the distal regions completely regenerated after testosterone propionate was administered to the castrated males. In the VP, androgen replacement simply returned the gland to its former size with moderate ductal distension; in the DLP, excessive epithelial infoldings and ductal distension were elicited in the distal regions of the ducts after 14 days of treatment with testosterone propionate. These results suggest that androgenic responsiveness and dependency are different in distal versus proximal ducts. Distal ducts are exquisitely androgen-dependent and androgen-sensitive; in proximal regions, androgen-dependency is not as strict.

Animals↗
PubMed1999

Central administration of corticotrophin releasing hormone but not arginine vasopressin stimulates the secretion of luteinizing hormone in rams in the presence and absence of testosterone.

This study tested the hypothesis that central administration of corticotrophin-releasing hormone (CRH) and/or arginine vasopressin (AVP) will affect the secretion of LH in rams and that testosterone is necessary for these actions to occur. Plasma LH levels were measured in castrated rams during 1 h infusion of either 100 microliter vehicle/mock cerebrospinal fluid (CSF) or mock CSF containing 25 microgram CRH, 25 microgram AVP or 25 microgram of each peptide through guide cannulae into the third cerebral ventricle. These intracerebroventricular (i.c.v.) infusions were given to the castrated rams following injections (i.m.) each 12 h of oil or 8 mg testosterone propionate for 7 days. Blood samples were collected every 10 min for 4 h before i.c.v. infusion, during infusion and for 4 h following the infusion. Infusion of vehicle did not affect any endocrine parameters. In contrast, the plasma concentrations of LH and the amplitude of LH pulses were increased significantly during and following infusion of CRH, and this effect was not influenced by whether the castrated rams were treated with testosterone propionate or whether the CRH was administered in combination with AVP. Infusion of AVP alone did not affect LH secretion. The frequency of LH pulses and the plasma concentrations of FSH did not change with any of the i.c.v. treatments. The plasma concentrations of cortisol were significantly increased by CRH and AVP infusions. The plasma concentrations of cortisol achieved during and following i.c.v. infusion of CRH and AVP combined were greater than the concentrations achieved as a result of treatment with AVP alone but were similar to those with CRH. There was no effect of testosterone propionate on cortisol levels. These results show that CRH, but not AVP, is capable of acting either centrally or at the pituitary level to increase the secretion of LH in rams and these actions are not affected by testosterone. The stimulatory effects of CRH on LH secretion are to increase the amplitude of GnRH pulses and/or the responsiveness of the pituitary to the actions of GnRH with no effect on the frequency of GnRH pulses. The secretion of FSH in rams is not influenced by either CRH or AVP. The effect of CRH to increase LH pulse amplitude occurs in the face of increased cortisol levels, further reinforcing our belief that this adrenal steroid does not affect the reproductive axis in this species.

Animals↗
PubMed1980

The influence of testosterone on the alkaline proteolytic activity in rat skeletal muscle.

The effects of testectomy and subsequent administration of testosterone propionate on the activity of the alkaline proteinases in rat skeletal muscle were investigated. Castration of the mature rat was followed by a short-term delay in protein accretion in skeletal muscle tissue as measured by the protein/DNA ratio and was paralleled by a 2-3-fold increase in specific activity of the alkaline proteinase(s). This increase of proteolytic activity was equally significant when expressed relative to microgram DNA. Although the gain in body weight was significantly lower in the castrated rats, nevertheless the protein/DNA ratio in muscle after 6 weeks approximated the values of sham-operated control rats without normalization of the proteolytic activity. Treatment of the castrated rats with testosterone propionate resulted in restoring normal levels of previously elevated levels of alkaline proteolytic activity in muscle tissue. The normalization of enzyme activity as well as protein accretion in muscle was dose-dependent. Treatment of the rats with a low dose (0.1 mg/day) of testosterone propionate failed to restore the proteolytic activity, but led to a small increase of th protein/DNA ratio as well as to a progressive increase in body weight. These data indicate a regulatory role of testosterone in the adaptive behaviour of the alkaline proteolytic system in rat skeletal muscle.

Animals↗
PubMed1991

Sexual dimorphism of the chromatographic profiles of I-compounds (endogenous deoxyribonucleic acid modifications) in rat liver.

DNA of all tissues studied thus far in untreated mammals contains as yet structurally unidentified, covalent modifications termed I (indigenous)-compounds, which are detectable by the 32P postlabeling assay for DNA adducts and increase with age. The purpose of this study was to determine the effects of sex, gonadectomy, and androgen administration on I-compound profiles and levels in order to gain insight into the factors involved in the biosynthesis of these DNA modifications. Liver DNA from various groups of 6-month-old Sprague-Dawley rats (untreated or gonadectomized males and females; animals with or without gonadectomy treated with testosterone propionate) was analyzed by a nuclease P1-enhanced version of the 32P postlabeling assay. Hepatic I-compound profiles of untreated animals exhibited pronounced sexual dimorphism. In addition to a number of I-compounds that differed quantitatively between sexes, 7 female-specific and 1 male-specific I-compounds were observed. In female rats, the total level amounted to 112 I-compounds in 10(9) DNA nucleotides and exceeded the level in males by 3-fold. Castration feminized and ovariectomy masculinized I-compound profiles and levels. Neonatal testosterone propionate failed to restore the male pattern of I-compounds lost by neonatal castration, so that an androgen-imprinting mechanism did not appear to be involved in the maintenance of the male I-compound phenotype and the suppression of the female pattern. Testosterone propionate administered to intact female animals lowered total I-compound levels significantly. The results indicate that estrogens play a dominant role in regulating sex-dependent formation of I-compounds in rat liver. The dependence of I-compound formation on both age and sex hormones suggests that the levels of these DNA modifications are developmentally controlled.

Animals↗
PubMed1975

Free amino acids of sex organs of the mouse: regulation by androgen.

Male mice were castrated at 2 mo and a pellet of testosterone propionate was implanted subcutaneously 2 wk later. Mice were killed after 11 days and tissue extracts were analyzed. All the common 20 amino acids were present in widely varying concentrations. Castration uniformly increased the concentration of all free amino acids of the seminal vesicle, excepy proline, cystine/2, and tryptophan; androgen restored values to normal. These changes were not entirely due to changes in quantity of seminal vesicle fluid. Concentrations of amino acids of the prostate were not significantly changed by castration or testosteronepropionate. Fifteen other ninhydrin-postive compounds were detected. Hypotaruine, taurine alpha-aminobutyric acid, and cysteic acid in seminal vesicles were greatly decreased and several other compounds were slightly decreased by castration and restored tp normal by testosterone propionate. In the prostate, hypotaurine, alpha-aminobutyric acid, cysteic/cysteinessulfinic acids, glycerophosphoethaniomine, cystathionine, and phosphoethanolamine were decreased and alpha-amino-n-butyric acid was increased by castration and restored to normal by testosterone propionate. Concentrations of taurine and 5 other compounds were not affected. Epidiymis and testis also contained appreciable pools of amino acids and the other compounds. Amino acids concentrations were lower in cauda than in caput epididymis; in the testis values were intermidate, with much higher concentrations of glutamic and aspartic acids. Taurine concentrations were twice as great in cauda as in caput epidiymis; concentrations of hypotaurine and the other sulfur-containing compounds were similar in both parts of the epidiymis. The most striking result in the testis was the high concentration of reduced glutathione.

Amino Acids↗
PubMed1976

Effect of androgens on maturation and metabolism of erythroid tissue.

Specific changes taking place in the erythroid tissue following depletion or replacement of androgens were studied in rats. The reduction of testosterone levels in blood of orchiectomized animals did occur in conjunction with a decline of erythrocyte glucose-6-phosphate (G6P) and lactate levels. No evidence of anemia was observed. The subcutaneous administration of testosterone propionate (16.0 mg/kg) to orchiectomized rats restored, within 12 hours, blood testosterone levels as well as erythrocyte G6P levels and lactate production. The in vitro incorporation of glucose-1-14C into rat erythrocytes incubated with testosterone was comparable to that of control cells. A radioautographic study of rat erythroid marrow pulsed with glucose-1-14C showed a lower labeling when testosterone propionate was administered. The authors conclude that testosterone does directly affect glucose metabolism of erythroid cells, via the pentose shunt pathway. The possible role of the androgen-dependent enhancement of erythroid glycolysis is discussed in relation to the function of testosterone receptocytes present in marrow cells and a 17beta-hydroxysteroid dehydrogenase present in erythrocytes.

Animals↗