Non-castrated Animals Research Articles

Hormonal profiles, behavioral responses, and short-term growth performance after castration of pigs at three, six, nine, or twelve days of age1,2

The objective of this study was to determine the effects of castration on short-term growth performance, hormone profiles, and behavior in pigs at 3, 6, 9, or 12 d of age. Ninety intact male pigs were assigned randomly to a treatment age by litter [3, 6, 9, or 12 d of age; n = 9 to 13 pigs per treatment (age) group]. Pigs within a single litter were then assigned to noncastrated (NC) or castrated (CAS) treatment groups according to BW. Pigs were nonsurgically fitted with jugular catheters, and blood samples were drawn immediately before castration (0 h) and at 0.5, 1, 1.5, 2, 24, and 48 h after castration. Body weights were obtained when pigs were catheterized and again at 24 and 48 h after castration. Serum samples were analyzed for cortisol, porcine corticosteroid-binding globulin, and dehydroepiandrosterone sulfate (DHEA-S). No differences were detected in initial BW of pigs, and there was no overall treatment effect on growth performance of pigs at 24 or 48 h posttreatment. A time x treatment interaction was detected (P < 0.01) for serum cortisol concentrations, such that cortisol was greater in CAS pigs than in NC pigs. No overall effect of age at castration was observed on cortisol concentrations. At 24 h after castration, serum cortisol concentrations returned to baseline in all treatment groups; however, at 48 h after castration, overall cortisol concentrations were elevated (P < 0.01) in the 6-, 9-, and 12-d-old pigs in both the CAS and NC groups compared with baseline concentrations. Total cortisol and porcine corticosteroid-binding globulin were used to calculate the free cortisol index (FCI). A time x treatment interaction was observed (P < 0.01) for FCI, such that FCI was greater in CAS males than in NC males. The FCI was also affected by age (P < 0.01). There was a time x treatment x age interaction (P < 0.01) for serum DHEA-S, such that DHEA-S concentrations decreased in CAS animals but increased in NC animals, and DHEA-S concentrations increased with age. During the first 2 h after castration, there was an overall age effect (P = 0.01) on the time that pigs spent standing, such that 3-d-old pigs stood more than 6-, 9-, or 12-d-old pigs. Treatment did not influence the time that pigs spent nursing, lying, standing, or sitting, although there was a trend (P = 0.08) for CAS pigs to be less active than NC pigs. These data indicate that castration is stressful regardless of age; however, the stress associated with handling seems to increase as pigs age.

Producción de carne bovina en praderas renovadas con Brachiaria brizantha cv. Marandú en el Piedemonte de los llanos Orientales de Colombia

En una finca ganadera del Piedemonte Llanero de Colombia se realizó un trabajo de recuperación de praderas de Brachiaria decumbens, degradadas por el ataque del "mión de los pastos" (Aeneolamia sp.) y con predominio de la gramínea nativa Homolepis aturensis ("paja amarga"). Los tratamientos consistieron en labranza vertical al comienzo de las lluvias, siembra de la gramínea Brachiaria brizantha cv. Marandú y de las leguminosas forrajeras Pueraria phaseoloides (Kudzú) y Arachis pintoi (maní forrajero). Además, se fertilizó con 200 kg.ha-1 de roca fosfórica y cal dolomítica, 50 kg.ha-1 de cloruro de potasio y 25 kg.ha-1 de flor de azufre. Se utilizaron 30 animales enteros o toros (sin castrar) y 30 novillos (castrados) Cebú comercial, los cuales pastorearon 15 ha de pradera mejorada y 30 ha de pradera de B. decumbens con el manejo tradicional del productor (testigo); los animales se llevaron hasta un peso al sacrificio de 460 kg/animal. En la pradera renovada la disponibilidad de forraje aumentó de 750 a2.500 kg.ha-1 MS con 28 días de descanso; el contenido de minerales y proteína también aumentó. A su vez, la carga animal en las praderas renovadas fue 1.9 veces la obtenida en las praderas con manejo tradicional. Los novillos y los toros de la pradera mejorada ganaron 233 y 270 kg.ha-1 /año más de lo que ganaron los animales de la pradera testigo. En el segundo año el ingreso neto en la pradera testigo fue de $240.000 y $146.000/ha/año para toros y novillos respectivamente, mientras que en la pradera renovada el ingreso neto correspondiente fue de $762.000 y $590.000/ha/año.

Liver microsomal biotransformation of albendazole in deer, cattle, sheep and pig and some related wild breeds

Albendazole (ABZ) biotransformation was studied in vitro in liver microsomes of adult noncastrated male farm animals (ram, buck, bull and boar), castrated adult males (wether, billy and hog), and free living males (fallow buck, red deer stag, mouflon ram, roe buck and wild boar). Liver microsomal fractions were incubated with either ABZ or racemic albendazole sulphoxide (ABZSO). ABZ was extensively metabolized to the (+) and (-) enantiomers of ABZSO, whereas ABZSO underwent a slow oxidation to albendazole sulphone (ABZSO2) in all species. In all species both ABZSO enantiomers were detected. The chiral ratio, (+)-ABZSO/(-)-ABZSO, was greater than one in farm animals, mouflon and wild boar, and less than one in three species of deer. For total ABZ sulphoxidation, deer like species had lower values compared to the other species. Mouflon ram and ram had lower total sulphoxidation rates compared to wethers, as well as ABZ suphoxidation towards (+)-ABZSO. No significant difference occurred comparing ABZSO formation in mouflon ram and ram, but ABZSO2 formation rate in mouflon ram was higher than in rams and wethers. Roe deer stag, fallow buck and red deer stag did not differ in both total-ABZSO and (-)-ABZSO synthesis rates and roe deer stag and fallow buck did not differ in synthesis rates of (+)-ABZSO and ABZSO2. The bull differed from other species in all metabolites studied, except for red deer stag and boar in (-)-ABZSO synthesis rate. The extent of ABZSO sulphonation to ABZSO2 in bull microsomes was more than twice that of other species.

Efeito da castração pré-púbere sobre o desenvolvimento corporal de equinos

Aiming to evaluate the effect of pre-puberty castration on traction horses' body development, the experiment was carried out with 18 cross breeding Mangalarga foals. The animals belonged to the same stallion offspring and were castrated at 2 months old. The following characteristics were measured at ages 2, 12 and 24 months: the hights of withers, back chine, hook, ribs and chest floor, the lengths of body and rump, the widths of thurl, hook and chest and the perimeters of limbs and thorax. Besides, loading, capacity, body, morphological, chest and dactyl-thorax indexes were also measured. The results showed that there were not significant differences between castrated and non-castrated animals for almost all measured characteristics. However, castrated horses had greater liveweight, thorax perimeter and index capacity than non-castrated animals. Thus, it was concluded that pre-puberty castration is feasible.

Castration in female rats modifies the development of the pilocarpine model of epilepsy

Previous studies have shown that the susceptibility to pilocarpine-induced status epilepticus (SE) in female rats changes according to estrous cycle phases. These studies have also shown that following pilocarpine administration changes occur in gonadal, hypophyseal and hypothalamic hormones that could contribute for the sequence of the epileptic events. Accordingly, the present work aimed to investigate the role of sexual hormones withdrawal on the development of the pilocarpine model of epilepsy in female rats. With this purpose, castrated and non-castrated adult female Wistar rats were injected with pilocarpine and some characteristic parameters of the experimental model were observed. The results showed increased mortality after pilocarpine injection in the castrated rats when compared with non-castrated females. The latency period for SE onset and for the first spontaneous seizure was decreased in castrated when compared with non-castrated animals. The mossy fiber sprouting measured by neo-Timm scale during the chronic period, reached grade 3 for castrated epileptic rats while the non-castrated epileptic rats showed grade 2. Our results indicate that castration interferes with the epileptogenesis in the pilocarpine model of epilepsy suggesting that female sexual hormones could have protective effects against pilocarpine-induced SE.

Expression of testosterone-dependent enzyme, carbonic anhydrase III, and oxidative stress in experimental alcoholic liver disease.

We studied the sequential immunohistochemical appearance of androgen-dependent carbonic anhydrase (CA III) during the development of ethanol-induced liver injury using liver samples from castrated and noncastrated male micropigs. In castrated micropigs, the baseline expression of CA III was either low or absent, while distinct positive immunoreactions were found in zone 3 hepatocytes at 5 and 12 months after the initiation of the ethanol diet. The CA III enzyme and protein adducts of lipid peroxidation-derived aldehydic products, malondialdehyde and 4-hydroxynonenal, appeared together in the perivenous region, suggesting that the enzyme functions in an oxidative environment. The positive staining became more abundant and widespread during the progression of alcoholic liver disease. After 12 months, CA III was significantly more abundant in both the ethanol-fed noncastrated and castrated micropigs than in the control animals (P < 0.001, P < 0.05, respectively). CA III content was strikingly high in the ethanol-fed noncastrated animals, consistent with a potential role of androgens in the regulation of ethanol-induced CA III expression. The strongly positive CA III immunoreactions in the ethanol-fed noncastrated micropigs were associated with scant evidence of aldehydic protein adducts and minimal histopathology. Thus, enhanced expression of CA III during ethanol consumption may also account in part for gender differences in the susceptibility for alcohol-induced liver injury.

Dehydroepiandrosterone: an inexpensive steroid hormone that decreases the mortality due to sepsis following trauma-induced hemorrhage.

Recent studies suggest that male sex steroids play a role in producing immunodepression following trauma-hemorrhage. This notion is supported by studies showing that castration of male mice before trauma-hemorrhage or the administration of the androgen receptor blocker flutamide following trauma-hemorrhage in noncastrated animals prevents immunodepression and improves the survival rate of animals subjected to subsequent sepsis. However, it remains unknown whether the most abundant steroid hormone, dehydroepiandrosterone (DHEA), protects or depresses immune functions following trauma-hemorrhage. In this regard, DHEA has been reported to have estrogenic and androgenic properties, depending on the hormonal milieu. To determine whether administration of DHEA after trauma-hemorrhage has any salutary or deleterious effects on immune responses, and whether it improves the survival of animals subjected to subsequent sepsis. Male C3H/HeN mice underwent laparotomy (ie, trauma-induced) and hemorrhagic shock (blood pressure, 35+/-5 mm Hg for 90 minutes) followed by fluid resuscitation, or sham operation. The animals then received 100 mg of DHEA (4 mg/kg) or propylene glycol (hereafter referred to as vehicle). At 24 hours after trauma-hemorrhage and resuscitation, the animals were killed and blood, spleens, and peritoneal macrophages were harvested. Splenocyte proliferation and interleukin (IL) 2 release and splenic and peritoneal macrophage IL-1 and IL-6 release were determined. In a separate set of experiments, sepsis was induced by cecal ligation and puncture at 48 hours after trauma-hemorrhage and resuscitation. For those studies, the animals received vehicle, a single 100-microg dose of DHEA, or 100 microg/d DHEA for 3 days following hemorrhage and resuscitation. Survival was monitored for 10 days after the induction of sepsis. Administration of DHEA restored the depressed splenocyte and macrophage functions at 24 hours after trauma-hemorrhage. Moreover, daily administration of DHEA for 3 days significantly increased the survival of animals subjected to subsequent sepsis (P=.01). The finding that DHEA markedly improves the depressed immune functions and survival of animals subjected to subsequent sepsis suggests that short-term treatment with DHEA after trauma-hemorrhage is a safe and novel approach for preventing immunodepression and for decreasing the mortality rate due to subsequent sepsis.

Free Fatty Acid Composition of the Adipose Tissue of Intact and Castrated Lambs Slaughtered at 12 and 30 Weeks of Age

Free fatty acids from adipose tissue of rams and wethers slaughtered at 12 and 30 weeks of age were isolated by a modified Bligh and Dyer method and analyzed by gas chromatography−mass spectrometry. A total of 15 free fatty acids were positively identified. At 12 weeks of age, rams had nonsignificantly higher levels of the flavor-significant compounds, 4-methyloctanoic and 4-methylnonanoic acids, than wethers. At 30 weeks of age, differences in the levels of these acids in rams and wethers became significant and 4-methyloctanoic and 4-methylnonanoic acids increased by 13- and 4-fold, respectively, in the noncastrated animals. Log odor unit values indicated that 4-methyloctanoic acid was present at or above its odor threshold value in rams and wethers of both slaughter ages, but that the value was much higher for 30-week-old rams. 4-Methylnonanoic acid was present below its odor threshold value in all samples. Keywords: Branched-chain fatty acids; fatty acids; adipose tissue; lamb; sheepmeat

Lack of influence of aromatase and 5 alpha-reductase inhibition on [3H]imipramine binding in the male rat brain.

In intact adult male rats an inhibitor of aromatase and an inhibitor of 5 alpha-reductase did not change the characteristics of [3H]imipramine binding sites in cerebral cortex, hypothalamus, and hippocampus. Testosterone, estradiol and dihydrotestosterone prevented the effect of castration on the number of [3H]imipramine binding sites, but had no effect in non-castrated animals. These data suggest that testosterone and its major metabolites, estradiol and dihydrotestosterone, are equally effective with regard to imipramine binding sites.

Major reproduction hormones as regulators of cell-to-cell interactions in humoral immune responses

The effects of chorionic gonadotropin (CG), estradiol, and progesterone on the cell mechanisms that determine the rate of the humoral immune response have been investigated in experiments on ovariectomized and noncastrated mice. CG (40 IU) injected into noncastrated animals increased the antibody response to sheep erythrocytes (SRBC), whereas a higher dose of the hormone (200 IU) had no effect. In contrast, both hormone doses inhibited the immune response in ovariectomized animals. Injection of estradiol (2.5 μg/day), but not progesterone (0.2 mg/day), into ovariectomized mice stimulated the immune response, indicating a possible role of estrogens as mediators of CG immuno-stimulating effect in noncastrated animals. Both CG doses inhibited suppressor cell generation in noncastrated mice, whereas in ovariectomized animals, the hormonal effect was directly opposite. Sex steroid hormones did not influence the formation of suppressor cells. In a syngeneic transfer system, the hormones under study did not change the activity of helper T cell precursors. However, CG administration to noncastrated recipients stimulated an adoptive immune response in a dose-dependent manner. Estradiol, but not progesterone, has the same effect in ovariectomized mice. CG administration (200 IU) to ovariectomized recipients inhibited the plaque-forming cell response. This CG effect depended upon prostaglandin synthetase activity.

3H]Imipramine binding in discrete brain areas is affected by castration in male rats

In adult male rats, castration induces a progressive decrease in the number of [ 3H]imipramine binding sites in the cerebral cortex and hypothalamus, and a progressive increase in the hippocampus. Testosterone completely prevents this effect of castration, but has no effect on the characteristics of brain imipramine binding sites in intact, non-castrated animals. These data suggest that threshold levels of testosterone are necessary for the maintenance of a normal number of imipramine binding sites in the rat brain, but that these binding sites are not modified by excess testosterone.

The relationship between inhibition of plasminogen-activator activity and prostatic involution

The role of plasminogen activators (PAs) as potential mediators of involution of the rat ventral prostate was investigated by using an approach involving the administration in vivo of anti-PA drugs. The prostates of castrated rats, which had been injected daily for 7 days with the anti-PA drugs 6-aminohexanoic acid, tranexamic acid, aprotinin and cortisol, were assayed for PA activity, weight and cell number. In the prostates from the castrated controls, there was a 10-fold increase in the mean PA activity and a 7-fold decrease in cell number relative to that of the non-castrated animals. Although this rise in enzyme activity could be decreased to some extent by all the drugs except aprotinin, only treatment with high doses of tranexamic acid or cortisol had a statistically significant effect. A similar pattern was observed with respect to the relative potency of the drugs in preventing the loss of prostatic weight and cell number after castration. The effects of cortisol were dose-dependent, with complete inhibition of both the rise in PA activity and cell loss occurring at a dose of about 15 mg/day. Since the concentration of the principal intranuclear androgen, dihydrotestosterone, was the same in the prostates from treated and untreated castrated rats, the effects of cortisol are not due to increased retention of this androgen. Rather, the high inverse correlation (r = 0.86) between the cellular concentration of PA activity and the cell population of the prostate implies that PAs are directly associated with prostatic involution and that cortisol, and to a lesser extent tranexamic acid, blocks the involution process through inhibition of PAs.

Effects of intrabulbar injections of 6-hydroxydopamine on ethyl acetate odor detection in castrate and non-castrate male rats

The function of norepinephrine-containing neurons which project to the olfactory bulb is poorly understood. Although there has been suggestion that norepinephrine (NE) may modulate general olfactory sensitivity by attenuating the inhibitory feedback of granule cells upon mitral and tufted cells, behavioral indices of olfactory sensitivity have not been measured in animals with depletions of bulbar NE. The present experiment used computerized olfactometry and signal detection methodology to assess the odor detection performance of castrate and non-castrate male rats to a range of perithreshold concentrations of ethyl acetate following 6-hydroxydopamine (6-OHDA) depletion of bulbar NE. Such depletion had no significant influence on odor detection performance at any of the odorant concentrations examined in either castrate or non-castrate animals, as indexed by the non-parametric sensitivity measure SI. This observation implies that general olfactory sensitivity is unaltered by major depletion of intrabulbar NE, but does not preculude the possibility that NE modulates sensitivity to select odorants or odorant mixtures, or alters detection ability under atypical states of arousal.

Castration and erection. An animal study.

Castrated dogs (n = 3) need a much higher threshold level of energy to induce erection by electrical stimulation of the cavernous nerve than noncastrated animals (n = 24). In addition the resulting quality of erection, measured as maximal intracavernous pressure (pCC) versus peak systolic blood pressure (BP), was weaker in castrated dogs (pCC = 57% of BP on average) than in noncastrated dogs (pCC = 80% of BP on average). A high venous outflow from the corpora cavernosa in castrated dogs can also explain the shorter duration of erection. This experimental model excludes the interference of subjective factors, such as erotic stimuli and libido on erection, and it seems that androgen deficiency has a direct effect on the neurophysiology of the erectile tissues resulting in a higher tonus of the detumescence factors, which can be explained by an incomplete relaxation of the sinusoidal smooth muscle.

Effect of prostaglandin D2 on the release of luteinizing hormone and prolactin in castrated and intact male rats.

One, 5 or 20 micrograms of prostaglandin D2 (PGD2) was infused into a lateral ventricle of the brain of anaesthetized intact or castrated male rats, and the response of luteinizing hormone (LH) and prolactin (Prl) was determined. PGD2 stimulated the release of LH in both groups of rats. The greatest LH-response was observed in the castrated rats, where the lowest dose of PGD2 (1 microgram) caused the greatest LH response. This dose was ineffective in the non-castrated animals. PGD2 had no effect on the release of Prl neither in intact nor in orchidectomized rats. It is concluded that PGD2 is capable of stimulating the release of LH in male rats and that the stimulating effect is intensified by removal of the gonadal negative feedback effect on the hypothalamo-pituitary unit.

Regulation of L-ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase in rat ventral prostate and seminal vesicle.

1. The activities of l-ornithine decarboxylase (EC 4.1.1.17) and S-adenosyl-l-methionine decarboxylase (EC 4.1.1.50) were dramatically enhanced in both the ventral prostate and the seminal vesicle of castrated rats in response to androgenic stimulation. The time course of the stimulation of ornithine decarboxylase together with the quantitatively different response of adenosylmethionine decarboxylase to testosterone treatment in the prostate gland and seminal vesicle indicated that the enhancement in polyamine synthesis in the ventral prostate may reflect both cellular proliferation and the restoration of the secretory functions of the organ. In the seminal vesicle, however, the stimulation of the polyamine-biosynthetic pathway more closely resembled the pattern found in other rat tissues, such as regenerating liver, undergoing compensatory growth. 2. Ornithine decarboxylase activity in the ventral prostate and especially in the seminal vesicle of sexually mature rat was diminished in vivo by various short-chain diamines such as 1,2-diaminoethane, 1,3-diaminopropane and putrescine (1,4-diaminobutane). These diamines had no direct effect on the enzyme activity in vitro. 3. In contrast with the marginal decrease in ornithine decarboxylase activity produced by diaminoethane in the ventral prostate of non-castrated animals, repeated injections of the latter amine completely prevented the intense stimulation of the enzyme activity in the ventral prostate and seminal vesicle of castrated rats at 24h after the commencement of testosterone treatment. 4. The decrease in ornithine decarboxylase activity observed after injections of diamines (putrescine) in the ventral prostate was apparently associated with a similar decrease in the amount of immunoreactive protein as revealed by immunotitration of the enzyme with antiserum to rat ornithine decarboxylase.

Control of Hormone Receptor Levels and Growth of 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors by Estrogens, Progesterone and Prolactin

The effect of various hormone treatments was investigated on the growth and hormone receptor levels of hormone-dependent (those which regressed after ovariectomy) dimethylbenz- (a)anthracene (DMBA)-induced mammary tumors in the rat. Hormone binding measured in die tumors which remained 5½ weeks after ovariectomy was low for estradiol-17β (E2) (0.6 ± 0.2 pmol/g tissue), R 5020 (0.9 ± 0.4 pmol/g tissue) and prolactin (PRL) (0.9 ± 0.4% of specific binding). In non-castrated animals, binding values were 2.9 ± 0.4 pmol/g tissue, 13.7 ± 2.0 pmol/g tissue and 3.2 ± 0.3% for E2, R 5020 and PRL, respectively. Administration of progesterone (P) alone (0.5 mg/day) for three weeks to castrated animals had no effect on tumor size or hormone binding. Treatment with E2 (0.5 μg/day) for the same period of time increased tumor size and hormone binding: E2, 3.0 ± 0.7 pmol/g tissue; R 5020, 14.8 ± 3.3 pmol/g tissue; PRL, 2.4 ± 0.6%. At a daily dose of 2 mg, PRL alone increased tumor size slightly while honnone binding remained low except for that of E2 which was increased to 2.0 ± 0.4 pmol/g tissue. Combination of E2 with P or PRL resulted in tumor growth greater than that observed after PRL or E2 alone. The levels of hormone binding present in the tumors at the end of these combined treatments were all increased to levels similar to those obtained with E2 alone. It can be concluded that the presence of estrogen receptors in the DMBA-induced mammary tumors is a veiy good index of hormone dependency. In fact, the levels of this receptor were high under all honnone treatments which led to stimulation of tumor growth. These studies also clearly demonstrate that the concentration of P receptors in the DMBAinduced mammary tumors, as well as the response of the tissue to P, depends upon E2.

Estradiol- and testosterone-induced alterations in phosphatidylcholine and triglyceride synthesis in hepatic endoplasmic reticulum

Pathways of phosphatidylcholine and triglyceride biosynthesis were studied in hepatic endoplasmic reticulum from castrated and noncastrated male rats pretreated with estradiol or testosterone. In vitro measurements of hepatic microsomal enzymes which catalyze phosphatidylcholine biosynthesis revealed a significant increase in the specific activity of the enzyme governing phosphatidylcholine biosynthesis by the sequential methylation of phosphatidylethanolamine in the estradiol-treated castrate animals. The specific activity of phosphorylcholine-glyceride transferase was decreased by estradiol treatment in both castrate and noncastrate animals. The specific activity of diglyceride acyltransferase, which catalyzes triglyceride biosynthesis, was decreased by estradiol pretreatment in both castrate and noncastrate animals and was increased by testosterone in the castrate animals. The changes in specific activity of the enzymes governing phosphatidylcholine biosynthesis may account for the previously noted increased in vivo incorporation of methyl groups of l-methionine into hepatic phosphatidylcholine in female and estradiol-treated animals; the data suggest that in female and estradiol-treated rats a greater proportion of hepatic phosphatidylcholine is synthesized by the stepwise methylation of phosphatidylethanolamine. The decrease in diglyceride acyltransferase specific activity seen after estradiol administration may account for the lipotropic-like effect of estradiol.

Prostaglandin F 2 ∝ and motility of the myometrium isolated from ovariectomized rats. Effects of 17-beta estradiol

The presence of prostaglandin F 2 ∝(PGF 2 ∝) in extracts of uterine horns removed from ovariectomized rats, from non-ovariectomized rats and from ovariectomized rats injected with 17-beta estradiol, was studied. Thin-layer chromatography determinations demonstrate the presence of PGF 2∝ in extracts of uterine horns from ovariectomized animals and ovariectomized animals injected with a very small dose of 17-beta estradiol (0.1 ug/day/3 days) but not in extracts from non-ovariectomized or from ovariectomized rats injected with a higher dose of the hormone (60 ug/day/3 days). The relative Isometric Developed Tension (IDT), expressed on dry tissue weight basis, as well as the stability of the IDT and of the frequency of contractions of myometrial strips isolated from castrated rats, were greater than those exhibited by preparations from non-castrated animals and from castrated animals injected with 17-beta estradiol (60 ug/ day/3 days). The influence of ovarian hormones on uterine PGF 2∝ and the possibility of some interrelation between uterine PGF 2∝ and the functional activity of isolated rat myometrium, is discussed.

Distribution of male and female steroid sex hormones in some organs of the male rat.

ABSTRACT [6,7-3H] 17β-Oestradiol with a specific activity of 42.4 Ci/mmole was injected intramuscularly into three to four month old male rats, castrated three days previously. The radioactivity in liver, skeletal muscle, blood, the anterior pituitary gland, the seminal vesicles and in the different prostatic lobes was measured by liquid scintillation counting at different intervals after the administration. A high and prolonged uptake of radioactivity was found in the anterior pituitary gland. The uptake by the accessory sex organs was much lower, but significantly higher than that by skeletal muscle. The uptake by the prostate and the seminal vesicles in castrated animals was similar to that in non-castrated animals. The pattern of radioactivity uptake in the anterior pituitary gland of castrated male rats given [3H] testosterone was distinctly different from that after administration of [3H] 17β-oestradiol. There was a rapid elimination of radioactivity from the adenohypophysis after the administration of [3H] testosterone.