Upregulation of cyclooxygenase-2 expression in porcine macula densa with chronic nitric oxide synthase inhibition.

The objective of this study was to investigate the effects of chronic inhibition of nitric oxide synthase (NOS) on cyclooxygenase-2 (COX-2) expression in the macula densa (MD) of swine, as well as the effects on expression of related proteins. Adult female Yucatan swine were given either tap water (control, n = 6) or water with N (G)-nitro-L-arginine methyl ester (L-NAME, 100 mg/liter, n = 5) for a minimum of 30 days. Duplicate samples of kidney were fixed or snap frozen. There was a significant (P = .0082) upregulation of COX-2 mRNA expression in the MD of L-NAME, as well as an apparent increase in COX-2 protein. Plasma renin activity also increased with L-NAME treatment (control, 0.34 ± 0.08 ng/ml; L-NAME, 1.26 ± 0.03 ng/ml; P = .00000003). There were no differences between groups in expression of either inducible NOS or renin protein or in serum electrolyte concentrations. In conclusion, with chronic inhibition of NOS, COX-2 in MD is upregulated, perhaps to compensate for loss of nitric oxide. Increases in COX-2 products may counteract renal arteriolar constriction and sustain renin release.

Age and body weight effects on glucose and insulin tolerance in colony cats maintained since weaning on high dietary carbohydrate.

High dietary carbohydrate is suggested to promote development of diabetes mellitus in cats. Glucose tolerance, insulin sensitivity, and insulin secretion were assessed in young [0.8-2.3 (median = 1.1) years, n = 13] and mature [4.0-7.0 (median 5.8) years, n = 12] sexually intact females of a large (n ≅ 700) feline colony in which only dry-type diets (35% metabolizable energy as carbohydrate) were fed from weaning. Insulin sensitivity was assessed from the 'late-phase' (60-120 min) plasma insulin response of intravenous glucose tolerance tests (IVGTTs) and from fractional change in glycaemia from baseline 15 min after an insulin bolus (0.1 U/kg, i.v.). Insulin secretion was assessed from the 'early-phase' (0-15 min) plasma insulin response of IVGTTs. Compared to the young cats, the mature cats had greater body weights [2.3-3.8 (median = 2.9) vs. 3.0-6.3 (median = 4.0) kg, p < 0.01], greater late-phase insulin responses (p < 0.05), lower insulin-induced glycaemic changes (p = 0.06), lower early-phase insulin responses (p < 0.05), and non-significantly different rates of glucose disposal. The late-phase insulin response was correlated with body weight and age (p < 0.05). When group assignments were balanced for body weight, the age-group differences and correlations became non-significant. The findings indicate that body weight gain is more likely than dry-type diets to induce the pre-diabetic conditions of insulin resistance and secretion dysfunction.

Laminitis and the equine metabolic syndrome.

Although much has been written about laminitis in the context of its association with inflammatory processes, recognition is growing that most cases of laminitis examined by veterinarians in private practice are those associated with pasture grazing, obesity, and insulin resistance (IR). The term 'endocrinopathic laminitis' has been adopted to classify the instances of laminitis in which the origin seems to be more strongly associated with an underlying endocrinopathy, such as either IR or the influence of corticosteroids. Results of a recent study suggest that obesity and IR represent the most common metabolic and endocrinopathic predispositions for laminitis in horses. IR also plays an important role in the pathogenesis of laminitis that develops when some horses or ponies are allowed to graze pastures at certain times of the year. The term equine metabolic syndrome (EMS) has been proposed as a label for horses whose clinical examination results (including both physical examination and laboratory testing) suggest heightened risk for developing laminitis as a result of underlying IR.

Seasonal and pulsatile dynamics of thyrotropin and leptin in mares maintained under a constant energy balance.

The objective of this study was to determine if seasonal and/or pulsatile variations occur in plasma concentrations of thyrotropin (TSH) and leptin in mares while maintaining a constant energy balance. Blood samples were collected every 20 min during a 24h period in winter and again in summer from six Quarter Horse type mares. Plasma concentrations of TSH, leptin, and T(4) were determined by radioimmunoassay. No differences were observed in body weight between winter (388.1+/-12.5 kg) and summer (406.2+/-12.5 kg; P=0.11). Plasma concentrations of TSH were greater in the summer (2.80+/-0.07 ng/ml) when compared to winter (0.97+/-0.07 ng/ml; P<0.001). Pulse frequency of TSH was not different between winter (6.17+/-0.78 pulses/24h) and summer (5.33+/-0.78 pulses/24h; P=0.49). Mean TSH pulse amplitude, pulse area, and area under the curve were all greater in summer compared to winter (3.11+/-0.10 ng/ml versus 1.20+/-0.10 ng/ml, 24.86+/-0.10 ng/ml min versus 13.46+/-1.90 ng/ml min, 3936+/-72.93 ng/ml versus 1284+/-72.93 ng/ml, respectively; P<0.01). Mean concentrations of leptin were greater in summer (2.48+/-0.17 ng/ml) compared to winter (0.65+/-0.17 ng/ml; P<0.001). Pulsatile secretion patterns of leptin were not observed in any horses during experimentation. Mean concentrations of T(4) were greater in winter (20.3+/-0.4 ng/ml) compared to summer (18.2+/-0.4 ng/ml; P<0.001). These seasonal differences between winter and summer provide evidence of possible seasonal regulation of TSH and leptin.

Equine endometrial fibrosis correlates with 11beta-HSD2, TGF-beta1 and ACE activities.

Endometrial periglandular fibrosis (EPF) contributes to embryonic and fetal loss in mares. Equine EPF correlates inversely with conception and successful gestation. In the modified Kenney endometrial biopsy classification system, EPF categories I, IIA, IIB, and III correspond to minimal, mild, moderate, and severe fibrosis (+/-inflammation), respectively. Paraffin sections of biopsy specimens were stained with H&E, and picrosirius red (specific for fibrillar collagens types I and III), to determine %EPCVF. Endometrial ACE-binding activity, TGF-beta1 and 11beta-HSD2 activities were also measured. Ultrastructural changes in EPF categories IIB and III endometria strongly suggested myofibroblastic transformation. ACE-binding activity was highest in EPF category IIB; however, endometrial TGF-beta1 and 11beta-HSD2 activities were significantly correlated to the severity of EPF (P<0.05). We conclude that, locally generated angiotensin II initiates the expression of TGF-beta1 resulting in myofibroblastic transformation. 11Beta-HSD2 in concert appears to modulate the severity of endometrial fibrosis.

Glucocorticoid receptors in peripheral blood lymphocytes from bovine leukemia virus-infected cows with persistent lymphocytosis.

Bovine leukemia virus-infected cows with persistent lymphocytosis have an expanded population of B-lymphocytes in the peripheral blood that is sensitive to glucocorticoids in vitro and in vivo. We examined peripheral blood lymphocytes from cows with persistent lymphocytosis for the presence of specific glucocorticoid receptors. Steroid binding in intact cells was determined by a whole cell competitive binding assay using [3H]dexamethasone. The binding of the glucocorticoid to receptor was characterized in terms of affinity, specificity, and kinetics of the reaction. We found that peripheral blood lymphocytes from three cows with persistent lymphocytosis had 5000 to 6600 specific glucocorticoid-binding sites/cell. Compared with that reported for human lymphoid cells, glucocorticoid receptors in the bovine lymphocytes were found to have a greater affinity for the steroid with an association rate that was three times faster and a dissociation rate that was less than one-half of the former. We examined the biological half-life of hydrocortisone in the normal cow and found it to be 69.3 min, which is shorter than that reported for other domestic species and humans. The kinetics and affinity of the steroid binding may explain why in vivo glucocorticoid sensitivity was demonstrated in these animals despite the fact that elevated levels of plasma corticoids were not maintained. These results suggest that glucocorticoid sensitivity may be influenced by the nature of the binding reaction between steroid and receptor.

Angiotensin-II-induced increase in transcoronary protein clearance: role of hypertension vs. nitric oxide or cyclo-oxygenase products.

Elevations in plasma angiotensin II (AngII) are associated with an efflux of plasma macromolecules into the perivascular and contiguous interstitial space. Whether this exudative response is related to associated hypertension or another effect of AngII is uncertain. We therefore monitored plasma and cardiac lymph total protein, albumin and fibronectin and calculated transvascular clearances for total protein (TVPC) and albumin (TVAC) and lymph fibronectin transport (LFT) every 30 min in open-chested, instrumented dogs. After baseline observations were obtained over 30 min, pressor (250 ng.kg.min-1) or nonpressor (11 ng.kg.min-1) doses of AngII were given intravenously for 90 min. Saline-treated, instrumented dogs served as controls. To address a potential secondary effect of AngII on vascular protein clearance, we monitored lymph prostaglandin E2 and cGMP (a marker of released nitric oxide, NO). At > or = 30 min, each dose of AngII was associated with a significant (P < or = 0.05) and comparable increase in TVPC, TVAC and LFT over baseline, indicating that increase in protein clearance was not related to elevated arterial pressure. Lymph cGMP rose significantly (P < or = 0.05) at 30 min for each dose of AngII and remained elevated thereafter. Lymph PGE2 was increased at > or = 60 min (P < or = 0.05) but only with the pressor dose. To determine the contribution of NO and PGE2 on AngII-induced transcoronary protein clearance, each dose of AngII was accompanied by co-administration of either the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the cyclo-oxygenase inhibitor, indomethacin. L-NAME completely inhibited the release of cGMP and the increase in protein clearance was not seen. Indomethacin suppressed the release of PGE2, but did not prevent the increase in protein clearance. Thus, AngII-induced increase in transcoronary protein clearance is not related to arterial hypertension or the release of PGE2, but instead appears to be mediated by NO release.

Steroids in fluids and sperm entering and leaving the bovine epididymis, epididymal tissue, and accessory sex gland secretions.

Ten steroids which may have a role in the process of sperm maturation within the epididymis were quantified by competitive protein binding or radioimmunoassay. Rete testis fluid (RTF) carrying testicular sperm into the epididymis was rich in dehydroepiandrosterone and testosterone (21 +/- 2 and 33 +/- 3 ng/ml) while cauda eipididymal plasma (CEP) around sperm which have completed maturation had high levels of progesterone, dihydrotestosterone, 3beta-androstanediol, dehydroepiandrosterone and testosterone (7.4 +/- 0.8, 20.3 +/- 1.1, 6.5 +/- 0.4, 8.0 +/- 0.7 and 11.5 +/- 0.7 ng/ml). About 4 mug of steroids enter the epidymis daily in RTF, but less than 1% was found in CEP; the balance presumably was absorbed by the epithelium in the proximal caput epididymidis. Nevertheless, tissue levels of total 17beta-OH androgens were lower in the proximal caput than in the distal caput or corpus epididymidis. In all zones of the epididymis, dihydrotestosterone accounted fro about 70% of the total 17beta-OH androgens found in the nuclear fraction. In the cytoplasmic fraction, however, dihydrotestosterone predominated only in the distal caput and corpus epididymidis. In the cauda epididymidis, CEP and sperm probably accounted for less than 35% of the total 17beta-OH androgens and less than 25% of the dihydrotesterone. The progesterone concentration of the cauda than in the caput epidymidis. Twice washed testicular sperm contained more testosterone than cauda epididymal or ejaculated sperm (16.6 +/- 1.9, 1.6 +/- 0.2 and 1.5 +/- 0.3 ng/10(9) sperm, respectively), but less progesterone (0.5 +/- 0.1, 1.3 +/- 0.2 and 1.0 +/- 0.4 ng/10(9) sperm, respectively). As a consequence of mixture with estrogen-rich prostatic fluid (150 +/- 9 pg/ml), ejaculated sperm contained a relatively high amount of estrogens (112 +/- 15 pg/10(9) sperm). These studies revealed marked differences in steroid profiles of fluids entering and leaving the epididymis and of infertile testicular and fertile cauda epididymal sperm.

Transcription and translation of estrogen receptor-beta in the male reproductive tract of estrogen receptor-alpha knock-out and wild-type mice.

Estrogen receptor-alpha (ERalpha) has been identified in the male reproductive tract, but the role of estrogen in the male has not been well characterized. In vivo mutations in ERalpha genes have demonstrated the necessity for ERalpha-mediated action in male fertility. We asked whether both ERbeta messenger RNA and protein were present in the male reproductive tract of wild-type and ERalpha knock-out (ERalpha KO) mice, and whether ERbeta could compensate for the lack of ERalpha in infertile male ERalpha KO mice. Immunohistochemical localization with both N- and C-terminal anti-ERbeta antibodies demonstrated that ERbeta is present in the Leydig cells of the testes and in the epithelium of both the efferent ductules and the initial segment of the epididymis. RT-PCR amplification was used to confirm ERbeta transcription in these tissues. In conclusion, we observed that ERbeta messenger RNA and protein continue to be expressed in the Leydig cells, elongated spermatids, efferent ductules, and the initial segment of the epididymides of ERalpha KO mice, but the presence of ERbeta is not able to compensate for the absence of ERalpha in male reproductive function.

Metabolic responses to exhaustive exercise in racing sled dogs fed diets containing medium, low, or zero carbohydrate.

Eighteen racing sled dogs were assigned to three diets containing protein, fat, and carbohydrate in proportions as follows: diet A, 39:61:0; diet B, 32:45:23; and diet C, 28:34:38 on an available energy basis. The dogs were studied through a 28-week training period and subjected to three special tests, the first after 12 weeks training, the second at 24 weeks, and the third 4 weeks later. Overnight fasting, resting blood samples were taken before exercise, then about 5 or 30 min after exercise in the first 2 tests, or 1,5...30 min after exercise in the third test. Negligible changes in the red cell indices or serum concentrations of total protein, sodium, and urea indicated that there were no major water shifts. Significant decrements were found in serum concentrations of albumin (3% of resting value), calcium (4%), magnesium (13%), and inorganic phosphorus (39%). Significant increments were found in serum concentrations of creatinine (50%) and activities of glutamic-pyruvic and glutamic-oxalacetic transaminases (31 and 52%, respectively). None of the above variables showed differences between diets, exercise bouts, or time after exercise. Significant decrements in plasma cholesterol (D, mg/100 ml) were linearly related to the initial concentration (I mg/100 ml); D - 0.161 I - 17 mg/100 ml. Hyperglycemic responses were exhibited by 14 dogs in the 3rd test, including five dogs on diet A. Resting plasma glucose concentrations, peak values after exercise, and removal rates were the same in dogs fed all three diets. Blood lactic acid concentrations were linearly related to plasma glance (two from each group) had significantly higher peak lactic/glucose ratios tthan the six "worst" dogs, but there was no significant difference between diets in other measures of glucose or lactic acid. Plasma concentrations of free fatty acids, acetoacetic acid and 3-OH-butyric acid reached a maximum 10 min after exercise. Peak values and mean increments of free fatty acids were highest in dogs fed diet A. Also, mean free fatty acid increment was significantly higher in the six best dogs than in the six worst. An enhanced ability to mobilize body fat should confer an advantage in a dog subjected to prolonged strenous exercise in which fatty acid oxidation accounts for most of the oxygen consumption.

Hormonal control of Leydig cell differentiation.

Leydig cell progenitors contain significant concentrations of androgen receptors. When the metabolism of DHT to 3 alpha-DIOL is blocked, DHT stimulates testosterone production by Leydig cell progenitors, most probably via an androgen receptor dependent mechanism. Rapid metabolism by 3 alpha-HSD may limit the potency of exogenous DHT to stimulate differentiation of Leydig cell progenitors in vitro. Insulin-like growth factor-I enhances androgen production by purified immature Leydig cells. The elevated sensitivity of immature Leydig cells versus adult Leydig cells to IGF-I stimulation indicates that this peptide hormone has a role in their differentiation during puberty.

Gender, exercise training, and eNOS expression in porcine skeletal muscle arteries.

Our purpose was to determine the effects of gender and exercise training on endothelial nitric oxide synthase (eNOS) and superoxide dismutase (SOD) protein content of porcine skeletal muscle arteries and to evaluate the role of 17beta-estradiol (E2) in these effects. We measured eNOS and SOD content with immunoblots and immunohistochemistry in femoral and brachial arteries of trained and sedentary male and female pigs and measured estrogen receptor (ER) mRNA and alpha-ER and beta-ER protein in aortas of male and female pigs. Results indicate that female arteries contain more eNOS than male arteries and that exercise training increases eNOS content independent of gender. Male and female pigs expressed similar levels of alpha-ER mRNA and protein and similar amounts beta-ER protein in their arteries. E2 concentrations as measured by RIA were 180 +/- 34 pg/ml in male sera and approximately 5 pg/ml in female sera, and neither was changed by training. However, bioassay indicated that biologically active estrogen equivalent to only 35 +/- 5 pg/ml was present in male sera. E2 in female pigs, whether measured by RIA or bioassay, was approximately 24 pg/ml at peak estrous and 2 pg/ml on day 5 diestrus. The free fraction of E2 in sera did not explain the low measurements, relative to RIA, of E2. We conclude that 1). gender has significant influence on eNOS and SOD content of porcine skeletal muscle arteries; 2). the effects of gender and exercise training vary among arteries of different anatomic origin; 3). male sera contains compounds that cause RIA to overestimate circulating estrogenic activity; and 4). relative to human men, the male pig is not biologically estrogenized by high levels of E2 reported by RIA, whereas in female pigs E2 levels are lower than in the blood of human women.

Simultaneous ultramicroanalysis of both 17-keto-and 17beta-hydroxy androgens in biological fluids.

Sensitive methods for quantifying androgens were lacking. Therefore, a relatively simple procedure for separating steroids was combined with highly specific assay methods so that eight androgens could be measured with high accuracy, precision and sensitivity. Semi-automated separations on Sephadex LH-20 columns used heptane:methylene chloride:ethanol:water (50:50:1:0.12) and a flow rate of 17.0 min/ml. The six peaks eluted contained androstenedine; androsterone, epiandrosterone and dihydrotestosterone; testosterone and dehydroepiandrosterone; 3alpha-androstanediol; 3beta-androstanediol; and androstenediol. Androstenedione, dehydroepiandrosterone and androstenediol were quantified using specific antisera (sensitivity less than or equal to 75 pg). Testosterone and dihydrotestosterone were measured by competitive protein-binding assays using rabbit TeBG (sensitivity less than or equal to 150 pg). 3alpha- and 3beta-androstanediol were similarly assayed using human TeBG (sensitivity approximately 150 pg). Androsterone was reduced with NaBH4 and the resulting 3alpha-androstanediol was assayed using human TeBG (sensitivity approximately 200 pg). Inter- and intra-assay variations were less than 10% for radioimmunoassays and less than 16% for competitive protein-binding assays over the entire dose response curve.

Radiometric quantitation of delta 4-3-ketosteroid-5 alpha-oxidoreductase utilizing high performance liquid chromatography.

A reliable isocratic high performance liquid chromatography (HPLC) procedure has been developed for the separation and subsequent radiometric quantitation of delta 4-3-ketosteroid-5 alpha-oxidoreductase enzyme activity. The specificity of this HPLC procedure has been confirmed through the use of authentic androgen radioisotopes, linearity of detector response, and mass spectral analysis. In conjunction with this we have also developed a simple Sep-Pak sample preparation procedure which allows the uniform complete isolation of these androgens from epididymal tissue homogenates. Utilizing these procedures we have determined the regional distribution of 5 alpha - reductase in the epididymis of the CD-1 mouse. Regional differences in enzyme activity were found between the caput-corpus and cauda regions. Enzyme activity (specific activity) was higher in the caput-corpus region (28.98 pmol 5 alpha - reduced androgens formed/h/mg protein) than the cauda region (6.20 pmol 5 alpha - reduced androgens formed/h/mg protein).

Effect of testosterone replacement on the alteration of steroid metabolism in the hypothalamic-preoptic area of male hamsters treated with melatonin.

Adult male hamsters were maintained under 14 hours of light per day and randomly assigned to groups that received daily afternoon melatonin (25 micrograms) or vehicle injections. Animals from both groups were killed following 4, 8, and 12 weeks of treatment. By 12 weeks, the melatonin-treated hamsters had significant reductions in the weights of the testes and seminal vesicles, serum testosterone levels, and activities did not differ between groups. In a second experiment, hamsters were hypothalamic-preoptic area (HPOA) aromatase activities. Hypothalamic-preoptic area 5 alpha-reductase activities did not differ between groups. In a second experiment, hamsters were again treated with melatonin or vehicle for 12 weeks prior to being killed. After 10 weeks of treatment, groups of melatonin-treated animals received subcutaneous silastic capsules (5, 10, or 20 mm) filled with testosterone. Animals in two other groups were given blank implants or no implants at all. Two weeks later, at autopsy, reproductive organ weights, serum testosterone levels, and HPOA aromatase activities were significantly suppressed by melatonin administration. 5 alpha-Reductase activity in the HPOA was not affected. Hamsters that had been given the 10- and 20-mm testosterone implants exhibited normal seminal vesicle weights and HPOA aromatase activities. These results suggest that melatonin-induced reduction of HPOA aromatase activity is mediated by decreased circulating levels of testosterone.

Influence of rete testis fluid deprivation on the kinetic parameters of goat epididymal 5 alpha-reductase.

A surgical technique to cannulate the rete testis of the goat was utilized to examine the effects of rete testis fluid (RTF) deprivation on the enzymatic activity of epididymal 5 alpha-reductase. Kinetic techniques were used to determine whether the regional enzymatic effect of RTF deprivation is to decrease the apparent number of 5 alpha-reductase active sites or the catalytic activity of each active site within the epididymal epithelium. Paired comparisons of (Vmax)app and (Km)app values between control and RTF-deprived epididymides indicated that RTF deprivation affected the value of (Vmax)app with no apparent change in the values of (Km)app in caput, corpus, and cauda epididymal regions. We conclude that RTF deprivation in the goat epididymis for 7 days results in a decreased number of apparent 5 alpha-reductase active sites within the epididymal epithelium.

Chronic mineralocorticoid excess and cardiovascular remodeling.

Chronic mineralocorticoid (MC) excess, whether due to elevated plasma aldosterone (ALDO) or deoxycorticosterone (DOC), is associated with a perivascular fibrosis of systemic and coronary arterioles. This remodeling of resistance vessels contributes to the appearance of hypertension. Chronic MC excess is also accompanied by cardiac myocyte necrosis, secondary to myocardial potassium depletion, and a subsequent reparative fibrosis that appears in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles. Fibrosis contributes to the appearance of ventricular arrhythmias and dysfunction. Herein, clinical and experimental evidence linking chronic, inappropriate (relative to dietary sodium) elevations in circulating ALDO and DOC with these reactive and reparative forms of fibrous tissue formation in the heart and other tissues is presented.

Gonadotoxic effects of 2-hexanone and 1,2-dibromo-3-chloropropane on the enzymatic activity of rat testicular 17 alpha-hydroxylase/C17,20-lyase.

In this study the gonadotoxic effects of 2-hexanone administered as a pretreatment and/or 1,2-dibromo-3-chloropropane administered as a challenge on the activity of several key steroidogenic enzymes in the rat testis were examined. Despite the absence of an effect when either treatment was administered individually, the pretreatment/challenge combination inhibited the steroidogenic capacity of the rat testis. The specific activity of testicular 17 alpha-hydroxylase was significantly reduced (P less than 0.05), with respect to the control, following the pretreatment/challenge combination. There were no significant differences between the control and the individual treatments. The inhibition of 17 alpha-hydroxylase activity occurred in the absence of significant differences in testis weight and testicular protein content. This inhibition of testicular steroidogenic enzyme activity was specific as the activity of another testicular enzyme, namely C17,20-lyase, was not affected by any treatment. The decline in rat testicular 17 alpha-hydroxylase activity 18 h after the 1,2-dibromo-3-chloropropane challenge precedes the reported alterations in the seminiferous epithelium following this same treatment. The results of the present study indicate that the steroidogenic cell of the testis, i.e. the Leydig cell, is a potential site for the primary toxic effects of these agents in the rat testis.

Inhibition of testicular steroidogenesis in the neonatal rat following acute ethanol exposure.

We have previously reported detrimental effects of in utero ethanol exposure on testicular steroidogenic enzyme activity in newborn rats. It is now reported that in utero ethanol exposure during Day 12 of gestation through birth has no apparent morphological effect on the testes of Day 1 neonatal rats. It appears that the detrimental effects of ethanol on testicular steroidogenesis can be manifested at the biochemical level in the absence of morphological effects. However, it remained unknown as to whether acute exposure to ethanol would elicit similar biochemical effects as chronic ethanol exposure on testicular steroidogenesis. To test this possibility ethanol was injected at 0, 1, or 2 g/kg intraperitoneally (IP) into rats of various postnatal ages. Plasma ethanol and testosterone levels as well as testicular 17 alpha-hydroxylase and C17,20-lyase activities were measured. The results indicate that acute exposure to ethanol significantly (p less than 0.05) inhibits the catalytic activity of testicular 17 alpha-hydroxylase in the newborn rat testis. This inhibition was specific since the activity of testicular C17,20-lyase was not affected. In conjunction with the reduction in testicular enzyme activity, plasma testosterone levels were reduced to 30% of the control levels in newborn animals receiving ethanol. In older animals, i.e., postnatal Day 20 and 40 rats, plasma testosterone levels were reduced, but not significantly, following ethanol treatment. Furthermore, testicular enzyme activity was not significantly reduced following ethanol treatment in these same older animals. These results suggest that the newborn rat testis is especially sensitive to the effects of ethanol.

Plasma and endometrial progesterone content following exogenous progesterone administration in mares.

Intact and ovariectomized pony mares were treated with either progesterone in-oil or repositol progesterone. Serum progesterone, endometrial progesterone and endometrial histology were examined. There were no differences in serum or tissue progesterone between intact and ovariectomized mares. Serum and tissue progesterone were greater for progesterone in-oil treated mares than for repositol treated mares. Both progesterone in-oil and repositol progesterone initiated endometrial gland proliferation with no difference in response observed between the two preparations.