Decrease In Plasma Testosterone Levels Research Articles

Urtica Dioica Leaf Extract Attenuates Oxidative Stress Induced by Environment Pollutant Benzo[a] Pyrene in Mouse Testicular Tissues

Background: Epidemiological studies have shown that elevated levels of air pollutants are associated with various adverse health effects, including infertility. Objective: We aimed to assess the protective effects of aqueous Urtica dioica leaf extract against benzo[a]pyrene -induced oxidative damage in mouse testis. Methods: Mice exposed to benzo[a]pyrene were treated with or without aqueous Urtica dioica extract for five weeks, and changes in body and testes weights, messenger RNA levels and activities of antioxidant enzymes, plasma testosterone levels, sperm characteristics, and testicular tissue histology were determined. Results: Exposure to benzo[a]pyrene remarkably reduced testis and body weights, the expression and activity of antioxidant enzymes, increased lipid peroxidation, decreased plasma testosterone levels and sperm count and motility, affected sperm morphology and viability, and damaged the seminiferous tubules. Treatment with aqueous Urtica dioica leaf extract attenuated benzo[a]pyrene -induced oxidative stress in the testicular tissue by increasing the expression of antioxidant genes. Further, Urtica dioica leaf extract reduced lipid peroxidation, increased antioxidative enzyme activity, enhanced sperm characteristics, increased plasma testosterone levels, and improved the morphology of the seminiferous tubules. Conclusion: Aqueous Urtica dioica leaf extract protects testicular tissue from benzo[a]pyrene -induced oxidative damage and could potentially reverse benzo[a]pyrene -induced infertility.

Biochemical Changes of Mancozeb-Induced Alternations in Testes and Thyroid gland of Male Albino Rats

Mancozeb manganese ethylenebis dithiocarbamate polymeric complex – with zinc salts is a very important protective non-systemicfungicide, classified as an ethylenebisdithiocarbamate fungicide. It is used to control fungal diseases for a wide variety of crops because its broad-spectrum fungicidal effects and high compatibility with agrochemicals. The objective of this study was to investigate the effects of the fungicide mancozeb at different doses on some biochemical parameters, reproductive performance and histological changes in testes and thyroid gland. The low dose equal 1/7 of LD50 manc-d1 and high dose equal 1/3.5 of LD50 manc-d1. Doses of mancozeb (manc-d1 and manc-d2) adjusted according to rat's body weights. The results showed that mancozeb significantly (P<0.05) decreased plasma testosterone level, sperm count, viability, motility, and significantly (P<0.05) increased abnormal sperms, altered acrosome and abnormal DNA. Treatment of rats with manc-d1 and manc-d2 significantly (P<0.05) decreased T3. Also, T4 significantly (P<0.05) decreased in the group treated with manc-d2. Treatment of rats with manc-d1 and manc-d2 significantly (P<0.05) increased TSH. Furthermore, the histological investigation revealed that exposure to mancozeb reduced number of mature spermatozoa, necrosis and basal vacuoles observed in some tubules. On the other hand, mancozeb reduce colloid in most follicles resulting in desquamation of the follicular epithelium into the lumen of the thyroid follicles. In conclusion, despite mancozeb exhibit low acute toxicity, it has been shown to cause detrimental effects on reproduction, thyroid gland and its secretion. For this reason, it should be necessary to be careful when using mancozeb in agricultural areas and should take precautions.

Prenatal and perinatal phthalate exposure is associated with sex-dependent changes in hippocampal miR-15b-5p and miR-34a-5p expression and changes in testicular morphology in rat offspring.

MicroRNAs are a large group of non-coding nucleic acids, usually 20-22 nt long, which bind to regulatory sections of messenger RNA (mRNA) and inhibit gene expression. However, genome activity is also regulated by hormones. Endocrine disruptors such as those from the phthalate group imitate or block these hormonal effects, and our previous study showed a long-lasting decrease in plasma testosterone levels in rat offspring exposed to a mixture of three phthalates in utero and postnatally. These effects were also observed at the behavioural level. To shed more light on these findings, in this new study we compared testicular tissue morphology between control and phthalatetreated males and investigated possible persistent changes and sex differences in the expression of two hippocampal microRNAs - miR- 15b-5p and miR-34a-5p - participating in the transcription of steroidogenic genes. Histologically observed changes in testicular tissue morphology of phthalate-exposed males compared to control support testosterone drop observed in the previous study. At the microRNA level, we observed more significant changes in phthalate-treated females than in males. However, we are unable to relate these effects to the previously observed behavioural changes.

Cypermethrin triggers YY1-mediated testosterone biosynthesis suppression

Cypermethrin (CYP), an extensively-used broad-spectrum pyrethroid pesticide, is regarded as a potential environmental endocrine disruptor with the anti-androgenic characteristic. To explore underlying roles of non-coding RNAs and the Jak/Stat pathway in CYP-mediated testosterone biosynthesis suppression, SD rats and Leydig cells were employed in this work. Results displayed that β-CYP decreased plasma testosterone levels and led to abnormal alterations of testicular histomorphology and ultrastructures. LncRNA XIST and miR-142–5p were co-localized in the cytoplasm of Leydig cells, but the expression of XIST was inhibited by β-CYP while that of miR-142–5p was induced. Then overexpressed miR-142–5p dampened the Jak1/Stat1 pathway by directly targeting Jak1. Transcription factors NFκB and YY1 impeded by β-CYP were positively regulated by the Jak1/Stat1 pathway. Bidirectional Co-IP and ChIP assays demonstrated that NFκB interacted with and modulated YY1 by directly binding to the promoter region of YY1. ChIP, qPCR, and YY1 knockdown/overexpression assays indicated that YY1 acted as a transcriptional activator to directly modulate steroidogenic StAR and 3β-HSD in Leydig cells. Taken together, miR-142–5p sponged by lncRNA XIST directly targets the Jak1/Stat1 pathway, which regulates steroidogenic StAR and 3β-HSD via NFκB and YY1, and ultimately dampens testosterone production in Leydig cells.

The gender-specific adverse association of polycyclic aromatic hydrocarbons on skeletal muscle mass and strength in the general adults and the possible mechanisms in experimental rats

Whether polycyclic aromatic hydrocarbons (PAHs) exposure is associated with muscle mass and muscle strength has been scantly investigated. The cross-sectional associations of urinary PAH metabolites with appendicular skeletal muscle mass and hand grip strength in adults were first investigated in the National Health and Nutrition Examination Survey (NHANES). Laboratory study was further carried out to examine the effect of PAHs on skeletal muscle mass and strength. 2742 and 2462 US adults were finally analyzed for muscle mass and muscle strength, respectively. In male participants, urinary PAH metabolites were found to show an inverse relationship with muscle mass and grip strength. In female participants, no significant relationship was found between urinary PAH metabolites with muscle mass or grip strength. In male Sprague-Dawley (SD) rats, administration of B [a]P induced muscle atrophy when compared with the control. However, muscle mass and strength were not significantly altered in female rats. The variations in muscle morphology parameters were accompanied by significant decrease in plasma testosterone levels in the B [a]P-treated male rats. Testosterone co-treatment significantly mitigated B [a]P mediated damages in skeletal muscle in male rats. The results of the present study indicate that there may be a gender-specific causal relationship between the PAHs and muscle atrophy.

In Experimental Dilated Cardiomyopathy Heart Failure and Survival Are Adversely Affected by a Lack of Sexual Interactions.

Nearly one in three people in the U.S. will develop heart failure (HF), characterized by fluid retention (edema) in the lungs and elsewhere. This leads to difficult breathing, deterioration of physical capacity, restriction of normal activities and death. There is little data about the safety and effects of sexual interactions in patients with HF. We tested whether a lack of sexual interactions affected pathophysiological outcomes in a pre-clinical mouse model of dilated cardiomyopathy that recapitulates the progressive stages of human HF. Male mice were randomly given access to, or deprived from, sexual interactions with female mice, which were confirmed by videography and generation of offspring. Cohousing with access to sexual interactions markedly prolonged survival, while cohousing without access to sexual activity did not. Sexual interactions improved systolic function, reduced HF-associated edema, altered transcription of heart contractile protein genes and decreased plasma testosterone levels. To determine whether testosterone levels contributed to survival, testosterone levels were experimentally reduced. Reduction of testosterone levels significantly prolonged survival. Taken together, in mice with dilated cardiomyopathy, sexual activity altered cardiac contractile gene transcription, improved systolic function, reduced edema and prolonged survival which may be in part due to lower testosterone levels.

Developmental, behavioral and endocrine alterations in male rats at early and late postnatal life following in utero exposure to low dose di-n-butylphthalate.

Environmental chemical pollutants that interfere with hormonal homeostasis or hormone signaling are the relevant agents inducing congenital or postnatally developed reproductive abnormalities in human beings, wild and domestic animals. In this study, we are examining reproductive effects of prenatal exposure of male rats to a low dose di-n-butylphthalate (DBP). Wistar female rats were given intragastrically DBP at a daily dose of 100mg/kg b.w. during 15th-21st days of pregnancy. Anogenital distance(AGD) in male offspring decreased on postnatal day (PND) 2 followed by its normalization on PND 7 and 10. There were no other visible teratogenic lesions in the newborns. The testicle descent into scrotum of control males occurred on PND 38.5 ± 0.1, while in DBP group it accelerated by 5.3days on the average. At the age of 6months, DBP-exposed animals exhibited double increase of blood plasma testosterone level as compared to controls, and hyperactive male sexual behavior in the presence of receptive female. The duration of latent periods of the first mount and the first intromission, as well as post-ejaculatory refractory period, have been shortened; the number of mounts with intromission and the number of ejaculations increased significantly. Histological examination of the testes indicated activation of Leydig cells. The female-type sexual behavior as evaluated by appearance of lordosis of orchidectomized and primed with estradiol and progesterone 10-month-old males in response to mount or approach of sexually active normal male was enhanced in DBP-group. Both 10-month-old and aging males (18months), castrated and hormone-primed, displayed homosexual type of behavior. Prenatal low dose DBP caused in 18-month-old males premature atrophy of the testes and accessory sexual glands, increased number of Leydig cell adenomas, a twice decrease of plasma testosterone level and exhausting of sexual potency. We concluded that prenatal exposition of male rats to low dose DBP determines epigenetic alterations of programming of sex brain differentiation and regulation of testicular steroidogenesis that leads to reproductive disorders and accelerated aging of reproductive system.

The Testicular Leptin System in Rats with Different Severity of Type 2 Diabetes Mellitus

Leptin is one of the major regulators of the reproductive system which targets all components of the hypothalamic—pituitary—gonadal axis. In type 2 diabetes mellitus (DM2), functions of the male reproductive system are impaired, which may be due to altered activity of the testicular leptin system. The aim of this work was to study the leptin level and the functional state of the leptin signaling system in the testes of male Wistar rats with different degrees of severity of DM2 induced by a high-fat diet and low-dose streptozotocin treatment. It was found that rats with highly severe DM2 (D-HS group) manifested marked hyperleptinemia, decreased plasma testosterone level, lower sperm count, and higher number of the abnormally shaped sperm accompanied by hyperglycemia, impaired glucose tolerance, insulin resistance, and increased levels of glycated hemoglobin and free fatty acids. The testes of this rat group had an increased leptin level, decreased number of leptin receptors, and attenuated phosphorylation of the effectory components of leptin signaling—transcription factor STAT3 at Tyr705 and Akt-kinase at Ser473. In rats with moderately severe DM2 (D-MS group), metabolic and hormonal disturbances, as well as a decrease in the plasma testosterone level and sperm abnormalities, were less pronounced. The plasma leptin level significantly exceeded that in control only after glycemic load. In the D-MS group’s testes, no statistically significant differences in levels of leptin and its receptor, as well as in STAT3 and Akt-kinase phosphorylation, were revealed compared to control. Thus, pathological changes in steroidogenesis and spermatogenesis in male rats with DM2 depend on the severity of metabolic and hormonal disturbances and the functional state of testicular leptin signaling, the severity of changes in which correlates positively with systemic hyperleptinemia.

EFFECT OF NIFEDIPINE ON APOPTOSIS, NECROSIS AND VIABILITY OF GERMINAL EPITHELIAL CELLS IN THE CONTRALATERAL TESTICLE AND PLASMA TESTOSTERONE LEVELS IN MALE WHITE RATS (RATTUS NORVEGICUS, WISTAR STRAIN) AFTER UNILATERAL TESTICULAR TORSION

Objective: To compare the number of apoptosis, necrosis and viability of germinal epithelial cells in the contralateral testicle (CT) and plasma testosterone (PT) levels in white male rats which administered Nifedipine after unilateral testicular torsion (TT) compared with control group. Material & Methods: This research was an experimental study using male white rats (Rattus Norvegicus, Wistar strain) aged 10-12 weeks and body weight 150-200 gram. A total of 30 rats were then randomly divided into 5 groups (n=6) which were negative control group (KN), positive control group (KP1 and KP2) and Nifedipine-administered group (N1 and N2). Each group performed unilateral left side torsion of testicular of 1080o anticlockwise except the KN group. There was 4-hour ischemic duration in the KP1 and N1 groups while 10 hours in the KP2 and N2 groups. Administration of Nifedipine 30 minutes before detorsion by intraperitoneal injection dosed 100 μg/kgBW. All groups performed right orchidectomy and plasma blood sampling. Measurement of apoptosis, necrosis and viability of germinal epithelial cells in the CT using flowcytometry. Measurement of PT levels using Enzyme-Linked Immunosorbent Assay (ELISA). Results: The number of apoptosis, necrosis and viability of contralateral testicular germinal epithelial cells and PT levels in the KN group compared with KP1 and KP2 groups were significantly different (p<0.05). There was no significant discrepancy in apoptosis (p>0.05) in KP1 group compared with N1 group, as well as in KP2 group compared with N2 groups. The number of necrosis, viability of germinal epithelial cells in the CT and PT level in KP1 group in compared with N1 group, as well as in KP2 group in compared with N2 group were significantly different (p<0.05). Conclusion: Nifedipine administration prior to testicular detorsion can maintain cell viability and decrease the amount of necrotic germinal epithelial cells in the CT and prevent the decrease in PT levels after unilateral TT.

SB223412, a neurokinin-3 receptor-selective antagonist, suppresses testosterone secretion in male guinea pigs

Guinea pigs are important zoo animals and have been recommended for animal-assisted activities or therapy, however there are problems concerning testosterone inducing aggressive or sexual behaviors in male guinea pigs. Testicular testosterone secretion is regulated by pulsatile gonadotropin releasing hormone (GnRH)/luteinizing hormone (LH) release in mammals. The mechanism generating GnRH/LH pulses is thought to be governed by kisspeptin neurons, which coexpress neurokinin B (NKB) and dynorphin A (Dyn), in the arcuate nucleus (ARC). Kisspeptin neurons in the ARC are frequently referred to as KNDy neurons. The purpose of this study was to examine whether the antagonization of NKB-neurokinin-3 receptor (NK3R) signaling can manipulate testosterone secretion in male guinea pigs. A single subcutaneous administration or 7 days of oral administration of an NK3R-selective antagonist, SB223412 (50 mg/body), significantly decreased plasma testosterone levels in male guinea pigs. In vitro binding assays confirmed that SB223412 has a high affinity to guinea pig NK3R. These results suggest that SB223412 could be used as an orally-available compound to suppress testosterone levels in male guinea pigs. Double labeling in situ hybridization of kisspeptin and either NKB or Dyn showed that kisspeptin-expressing neurons contained NKB (77.9%) or Dyn (62.3%) in the ARC, suggesting the presence of KNDy neurons in the ARC of guinea pigs. In conclusion, the present study shows that SB223412 could be a candidate compound to suppress testosterone secretion in male guinea pigs for controlling sexual and aggressive behaviors in the species.

Effect of dietary estrogens from bovine milk on blood hormone levels and reproductive organs in mice

Cows are often milked until 60 d before their next expected calving. Milk from cows in the third trimester of pregnancy contains up to 20 times more estrogens than milk from nonpregnant cows. The aim of this study was to evaluate whether exposure to known doses of estrogens from bovine milk could affect blood hormone levels in mice and influence their reproductive organs. This study was performed with 30 intact male and 30 ovariectomized female mice. Mice of each sex were randomly divided into 3 experimental groups, each with 6 animals of each sex, and a control group with 12 animals of each sex. The first experimental group received 4mL of milk each day from a pregnant cow with natural estrone (E1) and 17β-estradiol (E2) in concentrations 0.093 and 0.065ng/mL, respectively. The second experimental group received 4mL of the same milk each day, with an added 10ng/mL of both E1 and E2. The third experimental group received 4mL of the same milk each day, with an added 100ng/mL of both E1 and E2. The control group received no milk. After 8 d of treatment, mice were euthanized, blood was collected, and the uteruses, testes, and seminal vesicles were weighed. The results of our study demonstrated that consumption of native milk from a pregnant cow did not affect plasma E1 and E2 levels in either sex; uterine weight in females; or testosterone levels and testes and seminal vesicle weights in males. Similarly, we found no changes in the group that received the milk with an added 10ng/mL of E1 and E2. We did observe elevated plasma estrogens in both sexes, increased uterus weight in females, and decreased plasma testosterone levels in males from the group that received milk with an added 100ng/mL of E1 and E2. However, concentrations in the third group exceeded the physiological concentration of milk estrogens by 1,000 times, so it would be extremely unlikely to find such concentrations in native cow milk.

Effects of resveratrol on doxorubicin induced testicular damage in rats

The purpose of this study was to evaluate the likely protective effect of resveratrol (RES) on doxorubicin (DOX) induced testicular damage. Rats were divided into five groups: control, RES, dimethyl sulfoxide (DMSO), DOX and DOX+RES. At the end of treatment, the rats were sacrificed. Plasma testosterone levels, oxidative status, epididymal sperm parameters and testicular apoptosis were evaluated. MDA levels, GP-x and GSH activities were higher in the DOX group than in the control group. MDA levels were lower in the DOX+RES group than in the DOX group. The DOX group exhibited a significant decrease in plasma testosterone levels, sperm concentration and motility, and a significant increase in abnormal sperm rate and TUNEL (+) cells in the testis. A significant increase was observed in plasma testosterone levels and sperm concentration and motility, and a significant decrease in the abnormal sperm rate and TUNEL (+) cells in the DOX+RES group compared to the DOX group. A marked improvement in severe degenerative alterations in the germinative epithelium was also observed following treatment with RES. In conclusion, RES makes a positive contribution to fertility by exhibiting anti-apoptotic and antiperoxidative effects against DOX-induced testicular damage.

Responses of testis, epididymis, and sperm of pubertal rats exposed to functionalized multiwalled carbon nanotubes.

The present study investigated the response of testes, epididymides and sperm in pubertal Wistar rats following exposure to 0, 0.25, 0.5, 0.75, and 1.0 mg kg(-1) functionalized multi-walled carbon nanotubes (f-MWCNTs) for 5 days. The results showed that administration of (f-MWCNTs) significantly increased the activities of superoxide dismutase, catalase, and glutathione peroxidase in a dose-dependent manner in both testes and sperm compared with control group. Moreover, the significant decrease in the activity of glutathione-S-transferase and glutathione level was accompanied with significant elevation in the levels of hydrogen peroxide and malondialdehyde in both testes and sperm of (f-MWCNTs)-treated rats. The spermiogram of (f-MWCNTs)-treated rats indicated significant decrease in epididymal sperm number, sperm progressive motility, testicular sperm number and daily sperm production with elevated sperm abnormalities when compared with the control. Exposure to (f-MWCNTs) decreased plasma testosterone level and produced marked morphological changes including decreased geminal epithelium, edema, congestion, reduced spermatogenic cells and focal areas of tubular degeneration in the testes. The lumen of the epididymides contained reduced sperm cells and there was mild to severe hyperplasia epithelial cells lining the duct of the epididymis. Collectively, pubertal exposure of male rats to (f-MWCNTs) elicited oxidative stress response resulting in marked testicular and epididymides dysfunction.

Intermedin Attenuates LPS-induced Inflammation in the Rat Testis

First reported as a vasoactive peptide in the cardiovascular system, intermedin (IMD), also known as adrenomedullin 2 (ADM2), is a hormone with multiple potent roles, including its antioxidant action on the pulmonary, central nervous, cardiovascular and renal systems. Though IMD may play certain roles in trophoblast cell invasion, early embryonic development and cumulus cell-oocyte interaction, the role of IMD in the male reproductive system has yet to be investigated. This paper reports our findings on the gene expression of IMD, its receptor components and its protein localization in the testes. In a rat model, bacterial lippolysaccharide (LPS) induced atypical orchitis, and LPS treatment upregulated the expression of IMD and one of its receptor component proteins, i.e. receptor activity modifying protein 2 (RAMP2). IMD decreased both plasma and testicular levels of reactive oxygen species (ROS) production, attenuated the increase in the gene expression of the proinflammatory cytokines tumor necrosis factor alpha (TNFα), interleukin 6 (IL6) and interleukin 1 beta (IL1β), rescued spermatogenesis, and prevented the decrease in plasma testosterone levels caused by LPS. The restorative effect of IMD on steroidogenesis was also observed in hydrogen peroxide-treated rat primary Leydig cells culture. Our results indicate IMD plays an important protective role in spermatogenesis and steroidogenesis, suggesting therapeutic potential for IMD in pathological conditions such as orchitis.

Effect of honey on testicular functions in rats exposed to cigarette smoke

Summary Honey is traditionally consumed by the local Malaysian population as a nutrient, as well as for the enhancement of fertility. The decline in male reproductive health and fertility in the last 30 years has been linked to environmental toxicants including cigarette smoke (CS). In human and experimental studies, CS exposure has been associated with decreased plasma testosterone level, lower sperm count and increased percentage of abnormal sperm. The aim of this study, therefore, was to determine the possible protective role of honey against the toxic effects of CS on testicular functions in rats. Thirty-two adult Sprague-Dawley rats were randomly divided into 4 groups (8 rats per group) i.e. control group, honey-treated group (H), cigarette smoke-exposed group (CS) and honey-treated plus CS-exposed group (H+CS). Rats in control and CS groups received oral administration of distilled water daily while rats in H and H+CS groups received honey (1.2 g/kg body weight) orally by gavage daily. Rats in CS and H+CS groups were also exposed to CS for 8 min (3 times/day). After 13 weeks of treatment, each rat was sacrificed for reproductive parameters analysis. Rats in CS group had significantly lower sperm count, daily sperm production, percentage of motile sperm and testosterone level as well as a higher percentage of abnormal sperm compared to control and H groups. However, supplementation of honey significantly improved all these parameters in H+CS group. Administration of honey significantly attenuated the toxic effects of CS on spermatogenesis and testosterone level in rats. This study suggests that honey might have a protective effect against CS-induced impaired testicular functions in rats.

Involvement of selenoprotein P and GPx4 gene expression in cadmium-induced testicular pathophysiology in rat

To investigate the effect of co-exposure to cadmium (Cd) and selenium (Se) on selenoprotein P (SelP) and phospholipid hydroperoxide glutathione peroxidase (GPx4) gene expression in testis and to evaluate their possible involvement in Cd-induced testicular pathophysiology, male rats received either tap water, Cd or Cd + Se in their drinking water for 5 weeks. Cd exposure caused a down-regulation of SelP and GPx4 gene expression and a significant decrease in plasma and testicular concentrations of Se. These changes were accompanied by decreased plasma testosterone level, sperm count and motility, GSH content, protein-bound sulfhydryl concentration (PSH), enzymatic activities of catalase (CAT) and glutathione peroxidase (GSH-Px) as well as by increased glutathione-S-transferase (GST) activity, lipid peroxidation (as malondialdehyde, MDA) and proteins carbonyls (PC). The decrease of testicular SelP and GPx4 gene expression under Cd influence was significantly restored in Cd + Se group. Co-treatment with Cd and Se also totally reversed the Cd-induced depletion of Se, decrease in plasma testosterone level and partially restored Cd-induced oxidative stress and decrease in sperm count and motility. Taken together, these data suggest that down-regulation of SelP and GPx4 gene expression induces plasma and testicular Se depletion leading, at least in part, to Cd-induced testicular pathophysiology.

Influence of combined treatment with zinc and selenium on cadmium induced testicular pathophysiology in rat

The present study was conducted to evaluate the potential benefit of combined treatment with zinc (Zn) and selenium (Se) in reversing cadmium (Cd)-induced testicular pathophysiology compared to Se or Zn treatment alone in rats. For this purpose, male rats received either tap water, Cd, Cd+Zn, Cd+Se or Cd+Zn+Se in their drinking water, for 35days. Cd exposure caused a significant decrease in plasma and testicular concentrations of Se and Zn which was accompanied by decreased plasma testosterone level, sperm count and motility, enzymatic activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) as well as by increased lipid peroxidation (as malondialdehyde, MDA). With Se or Zn administration, during exposure to Cd, only partial corrective effects on depletion of testicular and plasma Se and Zn levels, sperm characteristics and oxidative stress have been observed. The combined treatment of Cd-exposed animals with Se and Zn assured a more significant decrease in plasma and testicular Cd concentrations and a more efficient protection against the observed testicular damage as evidenced by the total prevention of both Se and Zn deprivation and by the entire restoration of the sperm motility and the testicular antioxidant status.

Evaluation of involvement of testicular metallothionein gene expression in the protective effect of zinc against cadmium-induced testicular pathophysiology in rat

To investigate the effects of exposure to Cd and Zn on testicular MT-1 and MT-2 gene expression and evaluate their involvement in Zn protection against Cd-induced testicular pathophysiology, male rats received either tap water, Cd or Cd + Zn in their drinking water for 35 days. Cd induced histopathological changes in testicular tissues were accompanied by decreased plasma testosterone level, plasma and testicular Zn concentrations, oxidative stress, and by increased MT-1 and MT-2 gene expression. Co-treatment with Cd and Zn reversed the Cd-induced decrease testosterone level and SOD activity, decreased testicular Cd accumulation and partially restored Cd-induced histological changes, lipid peroxidation, and Zn depletion. The increase of testicular MT-1 and MT-2 gene expression under Cd influence was significantly reduced in Cd + Zn group. These data suggest that Zn enhances the protection against Cd-induced testicular pathophysiology through non-MT gene expression mechanisms but essentially by preventing Cd accumulation, Zn deprivation and by ameliorating the testicular antioxidant status.

Circulating steroid hormones in prostate carcinogenesis. Part 1 - Androgens.

The aim of this review is to identify circulating steroids associated with prostate cancer (PCa) in bibliographic reports. First, we summarize chronological reports comparing circulating steroid levels in men with a high risk of PCa, such as African-Americans (AAs), with men having a lower risk. Higher testosterone plasma levels in young AA men have been reported. However, the difference between AAs and Caucasians decreases with age. When measured, dihydrotestosterone (DHT) was found to be higher in AAs; however, these results must be taken with caution, as immunological assay of this steroid is difficult. Second, we summarize chronological reports concerning circulating steroids assayed in blood samples drawn several years before a diagnosis of PCa was made, compared to controls. These nested case-control studies did not lead to straightforward conclusions regarding an increase in circulating testosterone. However, large collaborative studies showed a trend of a decrease in plasma sex hormone binding globulin, consequently an increase in bioavailable plasma testosterone in PCa. These nested case-control studies failed to associate plasma DHT levels with PCa risk. Third, we summarize numerous chronological publications relating plasma concentrations, measured at the time of PCa diagnosis. Numerous results showed a decrease in plasma testosterone levels in aggressive PCa (high Gleason score, advanced stage with positive surgical margins). Testosterone levels returned to normal several months after prostatectomy. All plasma hormone assay levels were always carried out using immunological methods. We recommend replacing this methodology by mass spectrometry coupled with gas chromatography or liquid chromatography in these epidemiologic studies.

Resveratrol: Impact on Reproduction

Event Abstract Back to Event Resveratrol: Impact on Reproduction Eleana Kara1 and Paraskevi Papaioannidou1* 1 Aristotle University of Thessaloniki, Department of Pharmacology, Greece Resveratrol is a phytoestrogen found in the skin of red grapes. It binds to estrogen receptors, although with much weaker affinity than estradiol, and it may disrupt the endocrine system by acting as an estrogen receptor agonist or mixed agonist/antagonist. There is evidence that resveratrol can affect the development of the reproductive system, although the available data are controversial. Exposure of adult female rats to resveratrol has been reported to cause ovarian hypertrophy, menstrual cycle abnormalities and altered sociosexual behavior. Exposure of female rats to resveratrol during lactation has been reported to increase ovarian weight and decrease body weight, while exposure of male rats to resveratrol during lactation decreases plasma testosterone levels and seminal vesicle weight, increases testicular weight, alters sociosexual behavior and causes changes in cerebral development. Other studies have indicated no effects on spermatogenesis and sperm quality, on the morphology of the ovaries, and on fertility of mice exposed to resveratrol during gestation, lactation, puberty and adulthood. Studies on the action of resveratrol on mouse Leydig tumor cells have shown that resveratrol affects steroidogenesis by decreasing cAMP-stimulated progesterone secretion and steroidogenic acute regulatory mRNA expression. There is evidence that resveratrol prevents carcinogenesis, protects the brain from beta-amyloid neurotoxicity and slows-down the progression of cardiovascular disease. Despite these beneficial actions, further studies are necessary in order to investigate its potential detrimental effects on the human reproductive system during crucial periods of its development. Keywords: resveratrol, estrogen disruptors, Fertility, grapes Conference: 8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010, Thessaloniki, Greece, 1 Oct - 5 Oct, 2010. Presentation Type: Poster Topic: Xenobiotics and reproduction Citation: Kara E and Papaioannidou P (2010). Resveratrol: Impact on Reproduction. Front. Pharmacol. Conference Abstract: 8th Southeast European Congress on Xenobiotic Metabolism and Toxicity - XEMET 2010. doi: 10.3389/conf.fphar.2010.60.00138 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 28 Oct 2010; Published Online: 04 Nov 2010. * Correspondence: Dr. Paraskevi Papaioannidou, Aristotle University of Thessaloniki, Department of Pharmacology, Thessaloniki, Greece, ppap@auth.gr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Eleana Kara Paraskevi Papaioannidou Google Eleana Kara Paraskevi Papaioannidou Google Scholar Eleana Kara Paraskevi Papaioannidou PubMed Eleana Kara Paraskevi Papaioannidou Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.