Abnormal Testis Research Articles

Identification and functional characterization of the sex-determining gene doublesex in the sawfly, Athalia rosae\xa0(Hymenoptera: Tenthredinidae)

Sexual fate of the sawfly, Athalia rosae (Hymenoptera: Tenthredinidae) is determined by the complementary sex determination (CSD) mechanism as is the case in honeybees. However, to date, genes involved in sex determination have not been identified in this species. In this study, we attempted to identify orthologs of complementary sex-determiner (csd), feminizer (fem), and doublesex (dsx) from the A. rosae genome, all of which are crucial components of the sex determination cascade in the honeybee. As a result, we identified a sawfly ortholog of dsx (designated as Ardsx). Rapid amplification of cDNA ends (RACE) using total RNA extracted from male and female larvae identified three male-specific variants and three female-specific variants. Comparison between the full-length Ardsx cDNAs and the genomic sequence revealed that exon 5 was differentially spliced between the male- and female-specific variants. RT-PCR analysis demonstrated that Ardsx pre-mRNA was spliced alternatively in a sex-dependent manner at almost all the developmental stages. RNAi-mediated knockdown of Ardsx in males caused severe defects in the reproductive organs and, notably, induced development of the ovipository apparatus containing the dorsal pair of blades and the sheath. These males also showed abnormalities in testes and seminal vesicles and lacked mature sperm. The present study provides the first direct evidence that dsx is essential for sexual development in hymenopteran species.

Expression profile of the SOX9 gene in the testes of sexually immature and mature male goats (Capra hircus), and its potential influence on postnatal testis development

The aim of this study was to compare the expression levels of the SOX9 (SRY-box 9) gene in the testes of 18 White improved male goats (Capra hircus) divided into three age groups (one, 10 and 15 months of age with seven, eight and three individuals per group, respectively). Abnormalities in testis development were observed in three individuals from the group of 10-month-olds. Additionally, differences in SOX9 expression that may affect the process of testis maturation and testicular spermatogenic activity were investigated among individuals. The expression of the SOX9 gene in testicular tissues was analysed using qPCR. Maximal SOX9 expression was observed in 10-month-old males with normal testes, while expression was significantly reduced in the same age group of males with abnormal testes. Abnormalities in testis development were associated with low parameters of semen quality. The lowest expression levels of SOX9 were observed in 15-month-old goats. The results of the present study indicate that SOX9 expression changes significantly during the development of male goats.

688 - Blunt scrotal trauma in adults: A multi-institution experience evaluating the American Association for the Surgery of Trauma organ injury grading scale about 107 cases

The authors evaluated the usefulness of the American Association for the Surgery of Trauma (AAST) testis injury scale based on preoperative scrotal ultrasonography (US) and physical examination compared to peroperative findings. A retrospective review was performed on 107 patients (mean age=29,2±5.8 years) with a testis blunt trauma treated between January 2005 and August 2015. All patients underwent surgical scrotal exploration. Preoperative US was performed in all cases. Testis trauma was classified according to the AAST organ injury scale, preoperatively based on physical examination and scrotal US and then compared to peroperative definitif grading scale. Of the included patients, 14 were found to have abnormal testis contours on US, 25 had a rupture of the tunica albuginea, with a sensitivity of 70,8% and a specificity of 71,2%. Orchidectomy was performed in 12 cases, partial orchidectomy in 32 and tunica albuginea repair in 35 patients. Through this series, US was not a specific and sensitive exam to really precise the severity grade of testis trauma. Pre- and preoperative findings were significantly different. Thus, we continue to support history and clinical findings and we encourage surgical exploration when testis lesion is suspected.

The Role of Pnut and its Functional Domains in Drosophila Spermatogenesis.

The Drosophila Pnut protein belongs to the family of septins, which are conserved GTPases participating in cytokinesis and many more other fundamental cellular processes. Because of their filamentous appearance, membrane association, and functions, septins are considered as the fourth component of the cytoskeleton, along with actin, microtubules, and intermediate filaments. However, septins are much less studied than the other cytoskeleton elements. We had previously demonstrated that the deletion of the pnut gene leads to mitotic abnormalities in somatic cells. The goal of this work was to study the role of the pnut in Drosophila spermatogenesis. We designed a construct for pnut RNA interference allowing pnut expression to be suppressed ectopically. We analyzed the effect of pnut RNA interference on Drosophila spermatogenesis. Germline cells at the earliest stages of spermatogenesis were the most sensitive to Pnut depletion: the suppression of the pnut expression at these stages leads to male sterility as a result of immotile sperm. The testes of these sterile males did not show any significant meiotic defects; the axonemes and mitochondria were normal. We also analyzed the effect of mutations in the Pnut's conservative domains on Drosophila spermatogenesis. Mutations in the GTPase domain resulted in cyst elongation defects. Deletions of the C-terminal domain led to abnormal testis morphology. Both the GTPase domain and C-terminal domain mutant males were sterile and produced immotile sperm. To summarize, we showed that Pnut participates in spermiogenesis, that is, the late stages of spermatogenesis, when major morphological changes in spermatocytes occur.

Acoustic radiation force impulse (ARFI) elastography of testicular disorders in dogs: preliminary results

The aim of this study was to describe the use of acoustic radiation force impulse (ARFI) elastography in the evaluation of testicular disorders in dogs. Eighteen dogs with testicular disorders (thirty-six testicles) were assessed. Echotexture, size, contours and margins of testes were analysed by ultrasonography. Deformities and tissue stiffness (greyscale and homogenous or heterogeneous) were evaluated by qualitative elastography and shear velocity was determined quantitatively. Subsequent to orchiectomy, testicular samples were collected for histopathology analysis and thirty-six disorders were identified. Qualitative elastography revealed that normal healthy testicular tissues were homogenous and not pliable while the affected testicles had alterations in tissue stiffness and homogeneity. The values obtained for quantitative elastography of the testicular tissues were: normal/healthy - 1.30±0.12 m/s; degenerated - 0.97±0.08 m/s; atrophied - 2.00±0.35 m/s; hypoplastic - 0.82±0.2 m/s; cystic - 1.32±0.18 m/s; orchitis - 2.68±0.42 m/s; interstitial cell tumours - 3.32±0.65 m/s; sertolioma - 2.99±0.07 m/s and leydigoma - 2.73±0.37. ARFI elastography of abnormal testes proved to be an applicable and complementary technique in the diagnosis of testicular disease in dogs.

Excessive apoptosis and defective autophagy contribute to developmental testicular toxicity induced by fluoride

Fluoride, a ubiquitous environmental contaminant, is known to impair testicular functions and fertility; however the underlying mechanisms remain obscure. In this study, we used a rat model to mimic human exposure and sought to investigate the roles of apoptosis and autophagy in testicular toxicity of fluoride. Sprague–Dawley rats were developmentally exposed to 25, 50, or 100 mg/L sodium fluoride (NaF) via drinking water from pre-pregnancy to post-puberty, and then the testes of offspring were excised on postnatal day 56. Our results demonstrated that developmental NaF exposure induced an enhanced testicular apoptosis, as manifested by a series of hallmarks such as caspase-3 activation, chromatin condensation and DNA fragmentation. Further study revealed that fluoride exposure elicited significant elevations in the levels of cell surface death receptor Fas with a parallel increase in cytoplasmic cytochrome c, indicating the involvement of both extrinsic and intrinsic apoptotic pathways. Intriguingly, fluoride treatment also simultaneously increased the number of autophagosomes and the levels of autophagy marker LC3-II but not Beclin1. Unexpectedly, the expression of p62, a substrate that is degraded by autophagy, was also significantly elevated, suggesting that the accumulated autophagosomes resulted from impaired autophagy degradation rather than increased formation. Importantly, these were associated with marked histopathological lesions including spermatogenic failure and germ cell loss, along with severe ultrastructural abnormalities in testes. Taken together, our findings provide deeper insights into roles of excessive apoptosis and defective autophagy in the aggravation of testicular damage, which could contribute to a better understanding of fluoride-induced male reproductive toxicity.

Long-term and large-scale epidemiology of Brucella infection in baleen whales and sperm whales in the western North Pacific and Antarctic Oceans.

In a long-term, large-scale serologic study in the western North Pacific Ocean, anti-Brucella antibodies were detected in common minke whales (Balaenoptera acutorostrata) in the 1994–2010 offshore surveys (21%, 285/1353) and in the 2006–2010 Japanese coastal surveys (20%, 86/436), in Bryde’s whales (B. edeni brydei) in the 2000–2010 offshore surveys (9%, 49/542), in sei whales (B. borealis) in the 2002–2010 offshore surveys (5%, 40/788) and in sperm whales (Physeter macrocephalus) in the 2000–2010 offshore surveys (8%, 4/50). Anti-Brucella antibodies were not detected in 739 Antarctic minke whales (B. bonaerensis) in the 2000–2010 Antarctic surveys. This suggests that Brucella was present in the four large whale populations inhabiting the western North Pacific, but not in the Antarctic minke whale population. By PCR targeting for genes of outer membrane protein 2, the Brucella infection was confirmed in tissue DNA samples from Bryde’s whales (14%, 2/14), sei whales (11%, 1/9) and sperm whales (50%, 2/4). A placental tissue and an apparently healthy fetus from a sperm whale were found to be PCR-positive, indicating that placental transmission might have occurred and the newborn could act as a bacterial reservoir. Marked granulomatous testes were observed only in mature animals of the three species of baleen whales in the western North Pacific offshore surveys, especially in common minke whales, and 29% (307/1064) of total mature males had abnormal testes. This study provides an insight into the status of marine Brucella infection at a global level.

Epigenetic Effects of Endocrine Disrupting Chemicals

Recently, there is increasing evidences supported by animal studies emphasizing that exposure to environmental factors, nutritional conditions, xenobiotic chemicals, reproductive factors and low dose exposure to radiations can alter epigenetic programming and concomitantly enhance the risk of developing diseases. Endocrine disrupting chemicals (EDCs) can influence organization of developing brain, which may appear in expression of species typical social behaviors. Environmental exposures to EDCs are shown to increase the susceptibility against many kind of diseases. Currently, there are already several articles, books and journals about the epigenetic effects of EDCs available in media and internet. The aim of this thesis is to review these articles and to evaluate the possible consequences of being exposed to these agents in our daily life for the process of risk assessment of these chemicals. Epigenetic effects do not change the gene sequence. They affect the gene expression and therefore identification of expression profile in sensitive genes to epigenetic effects may be used as a biomarker for disease and environmental exposure. In the future, theses epigenetic biomarkers may help for early diagnosis of sensitivity of an individual for adult onset disease or maybe used to prevent the disease before the disease’s symptoms develop. When an organism grows and develops, precisely organized chemical reactions activate or deactivate parts of the genome at specific time and locations. The study of these chemical reactions and factors influencing them is called epigenetics. It has been observed that, transgenerationally modified progenies in their life are more prone to different kinds of diseases, such as mammary tumors, prostate disease, kidney disease, testis abnormalities and immune abnormalities. Our health depends on our normal development and reproductive ability. Healthy endocrine system is needed to have normal development and normal reproduction. Few years ago we thought that our life starts with the DNA we receive from our parents, but currents studies have shown that we receive more than just DNA from our parents. Famine, stress, fear and even drug use could all leave chemical marks on parent’s genetic material. Environmental exposure to EDCs during early development and pregnancy can modify epigenomes and induce trans-generationally asthma, autism, cancer, cardiovascular dysfunctions, diabetes, obesity, schizophrenia, infertility, reproductive diseases and dysfunction later in life. There is evidence showing that EDCs can induce epigenetic gene alterations by which these altered genes can be transferred into subsequent generations.

The Founder Strains of the Collaborative Cross Express a Complex Combination of Advantageous and Deleterious Traits for Male Reproduction.

Surveys of inbred strains of mice are standard approaches to determine the heritability and range of phenotypic variation for biomedical traits. In addition, they may lead to the identification of novel phenotypes and models of human disease. Surprisingly, male reproductive phenotypes are among the least-represented traits in the Mouse Phenome Database. Here we report the results of a broad survey of the eight founder inbred strains of both the Collaborative Cross (CC) and the Diversity Outbred populations, two new mouse resources that are being used as platforms for systems genetics and sources of mouse models of human diseases. Our survey includes representatives of the three main subspecies of the house mice and a mix of classical and wild-derived inbred strains. In addition to standard staples of male reproductive phenotyping such as reproductive organ weights, sperm counts, and sperm morphology, our survey includes sperm motility and the first detailed survey of testis histology. As expected for such a broad survey, heritability varies widely among traits. We conclude that although all eight inbred strains are fertile, most display a mix of advantageous and deleterious male reproductive traits. The CAST/EiJ strain is an outlier, with an unusual combination of deleterious male reproductive traits including low sperm counts, high levels of morphologically abnormal sperm, and poor motility. In contrast, sperm from the PWK/PhJ and WSB/EiJ strains had the greatest percentages of normal morphology and vigorous motility. Finally, we report an abnormal testis phenotype that is highly heritable and restricted to the WSB/EiJ strain. This phenotype is characterized by the presence of a large, but variable, number of vacuoles in at least 10% of the seminiferous tubules. The onset of the phenotype between 2 and 3 wk of age is temporally correlated with the formation of the blood-testis barrier. We speculate that this phenotype may play a role in high rates of extinction in the CC project and in the phenotypes associated with speciation in genetic crosses that use the WSB/EiJ strain as representative of the Mus muculus domesticus subspecies.

European Academy of Andrology Newsletter 2‐2015

s or, if open access is available, full texts are installed. The focus of this section is on news from ‘outside’ the EAA. An additional section of the new virtual library should reflect what is going on ‘inside’ EAA, and includes papers with high interest to our community published by the EAA centers. The papers are selected by the Centre directors. News from the EAA journal “Andrology” The first impact factor (IF) of “Andrology” has been released by the Thomson Reuters Web of Science. The IF is 2.3 and this figure is expected to increase next year because the first IF includes citations gathered within one year only (2014) to articles published during one year (2015), instead of the customary two-year period of citations and publications.

CRISPR/Cas9-mediated Dax1 knockout in the monkey recapitulates human AHC-HH.

Mutations in the DAX1 locus cause X-linked adrenal hypoplasia congenita (AHC) and hypogonadotropic hypogonadism (HH), which manifest with primary adrenal insufficiency and incomplete or absent sexual maturation, respectively. The associated defects in spermatogenesis can range from spermatogenic arrest to Sertoli cell only syndrome. Conclusions from Dax1 knockout mouse models provide only limited insight into AHC/HH disease mechanisms, because mouse models exhibit more extensive abnormalities in testicular development, including disorganized and incompletely formed testis cords with decreased number of peritubular myoid cells and male-to-female sex reversal. We previously reported successful clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated genome targeting in cynomolgus monkeys. Here, we describe a male fetal monkey in which targeted genome editing using CRISPR/Cas9 produced Dax1-null mutations in most somatic tissues and in the gonads. This DAX1-deficient monkey displayed defects in adrenal gland development and abnormal testis architecture with small cords, expanded blood vessels and extensive fibrosis. Sertoli cell formation was not affected. This phenotype strongly resembles findings in human patients with AHC-HH caused by mutations in DAX1. We further detected upregulation of Wnt/β-catenin-VEGF signaling in the fetal Dax1-deficient testis, suggesting abnormal activation of signaling pathways in the absence of DAX1 as one mechanism of AHC-HH. Our study reveals novel insight into the role of DAX1 in HH and provides proof-of-principle for the generation of monkey models of human disease via CRISPR/Cas9-mediated gene targeting.

Usefulness of 1H magnetic resonance spectroscopy in human testes: preliminary study

To identify and quantify the metabolites detected on proton magnetic resonance spectroscopy ((1)H-MRS) in human testes. The institutional review board approved the study, and all patients provided informed consent. A total of 27 patients consulting the Urology Department underwent single-voxel (1)H-MRS (4000ms repetition time [RT], 31ms echo time [TE], 128 averages for each TE) at 1.5T. Spectroscopy was not evaluable in one patient, and four patients had only one testis; thus, 48 testes were studied. Choline-containing compounds (Cho) and methylene lipid (Lip) values were measured and the Cho/Lip ratio was calculated. Testes were classified as normal or abnormal based on conventional magnetic resonance imaging (MRI) findings. The Mann-Whitney U-test was used for correlated data and bootstrapping to compare mean Cho/Lip ratios between normal and abnormal testes, and the area under the receiver operating characteristic curve (AUC) was calculated. Thirty testes were classified as normal and 18 as abnormal. The mean Cho/Lip ratio was 1.02±0.46 in normal testes and 0.45±0.36 in abnormal testes (Mann-Whitney U, p=0.001; bootstrapping mean difference, 0.57; 95% confidence interval (CI) 0.32-0.82; AUC=0.833). (1)H-MRS could be useful in routine clinical practice to identify the major metabolites in the testes and help discriminate between normal and abnormal testes.

Testis specific serine/threonine protein kinase 4 (TSSK4) leads to cell apoptosis relying on its kinase activity.

Testis specific serine/threonine protein kinase 4 (TSSK4) belongs to the TSSK family, and its members play an important role in spermatogenesis and/or spermiogenesis. Mouse TSSK4 has been reported to be expressed exclusively in the testis and can maintain its kinase activity through autophosphorylation at Thr-197. However, its biological function remains poorly understood. Here we found that GFP-TSSK4-overexpressed HeLa cells showed apoptotic bodies, indicating TSSK4 can lead to apoptosis in vitro. Furthermore, TSSK4 induced apoptosis in different cell lines including HeLa, Cos-7 and H1299 tested by flow cytometry but not its kinase-dead mutant TSSK4-K54M. TSSK4 knockout mice showed increased testes weight and decreased apoptotic spermatogonia and spermatocytes at 21st day after birth tested by TUNEL technology. So TSSK4 was able to induce cell apoptosis in vitro depending on its kinase activity, which leads to abnormal testes weight and apoptosis, shedding light on its function in the process of spermatogenesis and/or spermiogenesis.

Testis abnormalities in a population of the iconic Australian species, the eastern bearded dragonPogona barbata

Testis volume is generally correlated with sperm production. Their size is, therefore, considered informative, and is widely used as a surrogate for reproductive ability in a range of species. Gonadal abnormalities that influence adult reproductive function as a result of endocrine disruption compounds (EDCs) have been reported. In response to the observation that the population of the bearded dragon Pogona barbata had crashed in peri-urban Western Sydney, we investigated the nature and extent of testis deformity. It was observed that individuals collected in Western Sydney since the introduction of unleaded petrol in 1985 have a high level of deformities that are consistent with disruption of the endocrine processes. While deformities, such as missing testes, extreme asymmetry between testes, and flattened testes were not associated with any single aspect of the reproductive cycle, and they were found across the range of the species, the problem was much greater in Western Sydney than elsewhere in the sp...

Non classical function of vitamin d – influence on reproductive health, puberty and fertility

In the past few years, there has been growing appreciation for the many roles of vitamin D and its active metabolites in a large number of tissues. Most tissues in the body, not just those participating in the classic action of vitamin D such as bone, kidney and gut, have receptors (VDR) for the active form of vitamin D – 1,25 dihydroxyvitamin D. The recent data on vitamin D from retrospective, prospective observational studies, case-control and experimental studies confirm the essential role of vitamin D in a variety of physiological functions. Last time there has been growing interest in this substance observed in the scientific researches and biomedical literature, due to findings which demonstrate a vitamin D deficiency status in the population. This review is an analysis of the association between the vitamin D and the female and male reproduction and fertility. We highlight the latest findings from medical trials on vitamin D during last years. The aim of this article is to understand how vitamin D affects the female and male fertility. Vitamin D is a hormone which controls nearly 1/3 of human and mice genome, over 200 genes in a human body, including those responsible for cell cycle control: proliferation, differentiation, apoptosis. Apart from basic functions, which are maintaining calcium-phosphoric balance, vitamin D takes active part in process of cell proliferation, epidermal keratinocyte differentiation, immune system stimulation, insulin secretion, brain metabolism, adipocytes function, puberty, reproduction and fertility. The vitamin D receptors (VDR) and vitamin D metabolizing enzymes are found in reproductive tissues of women and men. VDR knockout mice have significant gonadal insufficiency, decreased sperm count and motility, and histological abnormalities of testis, ovary and uterus. Assuming that 30 ng/ml (75 nmol/l) is a lower limit of normal concentration of 25(OH)D3 in serum, the number of people with vitamin D deficit equals about 1 billion worldwide.

Active vitamin D deficiency mediated by extracellular calcium and phosphorus results in male infertility in young mice.

We used mice with targeted deletion of 25-hydroxyvitamin D-1 α-hydroxylase [1α(OH)ase(-/-)] to investigate whether 1,25(OH)2D3 deficiency results in male infertility mediated by 1,25(OH)2D3 or extracellular calcium and phosphorus. Male 1α(OH)ase(-/-) and their wild-type littermates fed either a normal diet or a rescue diet from weaning were mated at 6-14 wk of age with female wild-type mice on the same diet. The fertility efficiency of females was analyzed, and the reproductive phenotypes of males were evaluated by histopathological and molecular techniques. Hypocalcemic and hypophosphatemic male 1α(OH)ase(-/-) mice on a normal diet developed infertility characterized by hypergonadotropic hypogonadism, with downregulation of testicular calcium channels, lower intracellular calcium levels, decreased sperm count and motility, and histological abnormalities of the testes. The proliferation of spermatogenic cells was decreased with downregulation of cyclin E and CDK2 and upregulation of p53 and p21 expression, whereas apoptosis of spermatogenic cells was increased with upregulation of Bax and p-caspase 3 expression and downregulation of Bcl-xl expression. When serum calcium and phosphorus were normalized by the rescue diet, the defective reproductive phenotype in the male 1α(OH)ase(-/-) mice, including the hypergonadotropic hypogonadism, decreased sperm count and motility, histological abnormalities of testis, and defective spermatogenesis, was reversed. These results indicate that the infertility seen in male 1,25(OH)2D3-deficient mice is not a direct effect of active vitamin D deficiency on the reproductive system but is an indirect effect mediated by extracellular calcium and phosphorus.

The immunoexpression of androgen receptor, estrogen receptors alpha and beta, vanilloid type 1 receptor and cytochrome p450 aromatase in rats testis chronically treated with letrozole, an aromatase inhibitor.

The function of testis is under hormonal control and any disturbance of hormonal homeostasis can lead to morphological and physiological changes. Therefore the aim of the study was to investigate the expression of androgen and estrogen receptors (AR, ERs), vanilloid receptor (TRPV1), cytochrome P450 aromatase (P450arom), as well as apoptosis of cells in testis of adult rats chronically treated with letrozole (LT), a non-steroidal aromatase inhibitor, for 6 months. The testicular tissues were fixed in Bouin's fixative and embedded in paraffin. Immunohistochemistry with monoclonal antibodies (abs) against AR, ERa, P450arom, and polyclonalabs against ERβ, TRPV1, caspase-3 was applied. Long-lasting estradiol deficiency, as an effect of LT treatment, produced changes in the morphology of testis and altered the expression of the studied receptors in cells of the seminiferous tubules and rate of cell apoptosis. The immunostaining for AR was found in the nuclei of Sertoli cells and the cytoplasm of spermatogonia and spermatocytes in III-IV stages of the seminiferous epithelium cycle. The intensity of staining for P450arom was lower in the testis of LT-treated rats as compared to control animals. The immunofluorescence of ERα and ERβ was observed exclusively in the nuclei of Leydig cells of LT-treated rats. There were no changes in localization of TRPV1, however, the intensity of reaction was stronger in germ cells of the seminiferous epithelium after LT treatment. The apoptosis in both groups of animals was observed within the population of spermatocytes and spermatids in II and III stages of the seminiferous epithelium cycle. In testis of LT-treated rats the immunoexpression of caspase-3 was additionally found in the germ cells in I and IV stages, and Sertoli, myoid and Leydig cells. In conclusion, our results underline the important role of letrozole treatment in the proper function of male reproductive system, and additionally demonstrate that hormonal imbalance can produce the morphological abnormalities in testis.

Gonadal development and transcript profiling of steroidogenic enzymes in response to 17α-methyltestosterone in the rare minnow Gobiocypris rarus

It is well known that natural and anthropogenic chemicals interfere with the hormonal system of vertebrate and invertebrate organisms. How these chemicals regulate gonadal steroidogenesis remains to be determined. The main objective of this study was to evaluate the effects of 17α-methyltestosterone (MT), a synthetic model androgen, on gene expression profiles of six key steroidogenic genes in adult rare minnow. The full-length cDNA encoding 11β-hydroxysteroid dehydrogenase-2 (11β-HSD2) was firstly isolated and characterized by RT-PCR and RACE methods. The gonadal transcript changes of StAR, cyp11a1, 3β-HSD, cyp17a1, 11β-HSD2 and cyp19a1a in 6-month adult Gobiocypris rarus exposed to MT and 17α-ethinylestradiol (EE2) for 7, 14 and 21 days were detected by qRT-PCR. To make an effort to connect the transcriptional changes of steroidogenic enzymes with effects on higher levels of biological organization and on VTG, one remarkable sensitive target of steroids, body and gonad weights, histology of gonads, and hepatic vtg mRNA level were measured. MT caused varying degree of abnormalities in ovaries and testes. The hepatic vtg mRNA level was highly inhibited in females and slightly altered in males by MT. Transcripts of several steroidogenic genes including StAR, cyp17a1, and cyp11a1 showed high responsiveness to MT exposure in G. rarus. The gene expression profiles of these steroidogenic genes in MT-treated groups were much distinct with the EE2-treated group.

Pathological changes of testicular tissue in normal adult mice: A retrospective analysis

Mouse testicular experimental models are widely used in the study of andrology, reproductive toxicology and pharmacology. Under physiological conditions, a normal adult mouse is usually considered to have normal testes. However, whether normal adult mouse testes exhibit pathological changes has not been evaluated. The objective of this study was to investigate the pathological changes of testicular tissues in normal adult mice. A retrospective analysis of 720 adult male Kunming mice, used in previous studies as controls, was performed. Bilateral testicular tissues were stained with hematoxylin and eosin for pathological examinations. Among the 720 mice, nine had abnormal testes, an incidence of 1.3%. The nine mice with abnormal testes included two with microrchidia (22.2%) while the others had a normal testicular size. The observed pathological changes associated with microrchidia were seminiferous epithelial vacuolation, spermatogenesis arrest at the spermatocyte stage and the absence of sperm in all tubules. In other abnormal testes, pathological alterations included seminiferous epithelial vacuolation, severe hypospermatogenesis and symplasts composed of collapsed spermatids in tubules. The results demonstrate that normal adult male mice exhibit testicular pathological changes. Therefore, the possibility of abnormal testes in normal adult mice must be considered when using mice to establish a testicular experimental model.

Dose-dependent effect of deltamethrin in testis, liver, and Kidney of wistar rats

Objectives:Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, household pest control, protection of foodstuff, and disease vector control. Although initially thought to be least toxic, a number of recent reports showed its toxic effects in mammalian and non-mammalian animal species. The current study was performed to assess the dose-dependent deltamethrin toxicity on testes, liver, and kidney of male Wistar rats.Materials and Methods:Twenty-four rats were divided in four groups of 6 each. Group A served as normal control. Group B, C, and D were administered with different doses (2 or 3 or 6 mg/kg corresponding to 1/30th or 1/20th or 1/10th of LD50, respectively) of deltamethrin for 28 days.Results:Deltamethrin exposure caused a significant reduction in weight of reproductive organs, decrease in sperm count, sperm motility, serum testosterone (T), follicle stimulating hormones (FSH), and luteinizing hormones (LH) in testis. Glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione S transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx) were decreased in testis, liver and kidney of exposed rats. Deltamethrin exposure significantly increased sperm abnormalities in testis. Significant increase in lipid peroxidation (LPO) level was observed in testis, liver and kidney. Deltamethrin also caused histological alterations in testes, liver, and kidney.Conclusions:The results indicated that deltamethrin at a dose of 6 mg/kg exerts significant harmful effects on testes, liver and kidney as compare to 2 mg and 3 mg/kg. The study concluded that the system toxicity induced by deltamethrin was dose dependent.