Decrease In Plasma Testosterone Levels Research Articles

Evaluation of Testicular Toxicity Following Short-term Exposure to Cypermethrin in Albino Mice.

The present study was undertaken to assess the testicular toxicity following short-term exposure to cypermethrin (α-CP) in albino mice. Cypermethrin was dissolved in arachis oil and administered to two groups of mice (n = 12/group) orally at the dose rate of 250 mg/kg body weight, once a day for 28 days. Fifty percent of the animals in both the groups were sacrificed on day 14 and the remaining on day 28. Plasma samples were subjected to radioimmunoassay to determine testosterone levels. The testes were collected to determine the cholesterol levels and the activity of transaminases (AST and ALT) or epididymal alkaline phosphatase (ALP). Histological study of testicular tissue was also undertaken to examine the α-CP-induced ultrastructural changes using transmission electron microscopy (TEM). α-CP significantly (P<0.05) increased the activities of testicular AST (1.36±0.12 vs. 1.19±0.10), ALT(1.78±0.11 vs. 1.36±0.09), and significantly (P<0.05) decreased the testosterone levels (0.86±0.24 vs. 1.72±0.18). Testicular cholesterol levels were elevated in treated animals as compared to control (1.81±0.16 vs. 1.42±0.08). Epididymal alkaline phosphatase (ALP) activity was also decreased significantly (P<0.05) in treated animals (1.10±0.20 vs. 1.64±0.1). Histological studies on day 28 revealed rupture of spermatogonic cell membrane, shrinkage in the nucleus, stages of apoptosis, condensation of chromatin, and decreased cytoplasmic organelles. The study suggested that short-term exposure to α-CP in albino mice induced toxicopathological lesions in testicular tissue leading to decreased plasma testosterone levels.

Diabetic rat testes: morphological and functional alterations

Reproductive dysfunction is a consequence of diabetes, but the underlying mechanisms are poorly understood. This study investigated the histological and molecular alterations in the testes of rats injected with streptozotocin at prepuperal (SPI rats) and adult age (SAI rats) to understand whether diabetes affects testicular tissue with different severity depending on the age in which this pathological condition starts. The testes of diabetic animals showed frequent abnormal histology, and seminiferous epithelium cytoarchitecture appeared altered as well as the occludin distribution pattern. The early occurrence of diabetes increased the percentage of animals with high number of damaged tubules. The interstitial compartment of the testes was clearly hypertrophic in several portions of the organs both in SPI and SAI rats. Interestingly, fully developed Leydig cells were present in all the treated animals although abnormally distributed. Besides the above-described damages, we found a similar decrease in plasma testosterone levels both in SPI and SAI rats. Oxidative stress (OS) is involved in the pathogenesis of various diabetic complications, and in our experimental models we found that manganese superoxide dismutase was reduced in diabetic animals. We conclude that in STZ-induced diabetes, the altered spermatogenesis, more severe in SPI animals, is possibly due to the effect of OS on Leydig cell function which could cause the testosterone decrease responsible for the alterations found in the seminiferous epithelium of diabetic animals.

The effects of subchronic lithium administration in male Wistar mice on some biochemical parameters

Lithium salts are efficiently used for treatment of psychiatric disorders. However, prolonged treatment frequently involves adverse side effects. In this study, effects of lithium carbonate administration on some biochemical parameters were studied in male mice. Lithium carbonate (20, 40, or 80 mg/kg body weight corresponding to 3.77, 7.54, or 15.08 mg Li element/kg body weight, respectively) was injected daily for 14 or 28 days. The following parameters were recorded: drinking water consumption, body weight, lithium and testosterone serum concentrations, activities of catalase (CAT), superoxide-dismutase (SOD), and glutathione-peroxidase (GPX), and level of lipid peroxidation (expressed as TBARS) in liver was performed. Lithium treatment, especially at the highest dose for 28 days, was found to induce weight gain and polydipsia and a significant decrease of plasma testosterone level. Lipid peroxidation level and activities of SOD and GPX were increased in liver, which suggests a perturbation of the antioxidative status. Our results indicate that subchronic exposure to lithium, which induces weight gain and polydipsia under our experimental conditions, also damages the male reproductive system and triggers an oxidative stress in the liver.

The effects of subchronic lithium administration in male Wistar mice on some biochemical parameters

Lithium salts are efficiently used for treatment of psychiatric disorders. However, prolonged treatment frequently involves adverse side-effects. In the present work, effects of lithium carbonate administration on some biochemical parameters were studied in male mice. Lithium carbonate (20, 40 or 80 mg/kg body weight, corresponding to 3.77, 7.54 or 15.08 mg Li element/kg body weight, respectively) was injected daily for 14 or 28 days. The following parameters were recorded: water consumption, body weight, lithium and testosterone serum concentrations, activities of catalase (CAT), superoxide-dismutase (SOD) and glutathione-peroxidase (GPX) and level of lipid peroxidation (expressed as TBARS) in liver was performed. Lithium treatment, especially at the highest dose for 28 days, was found to induce weight gain, polydipsia and a significant decrease of plasma testosterone level. Lipid peroxidation level and activities of SOD and GPX were increased in liver which suggests a perturbation of the antioxidative status. Our results indicate that subchronic exposure to lithium, which induces weight gain and polydipsia under our experimental conditions, also damages the male reproductive system and triggers an oxidative stress in the liver.

Alteration in plasma testosterone levels in male mice lacking soluble epoxide hydrolase.

Soluble epoxide hydrolase (Ephx2, sEH) is a bifunctional enzyme with COOH-terminal hydrolase and NH(2)-terminal phosphatase activities. sEH converts epoxyeicosatrienoic acids (EETs) to dihydroxyeicosatrienoic acids (DHETs), and the phosphatase activity is suggested to be involved in cholesterol metabolism. EETs participate in a wide range of biological functions, including regulation of vascular tone, renal tubular transport, cardiac contractility, and inflammation. Inhibition of sEH is a potential approach for enhancing the biological activity of EETs. Therefore, disruption of sEH activity is becoming an attractive therapeutic target for both cardiovascular and inflammatory diseases. To define the physiological role of sEH, we characterized a knockout mouse colony lacking expression of the Ephx2 gene. Lack of sEH enzyme is characterized by elevation of EET to DHET ratios in both the linoleate and arachidonate series in plasma and tissues of both female and male mice. In male mice, this lack of expression was also associated with decreased plasma testosterone levels, sperm count, and testicular size. However, this genotype was still able to sire litters. Plasma cholesterol levels also declined in this genotype. Behavior tests such as anxiety-like behavior and hedonic response were also examined in Ephx2-null and WT mice, as all can be related to hormonal changes. Null mice showed a level of anxiety with a decreased hedonic response. In conclusion, this study provides a broad biochemical, physiological, and behavioral characterization of the Ephx2-null mouse colony and suggests a mechanism by which sEH and its substrates may regulate circulating levels of testosterone through cholesterol biosynthesis and metabolism.

Abnormal pituitary-gonadal axis may be responsible for rat decreased testicular function under simulated microgravity

Space flight and simulated microgravity lead to suppression of mammalian spermatogenesis and decreased plasma testosterone level. In order to explain the mechanism behind the depression, we used rat tail-suspended model to simulate weightless conditions. To prevent cryptorchidism caused by tail-suspension, some experimental animals received inguinal canal ligation. The results showed that mass of testis decreased significantly and seminiferous tubules became atrophied in rats after tail-suspension. The levels of plasma testosterone (T), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in tail-suspended rats with or without inguinal canal ligation decreased significantly compared with controls, and an increased level of plasma estradiol ( E 2 ) was revealed in tail-suspended rats. The results indicate that besides the direct influence of fluid shift upon testis under short-term simulated microgravity, the pituitary function is also disturbed as a result of either immobilization stress or weight loss during tail-suspension treatment, which is responsible to some extent for the decreased testosterone secretion level and the atrophia of testis. The conversion of testosterone into E 2 under simulated microgravity is another possible cause for the decline of plasma testosterone.

The aging male – diagnosis and therapy of late‐onset hypogonadism

Managing the clinical features of hormone insufficiency in aging men is an important field of activity for dermatologists and in particular for dermatologists specialized in andrology. Potential consequences of age-associated decrease in plasma testosterone levels include long-term changes in diverse organ systems including changes of bone architecture, body composition, muscular strength, cognitive functions, and mood as well as negative effects on skin and hair. Indications and contraindications for a hormone replacement therapy as well as therapy monitoring are well-defined. Replacement of testosterone in the case of late-onset hypogonadism is not a standardized therapy. Previous studies suggest that testosterone replacement therapy has positive clinical effects. Dermatologic effects of testosterone replacement therapy have not yet been investigated. Further research is required to identify potential benefits and risks of hormone replacement therapy in aging men.

Imbalance in Sex Hormone Levels Exacerbates Diabetic Renal Disease

Studies suggest that the presence of testosterone exacerbates, whereas the absence of testosterone attenuates, the development of nondiabetic renal disease. However, the effects of the absence of testosterone in diabetic renal disease have not been studied. The study was performed in male Sprague-Dawley nondiabetic, streptozotocin-induced diabetic, and streptozotocin-induced castrated rats (n=10 to 11 per group) for 14 weeks. Diabetes was associated with the following increases: 3.2-fold in urine albumin excretion, 6.3-fold in glomerulosclerosis, 6.0-fold in tubulointerstitial fibrosis, 1.6-fold in collagen type I, 1.2-fold in collagen type IV, 1.3-fold in transforming growth factor-beta protein expression, and 32.7-fold in CD68-positive cell abundance. Diabetes was also associated with a 1.3-fold decrease in matrix metalloproteinase protein expression and activity. Castration further exacerbated all of these parameters. Diabetes was also associated with a 4.7-fold decrease in plasma testosterone, 2.9-fold increase in estradiol, and 2.1-fold decrease in plasma progesterone levels. Castration further decreased plasma testosterone levels but had no additional effects on plasma estradiol and progesterone. These data suggest that diabetes is associated with abnormal sex hormone levels that correlate with the progression of diabetic renal disease. Most importantly, our results suggest an important role for sex hormones in the pathophysiology of diabetic renal complications.

Effects of Maternal Exposure to 3,3′,4,4′,5‐Pentachlorobiphenyl (PCB126) or 3,3′,4,4′,5,5′‐Hexachlorobiphenyl (PCB169) on Testicular Steroidogenesis and Spermatogenesis in Male Offspring Rats

On days 7-21 of gestation, Sprague-Dawley rats were orally administered 3 or 30 mug/kg/d of 3,3',4,4',5-pentachlorobiphenyl (PCB126) or 3,3',4,4',5,5'-hexachlorobiphenyl (PCB169) daily. Their male offspring were autopsied at 3, 6, and 15 weeks after birth to investigate the effects of the 2 polychlorinated biphenyls (PCBs) on spermatogenesis and steroidogenesis in their testes. PCB treatment caused a decrease in the area ratio of 3beta-hydroxysteroid dehydrogenase (HSD)-expressing cells (Leydig cells)/testis at 3 weeks after birth. When PCB126 was administered to pregnant rats, the plasma testosterone levels in their offspring were decreased at 3 weeks. The expression levels of P450scc, 3beta-HSD, and P450(17alpha) mitochondrial RNAs (mRNAs) were unchanged, although the StAR (steroidogenic acute regulatory protein) mRNA expression level was increased at 6 weeks. On the other hand, when PCB169 was administered, plasma testosterone levels were decreased at 3 and 6 weeks and were increased at 15 weeks. Plasma luteinizing hormone (LH) levels were decreased at 6 weeks, and plasma follicle-stimulating hormone (FSH) levels were increased at 15 weeks. The expression levels of 3beta-HSD and P450(17alpha) were increased, and the mRNA level of 5alpha-reductase 1 was decreased at 15 weeks. PCB169 treatment suppressed the conversion of round spermatids between stages VII and VIII. These results indicate that in utero and lactational exposure to PCB126 or PCB169 decreases plasma testosterone levels in 3-week-old rats, with no change in the expression levels of the mRNAs of enzymes, and that PCB169 inhibits testicular steroid synthesis more strongly than PCB126. PCB169 greatly altered the concentration of testosterone, indicating a stronger inhibitory effect on spermatogenesis. Low testosterone and LH levels in prenatally PCB169-exposed rats until 6 weeks after birth presumably retard the functional differentiation of testicular Leydig cells; however, the increased testosterone levels at 15 weeks suggest that Leydig cells in PCB-exposed rats are virtually mature by the 15th week.

Effect of ‘PC Game Room’ use and polycyclic aromatic hydrocarbon exposure on plasma testosterone concentrations in young male Koreans

'PC Game Rooms' were first popularized in Korea, although the concept is now becoming popular worldwide. PC Game Rooms provide users with high-performance PC connected to the high-speed internet, and access to computer games. However, PC Game Room users are exposed to various hazardous agents such as cigarette smoke in a confined environment, and thus it is likely that excessive PC Game Room use involves abnormal exposure to polycyclic aromatic hydrocarbons (PAH) as well as being associated with disturbed sleep or circadian rhythm. In this cross-sectional study, the exposure to PAH was evaluated by measuring urinary 1-hydroxypyrene (1-OHP) and 2-naphthol. The correlations between PC Game Room use and PAH exposure and plasma testosterone and LH levels were analysed in 208 young male Koreans. Urinary 1-OHP concentrations increased (P = 0.0001) and plasma testosterone levels decreased (P = 0.0153) significantly with increased duration of PC Game Room use. Correlation analysis showed that plasma testosterone concentrations were significantly negatively correlated with urinary 1-OHP (r = -0.22, P = 0.0012) and 2-naphthol (r = -0.15, P = 0.0308) concentrations. Moreover, these associations persisted after adjusting for other independent variables. However, the duration of PC Game Room use itself was not found to be an independent significant determinant of plasma testosterone level. Rather, PC Game Room use increased PAH exposure, which decreased plasma testosterone level. The younger age group (15-19 years) showed a more prominent decrease in plasma testosterone concentrations with increasing duration of PC Game Room use than the older age group (20-24 years) (r2 = 0.355, P = 0.0301 versus r2 = 0.213, P = 0.0001). These results imply that the excessive use of PC Game Rooms is related to an adverse impact on sex hormonal status in young male Koreans via PAH exposure. This effect was more prominent in the younger age group.

A Causative Factor of Copulatory Disorder in Rats Following Social Stress

We investigated the causative role of testosterone in copulatory disorder and the expression of c-fos messenger (m)RNA in the medial preoptic area in rats after social stress. To generate copulatory disorder rats in the experimental defeated group were attacked by residents for 10 minutes daily for 7 consecutive days (social stress). We then investigated the effect of repeat defeat on the frequency of mounting behavior and plasma testosterone levels. The effects of testosterone replacement and/or apomorphine (100 microg./kg. subcutaneously), a dopamine receptor agonist, on the frequency of mounting behavior were also studied. After experiencing social stress the brain area within the medial preoptic area was removed for analysis of c-fos and androgen receptor mRNA expression. Real-time reverse transcription-polymerase chain reaction was done to analyze gene expression. Rats in the defeated group showed a reduced frequency of mounting behavior and a decrease in plasma testosterone levels compared with values in control rats (p <0.01). After testosterone replacement the frequency of mounting behavior became significantly higher than that of socially stressed rat (p <0.05) but did not achieve control levels. The frequency of mounting behavior by socially stressed rats after apomorphine treatment was significantly higher than that of vehicle treated rats (p <0.05) but the frequency produced by the combination of testosterone replacement and apomorphine injection did not achieve control levels. After the social stress experience c-fos mRNA expression was significantly increased compared with that in control rats (p <0.05). The expression of androgen receptor mRNA was not affected by social stress. Testosterone replacement significantly reduced the expression of c-fos mRNA in the medial preoptic area (p <0.05). Our results indicate that a reduction in plasma testosterone may have a causative role in copulatory disorder induced by social stress. Changes in c-fos mRNA expression in the medial preoptic area correlated with copulatory disorder and, thus, they are suitable for monitoring that disorder.

Cortisol affects testicular development in male common carp, Cyprinus carpio L., but not via an effect on LH secretion

Previous work showed that prolonged elevated cortisol levels, implicated in the stress adaptation, inhibits testicular pubertal development in male common carp, as well as an impairment of the synthesis of the 11-oxygenated androgens. This may be a direct effect of cortisol on the testis or via the gonadotropin secretion by the pituitary. The aim of the present study was to investigate whether cortisol has an effect on pituitary LH secretion. Juvenile common carp were fed with cortisol containing food pellets. Elevated cortisol levels blocked the increase in testosterone levels and pituitary LH content, but induced higher plasma LH levels at the end of puberty. The in vitro LH release capacity was correlated to the pituitary LH content. At the final stage of pubertal development, when a significant difference in pituitary LH content was observed, sGnRHa-induced LH release was also decreased. Testosterone has been shown to induce development of pituitary gonadotrophs, leading to an increase in LH content and GnRH-inducible LH release, but a decrease in plasma LH levels. We observed decreased plasma testosterone levels as a consequence of prolonged cortisol treatment. It is hypothesised that cortisol inhibits the testicular testosterone secretion and thereby, prevents LH storage. In vitro, this leads to a reduced GnRH-inducible LH release, but in vivo to increased LH plasma levels. It is very unlikely that the impaired testicular development is due to an effect of cortisol on LH secretion.

Behavioral and hormonal responses to corticosterone in the male red-sided garter snake, Thamnophis sirtalis parietalis

Stress and glucocorticoids are generally thought to suppress reproductive function at multiple levels. We tested the hypotheses that exogenous corticosterone would suppress sexual behavior in a dose-dependent manner, as well as drive a decrease in plasma testosterone levels in the male red-sided garter snake, Thamnophis sirtalis parietalis. We examined this by challenging individual males with intraperitoneal injections of exogenous corticosterone, and subsequently exposing them to sexually attractive females or taking a blood sample. Previous work has demonstrated a hormonal but no behavioral response to stress in this species. In this study, increasing concentrations of exogenous corticosterone rapidly suppressed mating behavior in a threshold manner. However, exogenous corticosterone had no effect on plasma levels of testosterone. Thus, these data suggest that the mechanism is in place for corticosterone to suppress mating behavior in this species and that these effects do not occur because of an indirect effect on plasma levels of testosterone but rather are the direct effect of the hormone itself. In addition, the negative relationship observed previously between plasma levels of corticosterone and testosterone in this species was probably not the direct result of corticosterone acting on the hypothalamic–pituitary–gonadal (HPG) axis. Rather, our results seem to indicate that the negative associations between the hypothalamic–pituitary–adrenal axis (HPA) and the HPG axis occur at other levels of these neuroendocrine pathways.

Inverse relationship between plasma epinephrine and testosterone levels during acute glucoprivation in healthy men

In healthy men, a decrease in plasma testosterone levels was observed in the context of metabolic stress. While physiological mechanisms underlying this response are unclear, there are several lines of evidence suggesting circulating epinephrine's influence on plasma testosterone levels. The purpose of this study was to directly relate stress-induced changes in plasma testosterone and epinephrine. The stressor used was blockade of glucose metabolism with pharmacological doses (40mg/kg) of 2 deoxyglucose (2DG). Arterial plasma samples from 10 healthy males were assayed at 20 minutes intervals for 60 minutes for the concentrations of testosterone, epinephrine and related biochemicals. Bolus administration of 2DG resulted in progressive decline in testosterone and increases in epinephrine and norepinephrine plasma levels (mean change from baseline: 29, 2530 and 186%, respectively). Inverse correlation was detected between both absolute (r s=−0.72; df=8; p=0.017) and baseline-corrected testosterone concentrations at the 60 minute time point and epinephrine area under the curve values. Our results suggest that adrenomedullary activation may be involved in stress-induced testosterone effects. The implications of these data for the understanding of the role of catecholamines in glucoprivic stress response are discussed.

Enhanced testicular antioxidant system by ascorbic acid in alloxan diabetic rats

The diabetic subject is at significantly increased risk of developing testicular changes. Its etiology may involve oxidative damage by free radicals and protection against such damage can be offered by antioxidant supplementation. Alloxan elicited significant inhibition of antioxidants including superoxide dismutase, catalase and glutathione reductase activities and decreased glutathione content in testis. These effects were accompanied by significant elevation of testicular lipid peroxidation, decreased plasma testosterone level and a drop in copper and zinc concentrations in testis. The administration of ascorbic acid after alloxan treatment interfered and prevented alloxan action. Ascorbic acid blunted the increased testicular lipid peroxidation and the decreased plasma testosterone level probably by protecting antioxidants and the loss of copper and zinc from testes. The data suggested that ascorbic acid has a protective effect on alloxan-induced damage by maintaining the activity of cellular antioxidants.

Long-term effects of cigarette-smoke exposure on plasma testosterone, luteinizing hormone and follicle-stimulating hormone levels in male rats.

To determine the effects of long-term cigarette smoking on the levels of plasma testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in male adult rats and to examine morphological and histological changes in the testes. Cigarette smoke was generated by a smoking-machine and 12 rats were exposed to cigarette smoke diluted with 90% air for 60 days (2 h/day). Twelve rats were exposed to room air only under similar conditions as controls. The concentrations of plasma testosterone, LH and FSH were measured before and after exposure using a radio-immunoassay and the testes were examined histologically. In rats exposed to smoke, the mean plasma testosterone level decreased significantly but there were no significant changes in testosterone in the control rats. The mean plasma LH and FSH levels of the two groups did not change significantly after exposure. In rats exposed to smoke, histological examination of the testes showed fewer Leydig cells and degeneration of the remaining cells. These results indicate that the decrease in plasma testosterone levels induced by exposure to smoke was not associated with changes in plasma gonadotrophin levels. The decrease in testosterone levels may be related to the toxic effects of smoke on Leydig cells.

Effect of a diphenylethylenediamine platinum complex on steroidogenesis in rats

Although less cytotoxic, the new platinum complex [meso-1,2-bis(2,6-difluoro-4-hydroxyphenyl)-ethylenediamine]sulfatopl atinum (II) (2) is equipotent to cisplatin (1) in the oestrogen-dependent MXT mammary tumour of the mouse. As this may be due to oestrogen level-lowering properties, we compared the effect of 1 and 2 on steroidogenesis in the rat. A single dose of 1 and 2 (20 mumol/kg s.c.) decreased plasma testosterone level in male rats by 90% (1, day 3) and 80% (2, day 7). Luteinizing hormone level remained unchanged in intact and in ovariectomized rats. The activities of the following testicular enzymes were decreased (day 7): cholesterol side-chain cleavage enzyme (1: 33%; 2: 36%), 3 beta-hydroxysteroid dehydrogenase/delta 4,delta 5-isomerase (1: 31%; 2: 48%) and 17 alpha-hydroxylase/17,20-lyase (1: 21%; 2: 15%). Testicular microsomal cytochrome P450 content was also diminished (1: 60%; 2: 49%, day 7). Corticosterone level in plasma and biosynthesis in adrenal explants was not affected, indicating the selectivity of action at the gonadal level. In vitro, neither 1 nor 2 (2 and 20 microM) influenced binding of human chorionic gonadotropin to testis interstitial cells during an observation period up to 21 h. These results suggest that 1 and 2 act at the gonadal level by inhibiting the expression of the steroidogenic enzymes. They do not, however, inactivate the luteinizing hormone receptor.

Immobilization-induced stress decreases lipogenesis in sebaceous glands as well as plasma testosterone levels in male Syrian hamsters

The effects of immobilization-induced stress on plasma testosterone levels and lipogenesis in the sebaceous gland were examined in male Syrian hamsters. To induce immobilization stress, the animals were placed in the prone position and wrapped with flexible steel wire gauze at room temperature. Plasma testosterone levels were determined by radioimmunoassay (RIA) of blood samples and sebaceous lipogenesis was determined by measurement of the incorporation of a lipid precursor, 14C-acetate, in ear skin biopsy samples. Both specimens were obtained immediately after the hamsters were decapitated. Immobilization stress for 4 consecutive days produced a marked fall in plasma testosterone levels and sebaceous lipogenesis. These reductions were reversible, the decreased plasma testosterone levels and decreased sebaceous lipogenesis recovering to the nonstressed or prestimulus levels after approximately 1 week. In 4-day stressed animals in occurrence with a decrease in plasma testosterone, sebaceous lipogenesis in ear with topical application of a small dose of testosterone, which have no effect on plasma testosterone level, was equivalent to that in nonstressed animals. These findings indicated that immobilization-induced stress lowered testosterone secretion, and consequently the testosterone levels in the skin, resulting in decreased lipogenesis in the skin. These results thus suggest that psychological or physiological stress can influence cutaneous function by inducing changes in the neuroendocrine system.

The male reproductive organs in experimental Chagas' disease: III. Plasma testosterone and accessory sex glands in the acute phase of the disease

Male Wistar rats were injected i.p. with 2 x 10(5) trypomastigotes of the Bolivia strain. Fifteen days later, few parasite nests were observed in the fibromuscular layer surrounding the seminal vesicle acini of chagasic animals and no parasites were detected in the testis and ventral prostate. A significant decrease was observed in the absolute weight and fructose content of the seminal vesicle and ventral prostate of chagasic rats, which also presented a sharp decrease in plasma testosterone levels.

Effect of a long‐lasting gonadotrophin hormone‐releasing hormone agonist in six cases of severe male paraphilia

Six men with severe paraphilia had been treated with depot gonadotrophin luteinizing releasing hormone analogue (GnRHa) (triptorelin 3.75 mg per month intramuscularly). In 5 cases, the treatment ended their deviant sexual behavior and markedly decreased their sexual fantasies and activities without further significant side effects than those related to hypoandrogenism. This clinical improvement was parallel to the gradual decrease of plasma testosterone level to castration values within the first month. The beneficial effect of this treatment had been maintained at follow-up varying from 7 months to 3 years. One patient interrupted the treatment at the end of the first year and relapsed within 10 weeks. GnRHa treatment, which leads to reversible castration, may constitute a promising treatment of paraphilic behavior and may favor the possibility of concurrent psychotherapy.