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PubMed1987

Relationship of testosterone, sex hormone binding globulin, and calculated free testosterone to subsequent clinical progress in patients with carcinoma of the prostate treated with bilateral orchidectomy or estrogens.

The concentration in serum of testosterone, sex hormone binding globulin (SHBG), and albumin has been measured, and from these measurements free testosterone has been calculated in 75 patients with carcinoma of the prostate treated with either bilateral orchidectomy, stilbestrol, or estramustine phosphate (Estracyt). After exclusion of 3 noncompliant patients, total testosterone did not differ significantly between treatments, but free testosterone was lower in estrogen-treated patients (5.9 +/- 0.9 (SEM) pmol/l, n = 28) compared with the orchidectomized patients (23 +/- 1.4 pmol/l, n = 44) (P less than 0.001); all of the estrogen-treated patients falling in the lower third of the range of the orchidectomized patients. Free testosterone did not change systematically during several years of treatment and there was no evidence of a rise with clinical deterioration. In the 33 patients with metastatic cancer treated with orchidectomy, the third with the lowest free testosterone or total testosterone showed a better survival over 2 years than the two-thirds with higher free or total testosterone; thereafter, the advantage was lost.

Aged↗

PubMed1976

Distinct testicular 17-ketosteroid reductases, one in interstitial tissue and one in seminiferous tubules. Differential modulation by testosterone and metabolites of testosterone.

The final step in the biosynthesis of testosterone is the reduction of androstenedione, which is catalyzed by the microsomal enzyme 17-ketosteroid reductase. Evidence is presented which suggests that there are two distinct 17-ketosteroid reductases in rat testes, one in interstitial tissue and one in seminiferous tubules. The two enzymes have different pH optima, 5.6 for the one from interstitial tissue and 6.5 for the one from seminiferous tubules. At the optimum pH, a 70-fold difference in Km values was observed, 17 muM for the interstitial tissue enzyme and 0.25 muM for the enzyme from seminiferous tubules. Testosterone and metabolites of testosterone have very different effects of each of these enzyme activities. The interstitial tissue enzyme activity is inhibited by testosterone and several 5alpha-reduced metabolites of testosterone and by estrogens. The most potent inhibitor of the steroids investigated was 5alpha-androstane-3alpha, 17beta-diol, followed by 17beta-estradiol approximately equal to dihydrotestosterone greater than testosterone greater than estrone greater than estriol. 5alpha-Androstane-3alpha, 17beta-diol and 17beta-estradiol were shown to act by competitive inhibition with apparent Ki values of 2.2 and 3.7 muM, respectively. In contrast, it was demonstrated that among the above steroids, only dihydrotestosterone inhibits the 17-ketosteroid reductase activity of seminiferous tubules and this inhibition was only observed at very high concentrations of inhibitor. Testosterone stimulated the 17-ketosteroid reductase activity of seminiferous tubules. 5alpha-Androstane-3alpha, 17beta-diol at low concentrations stimulated the enzyme activity from seminiferous tubules, while it had no effect at high concentrations. The remainder of the steroids tested had no effect on the 17-ketosteroid reductase activity of seminiferous tubules. The difference in response of the two enzyme activities suggests a mechanism for local regulation of testosterone synthesis in each testicular compartment that does not involve directly pituitary gonadotropins.

17-Ketosteroids↗

PubMed1988

Developmental changes in brain and serum binding of testosterone and in brain capillary uptake of testosterone-binding serum proteins in the rabbit.

Developmental changes in the brain uptake of circulating testosterone and of testosterone-binding proteins, such as testosterone-binding globulin (TeBG) or albumin, may play a role in the sexually dimorphic changes in brain structure that are mediated by circulating testosterone. The present studies examine developmental changes in binding of testosterone in both the serum and brain compartments in postnatal rabbits in vivo and developmental changes in the uptake of [3H]TeBG or [3H]albumin by capillaries isolated from developing rabbit brain. The results show that between 10 and 15 days postnatally both the brain sequestration of testosterone and rabbit serum binding of the hormone are markedly increased relative to the newborn period. In addition, both [3H]TeBG and [3H]albumin were taken up by microvessels isolated from 28-day-old rabbit brain, and this process for [3H]TeBG was more active in capillaries obtained from neonatal rats as opposed to adult rats. In summary, these studies show that the binding systems for testosterone are modulated in a parallel fashion in both the serum and brain compartments. In addition, uptake mechanisms for serum testosterone-binding proteins such as TeBG and, to a lesser extent, albumin exist in the capillaries of developing rabbits. These brain capillary plasma protein uptake systems may allow for the distribution into brain of circulating serum proteins such as TeBG and, to a lesser extent, albumin, in developing rabbits.

Aging↗

PubMed1985

Intratesticular regulation of testosterone secretion: comparison of the effects and interactions of hCG, an LHRH agonist and testicular interstitial fluid on Leydig cell testosterone secretion in vitro.

The stimulatory effects on Leydig cell testosterone secretion of a polypeptide(s) factor present in testicular interstitial fluid (IF) were compared with those of hCG and an LHRH agonist (LHRH-A). The actions of IF and LHRH-A were similar in showing (1) a delayed onset of action, (2) enhancement of testosterone production in response to a maximally stimulating concentration (5 nM) of hCG, and (3) near cessation of stimulation following their removal from the incubation medium. However, addition of an LHRH antagonist blocked only the actions of LHRH-A. Moreover, IF continued to stimulate testosterone production up to at least 20 h either on its own or in the presence of 5 nM hCG, whereas the stimulatory effects of LHRH-A disappeared beyond 6 h. IF was also able to enhance testosterone production in response to LHRH-A or in response to hCG + LHRH-A. IF enhanced testosterone production over 4-20 h in response to all doses of hCG and increasing concentrations of IF caused dose-dependent increments in the rate of hCG (5 nM) stimulated testosterone production. With submaximally stimulating doses of hCG or with LHRH-A alone, the stimulatory effect of IF was more or less additive, whereas with maximally stimulating doses of hCG the effect of IF was clearly synergistic. Thus, whereas the rate of testosterone production by Leydig cells in response to 5 nM hCG declined progressively from 4 to 20 h, addition of IF attenuated or prevented this decline. These findings have implications with respect to the physiological control of intratesticular testosterone levels and with respect to the regulation of steroidogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Testosterone and zinc supplementation in castrated rats: Effects on plasma leptin levels and relation with LH, FSH and testosterone.

The present study aims to examine how zinc and testosterone supplementation, in combination and separately, affect plasma LH, FSH and leptin levels in castrated rats. Eighty experimental animals used in the study were allocated to 8 groups, each containing an equal number of rats. Group 1, control group; Group 2, castration group; Group 3, testosterone group (5 mg/kg/day); Group 4, zinc-supplemented group (3 mg/kg/day); Group 5, testosterone and zinc-supplemented group; Group 6, zinc-supplemented castration group; Group 7, testosterone and castration group; and Group 8, zinc-supplemented, testosterone and castration group. Plasma zinc, leptin, LH, FSH and free and total testosterone levels were determined in the blood samples collected from the animals by decapitation. Group 2 had the highest leptin levels and together with group 6, it also showed the highest LH and FSH levels (p<0.01). The lowest leptin levels were observed in groups 3 and 7 (p<0.01). Leptin levels in groups 4 and 6 were higher than those in groups 1, 5 and 8 (p<0.01). LH levels in group 4 were lower than those in groups 2 and 6 and higher than those in all other groups (p<0.01). Free and total testosterone levels in groups 7 and 8 were lower than those in groups 3 and 5, but higher than those in all other groups (p<0.01). Plasma LH levels may be more effective than testosterone on plasma leptin and zinc may be an important mediator of the effect LH has on leptin.

Animals↗

PubMed2000

Salivary testosterone is associated with higher lumbar bone mass in premenopausal healthy women with normal levels of serum testosterone.

The relationships among lumbar and femoral bone mineral density (BMD) and different forms of testosterone--total, salivary testosterone and free testosterone index (FTI) calculated with the sex hormone binding globulin (SHBG)--, body mass index (BMI) and body fat distribution (waist-to-hip ratio and breast-to-hip ratio) were analysed in a cross-sectional study with 66 Spanish premenopausal healthy women aged 42 years and with normal levels of serum testosterone. BMD was measured using dual-energy X-ray absorptiometry (Hologic QDR 1000), and salivary and blood samples were obtained during early follicular phase. In a multiple stepwise regression analysis, lumbar BMD was positively predicted by salivary testosterone and negatively by SHBG adjusted by BMI (R2 = 0.20; p < 0.02). The most femoral BMDs were negatively predicted by SHBG and positively by breast-to-hip ratio (R2 = 0.22-0.33, according to the site measured), but neck BMD was not predicted by any variable. When FTI was entered into the regression model instead of SHBG, it was not an independent predictor of BMD. The waist-to-hip ratio was positively correlated with several femoral BMD sites, but breast-to-hip ratio was better predictor. After adjusting by SHBG, the BMI was only predictor for intertrochanter BMD. All women with elevated salivary testosterone (n = 12) had higher lumbar BMD than those with normal value (1.120 +/- 0.112 vs. 1.026 +/- 0.118; p < 0.01) without differences in other confounding variables. As a conclusion, in premenopausal healthy women of the same age with normal levels of serum testosterone, low levels of SHBG and high levels of salivary testosterone are associated with higher lumbar BMD, whereas low levels of SHBG together with higher breast-to-hip ratio are associated with higher femoral BMD.

Absorptiometry, Photon↗

PubMed1971

Testosterone action in the rat ventral prostate. The effects of diethylstilboestrol and cyproterone acetate on the metabolism of ( 3 H)testosterone and the retention of labelled metabolites by rat ventral prostate in vivo and in vitro.

Recent reports have indicated that the prior metabolism of testosterone by the secondary sexual tissues may be necessary for its androgenic effect. The effects of two anti-androgens, diethylstilboestrol and cyproterone acetate (17alpha-acetoxy-6-chloro-1,2alpha-methylenepregna-4,6-diene-3,20-dione) used in the chemotherapy of human prostatic carcinoma, have been examined on both the metabolism of testosterone and the retention of its metabolites by the rat ventral prostate gland. Cyproterone acetate was found to inhibit the retention of labelled metabolites of [(3)H]-testosterone by prostatic nuclei, both in vivo and in vitro. This inhibition appeared to be competitive. In contrast with its effect on nuclear retention of metabolites of testosterone, cyproterone acetate had no significant effect on the metabolism of [(3)H]testosterone by rat ventral prostate tissue. Diethylstilboestrol similarly had little effect on the metabolism of [(3)H]testosterone by prostatic tissue, although it did appear partially to inhibit its initial metabolism in all the incubation systems used. Diethylstilboestrol inhibited the nuclear retention of dihydrotestosterone when both [(3)H]testosterone and diethylstilboestrol were injected intraperitoneally in vivo, but had no effect on dihydrotestosterone retention when both testosterone and diethylstilboestrol were supplied directly to the prostate either in vivo or in vitro. It was concluded that if diethylstilboestrol has an anti-androgenic effect at the level of the target organ as distinct from its effect on androgen production by the testes, then it is probably due to a mechanism differing from that of cyproterone acetate.

Androgen Antagonists↗

PubMed1999

The effect of microsurgical varicocelectomy on serum follicle stimulating hormone, testosterone and free testosterone levels in infertile men with varicocele.

OBJECTIVES: To analyse the effects of varicocelectomy on serum follicle-stimulating hormone (FSH), testosterone and free testosterone levels, and to investigate the interrelationships between seminal and hormonal variables. PATIENTS AND METHODS: The records were retrospectively evaluated for 78 infertile patients who underwent microsurgical inguinal varicocelectomy, with documented serum FSH, testosterone, free testosterone levels, sperm concentration and sperm motility before and after surgery. Left and bilateral varicoceles were detected in 40 and 38 patients, respectively. In addition, serum hormonal values of 10 fertile men in whom physical examinations and Doppler ultrasonography revealed no evidence of varicocele were recorded and used as a control group. RESULTS: The mean (sd) serum FSH levels of all patients decreased from 15.21 (3.34) before surgery to 10.82 (2.93) mIU/mL afterward (P=0.01), and serum testosterone levels increased from 5.63 (1.40) to 8.37 (2.2) ng/mL (P=0.01), whereas free testosterone levels increased from 23.13 (3.19) to 32.83 (4.37) pg/mL (P<0.001). In contrast to the significant difference in sperm motility before and after surgery of all patients (P<0.01), the difference in sperm count was insignificant (P>0.05). Thirty-six patients with high serum FSH levels before surgery had significantly lower levels afterward (P=0.001). In this group, the sperm concentration and motility also increased, from 17.66 (4.35) to 20.76 (4.37) million/mL (P=0.05) and from 30.9 (4.4)% to 37.5 (4.34)%, respectively (P=0.01). In the remaining 42 patients who had normal preoperative serum FSH levels, there was a slight decrease after surgery (P=0.02). Their sperm concentration increased slightly (P=0. 04), and motility also increased (P=0.001). Sixty patients had a significantly higher testosterone level after surgery; in this group the sperm concentration and motility increased (P=0.01). CONCLUSION: Varicocelectomy promotes Sertoli and Leydig cell function. The significant increase in serum free testosterone level results in a significant improvement in sperm concentration and motility.

Adult↗

PubMed2004

Elevation of serum testosterone and free testosterone after embolization of the internal spermatic vein for the treatment of varicocele in infertile men.

BACKGROUND: To evaluate the effect of internal spermatic vein (ISV) embolization on levels of serum testosterone and free testosterone and on spermatogenesis. METHODS: The files of 83 infertile men treated for varicocele were reviewed for changes in serum testosterone, free testosterone and spermatogenesis after ISV embolization. RESULTS: Mean serum testosterone concentration rose after embolization by 43%, from 12.07 +/- 6.07 nmol/l to 17.22 +/- 8.43 nmol/l (P<0.001). Mean serum free testosterone concentration rose by 72%, from 5.93 +/- 2.44 nmol/l to 10.21 +/- 7.69 nmol/l (P<0.001). Mean sperm concentration increased from 7.49 +/- 1.73 x 10(6)/ml to 18.14 +/- 2.36 x 10(6)/ml (P<0.001); mean sperm motility increased from 21.74 +/- 2.47 to 34.47 +/- 2.27% (P<0.001); and mean sperm morphology increased from 6.63 +/- 1.07 to 13.08 +/- 1.44% (P<0.001). CONCLUSIONS: ISV embolization apparently induces an increase in both serum testosterone and free testosterone concentrations and in sperm parameters in infertile patient with varicocele, regardless of the size of the varicocele.

Adult↗

PubMed2000

Failure to achieve castrate levels of testosterone during luteinizing hormone releasing hormone agonist therapy: the case for monitoring serum testosterone and a treatment decision algorithm.

PURPOSE: We report the failure to achieve a castrate level of testosterone associated with 3-month depot luteinizing hormone releasing hormone (LH-RH) agonist therapy, which to our knowledge is a previously unrecognized outcome. MATERIALS AND METHODS: We prospectively enrolled in our study 38 men with prostate cancer on 3-month depot LH-RH agonist therapy. We monitored total serum testosterone and prostate specific antigen every 28 days beginning 90 days after the last depot LH-RH agonist injection. Data were analyzed with castrate testosterone defined as less than 50 and 20 ng./dl. or less. RESULTS: Using the 50 and 20 ng./dl. definitions of castrate testosterone 2 (5%) and 5 (13%) of the 38 men, respectively, failed to achieve castrate testosterone. A patient with a nadir testosterone of 70 ng./dl. subsequently underwent orchiectomy and testosterone decreased to 10 ng./dl. thereafter. CONCLUSIONS: A small but potentially important subgroup of men on depot LH-RH agonist therapy fail to achieve a castrate level of testosterone. Our findings support monitoring testicular response when LH-RH agonist therapy is initiated.

Aged↗

PubMed1982

Salivary testosterone: relationship to unbound plasma testosterone in normal and hyperandrogenic women.

A sensitive radioimmunoassay (RIA) was used to measure salivary testosterone levels in normal women, in patients with polycystic ovaries (PCO), and in women with hirsutism. There was a highly significant correlation (r = 0.79, P less than 0.001) between the concentration of testosterone in saliva [12.3 +/- 7.8 (SD) pg/ml] and the concentration of unbound testosterone in plasma (5.2 +/- 3.1 pg/ml) in matched samples collected from 56 women including normals, patients with clinical signs of hyperandrogenism, and women treated with a combination of cyproterone acetate (CA) and ethinyl oestradiol (EE). The unbound plasma testosterone was measured in the dialysate directly using a sensitive RIA. Salivary and plasma testosterone levels in patients with PCO (20.6 +/- 8.5 and 626 +/- 187 pg/ml respectively, n = 14) and in those with hirsutism (13.9 +/- 5.6 and 421 +/- 170 pg/ml, n = 30) were significantly higher (P less than 0.001) than levels in normal women (7.7 +/- 2.6 and 196 +/- 68 pg/ml, n = 36). Treatment for 3 months with CA and EE resulted in a decrease (mean 68%) in salivary testosterone levels in all patients studied (n = 15), but the suppression of plasma testosterone (mean 34%) was not observed in all cases. It is concluded that measurement of salivary testosterone gives a useful indication of levels of biologically available androgen in hyperandrogenic women, before and during CA/EE therapy.

Adolescent↗

PubMed1975

Radioimmunoassay of serum LH and testosterone in male rabbits actively immunized against testosterone.

Five male rabbits were actively immunized against testosterone to determine if this procedure could permanently inactivate circulating testosterone. To assess the response to immunization, serum LH, serum testosterone and antitestosterone titer (titer) were measured by radioimmunoassay at various times after immunization. All rabbits produced antisera to testosterone and developed serum LH levels similar to those measured in castrated males. The rise in serum LH was particularly pronounced after a booster immunization but these elevated levels were not maintained which suggests that biological neutralization was only transient. Serum testosterone rose dramatically after immunization and was directly correlated with titer. High serum testosterone concentrations were associated with both high and low serum LH. No correlation existed between titer ans serum LH. It is concluded that active immunization against testosterone does not necessarily result in a permanent neutralization of circulating testosterone and that titer alone is an inadequate criterion of neutralization.

Animals↗

PubMed1986

Effect of testosterone on gonadotrophin-releasing hormone receptors in the castrated rat: preliminary evidence for a stimulatory effect of testosterone on gonadotrophin function in the male rat.

In the long-term castrated rat the negative feedback effect of testosterone is markedly reduced and the raised levels of plasma LH seen in the castrated animals are not suppressed by physiological concentrations of plasma testosterone. In this study we have measured pituitary gonadotrophin-releasing hormone (GnRH) receptor content as well as plasma and pituitary LH on days 1, 10 and 40 after castration and noted the effect of testosterone replacement on these parameters. We found that the negative feedback effect of physiological concentrations of testosterone on plasma and pituitary LH, pituitary GnRH receptor content and response to exogenous GnRH was attenuated 10 and 40 days after castration. It is suggested that the lack of effect of testosterone in the long-term castrated rat is due to its inability to reduce the pituitary GnRH receptor content. On increasing testosterone to supraphysiological levels, the negative feedback effect was reinstated. We also found that in rats 40 days after castration, physiological and subphysiological concentrations of testosterone significantly increased pituitary GnRH receptor content and this may explain the previous findings that low concentrations of testosterone can enhance the effect of GnRH and increase plasma LH levels.

Animals↗

PubMed1989

Dynamics of testosterone secretion by the rat testis: implications for measurement of the intratesticular levels of testosterone.

Testosterone concentrations have been measured in testicular interstitial fluid (IF), and in blood plasma sampled from various parts of the rat testis and spermatic cord, to assess (1) the most accurate method for determination of the intratesticular levels of testosterone, and (2) the route of secretion of testosterone from the testis. In untreated adult rats, testosterone concentrations were highest in blood collected from veins on the surface of the testis (269.50 +/- 30.63 (S.E.M.) nmol/l), but were reduced by 56% on average in blood collected from veins at the proximal end of the spermatic cord (123.06 +/- 24.75 nmol/l), and were reduced considerably in peripheral venous blood (4.55 +/- 0.55 nmol/l). Similar changes occurred in adult rats in which steroidogenesis was either stimulated (by treatment with human chorionic gonadotrophin; hCG) or inhibited (by treatment with aminoglutethimide; AMG), and in rats of various ages during sexual maturation. The reduction in testosterone levels during passage of blood from the testis up the spermatic cord is probably due mainly to dilution by incoming arterial blood which transfers to venous blood via anastomoses in the spermatic cord. Venous-arterial transfer of testosterone in the cord contributed to this in only a minor way. Concentrations of testosterone in testicular IF were always greater than testicular venous concentrations in control, developing and hCG-stimulated rats, but were comparable in rats treated with AMG to suppress Leydig cell steroidogenesis. These and other results demonstrate that the method of drip-collection of IF results in over-estimation of the actual intratesticular levels of testosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Effects of ovine LH, GH and prolactin, and testosterone on serum testosterone and estradiol-17 beta levels, and seminal vesicle and testicular activity in the catfish Clarias batrachus (L.).

Intraperitoneal administrations of testosterone (0.5 microgram/g body wt), and ovine LH (1.0 microgram/g body wt), GH (5 micrograms/g body wt) and prolactin (10 micrograms/g body wt) daily for 7 days during early prespawning phase (May) in C. batrachus produced varied effects on seminal vesicle (SVSI) and testicular (GSI) weights and biochemical correlates. Testosterone and LH treatments significantly increased serum testosterone level and concentrations of total proteins, fructose, hexosamines and sialic acid in both seminal vesicles and testis. Serum E2 levels increased significantly only after testosterone treatment. GH treatment increased significantly serum testosterone level and only the concentrations of SV hexosamines and testicular protein. Prolactin, however, significantly lowered serum testosterone level and concentrations of total protein, hexosamines in both SV and testis, and testicular fructose and sialic acid levels. The results show that the stimulating effect of LH and GH on SV and testicular activity is mediated through the increased secretion of testosterone and the inhibitory effect of prolactin by decreased testosterone secretion.

Animals↗

PubMed1979

[Plasma testosterone, free testosterone fraction LH and FSH in males during the early stage of acute myocardial infarction (author's transl)].

In 18 males (age 49--79 yrs) without endocrine diseases, testosterone, free testosterone fraction, LH, FSH and cortisol (as indicator for stress) were determined in the early stage of an acute myocardia infarction. Blood was taken on admission as well as every 4 hours up to meanly 43 hours. The patients were separated in 2 groups for proving whether alterations of the parameters may depend on the severity of the myocardial infarction (group A=severe infarction; group B=not severe infarction). Testosterone showed a rapid decrease in the first 11 hours after admission, which continued less striking to the end of the investigation. Testosterone was significantly decreased in group A in comparison to group B. LH and FSH in both groups together were remarkably reduced during the whole time. Whereas group A demonstrated a tendency to decreased values in comparison to group B for LH, there were not any essential differences between the two groups for FSH. The free testosterone fraction was not altered. Cortisol in group A was twice as high as in group B during the entire investigation. The systolic pressure in group A was generally lower than in group B during the whole time. The results demonstrate an important reduction of the secretion of testosterone, LH and FSH during the early stage of the acute myocardial infarction. The testosterone suppression seems to be dependent on the severity of the myocardial infarction. These alterations may be caused by a general impaired perfusion as a consequence of myocardial infarction and a suppressive effect of increased cortisol values on testosterone levels.

Aged↗

PubMed1981

Male sex behavior and testosterone concentrations in gilts administered testosterone propionate.

Two gilts were administered testosterone propionate and their subsequent plasma testosterone concentrations and male sex behavior were recorded. These were compared to testosterone concentrations and male sex behavior in boars. Testosterone propionate (75 mg) was administered to the gilts every other day for 20 days (induction scheme) and every 10 days there-after (maintenance scheme). Concentrations of testosterone in plasma were elevated to concentrations detected in the boars during the induction scheme. During the maintenance scheme, concentrations of testosterone appeared to be lower than in boars. At 20, 30 and 40 days following the first injection, sniffing, nosing and mating song behaviors were exhibited by the testosterone treated gilts similar in frequency to the boars. Mounting behavior was first detected 30 days following the first testosterone propionate injection, and by day 40, the frequency of mounting was greater than observed in boars.

Journal Article↗

PubMed2005

Polychlorinated biphenyls (PCB 153 and PCB 126) action on conversion of 20-hydroxylated cholesterol to progesterone, androstenedione to testosterone, and testosterone to estradiol 17beta.

To look for one of the possible mechanisms of action we investigated the effect of two congeners of polychlorinated biphenyls (PCB153 as one of the most prominent environmental contaminants and PCB 126 as one of the most toxic contaminants similar to dioxin) on the cellular conversion of steroid precursors as an indicator for enzyme activity (20-hydroxylated cholesterol to progesterone for P450 (scc,) androstendione to testosterone for 17-beta-HSD, and testosterone to estradiol for P450 (arom)). The net synthesis and secretion of particular steroids was used as the indicator of enzyme activity. Co-culture of pig granulosa and theca cells isolated from small (SF) and large (LF) follicles, was carried out in medium M199 supplemented with 100 ng/ml of PCB 153 or 100 pg/ml of PCB 126. The inhibitory action of both PCB 126 and PCB 153 on progesterone secretion by cells isolated from SF and LF follicles was reversed in the presence of 20-hydroxylated cholesterol. The addition of PCB 126 into the culture medium caused a decrease in testosterone secretion by cells isolated from both SF and LF and this effect was reversed in the presence of androstendione. The inhibitory action of PCB 153 on testosterone secretion was reversed by the addition of androstendione to the culture medium in SF, while it caused even additional stimulatory action on cells collected from LF. No effect of PCB 126 and statistically significant decrease in estradiol secretion by cells collected from SF under the influence of PCB153 was observed. The inhibitory effect of PCB 153 was reversed when the culture was supplemented with testosterone. The opposite effect of both tested congeners on estradiol secretion in both basal and testosterone supplemented culture was seen in LF. PCB 126 increased it while PCB 153 decreased both, the basal and testosterone-stimulated estradiol secretion. In conclusion, the presented results suggest that the effect of both PCBs on steroid secretion observed in an early stage of the follicular phase of the estrus cycle is due to the inhibition of cholesterol mobilisation and thus insufficient substrate availability for hormone synthesis. On the contrary, in large preovulatory follicles inhibition of testosterone secretion is due to their action on 17-beta-HSD while stimulatory or inhibitory action on estradiol secretion is the result of their action on P450 aromatase activity.

Animals↗