Transcriptomic analysis reveals the endocrine toxicity of tributyltin and triphenyltin on the whelk Reishia clavigera and mechanisms of imposex formation.

Organotin compounds (OTs) are endocrine disruptors that induce imposex in hundreds of gastropods, but little is known about their underlying molecular mechanisms. This study aimed to investigate the endocrine toxicity and molecular responses to tributyltin (TBT) and triphenyltin (TPT) exposure in the whelk Reishia clavigera, which often serves as a biomonitor for OT contamination. Over a 120-day exposure to environmentally relevant concentrations of TBT (1000 ng L-1) and TPT (500 ng L-1), we observed a significant increase in penis length in both male and female whelks. Notably, TPT exhibited a stronger potency in inducing pseudo-penis development and female sterility, even at a half dose of TBT. Bioaccumulation analysis also revealed higher persistence and accumulation of TPT in whelk tissues compared to TBT. Differential expression analysis identified a substantial number of differentially expressed genes (DEGs), with TPT exposure eliciting more DEGs than TBT. Our results demonstrated that OTs induced xenobiotic metabolism and metabolic dysregulation in the digestive gland, impaired multiple cellular functions and triggered neurotoxicity in the nervous system, and disrupted lipid homeostasis and oxidative stress in the gonads. Furthermore, imposex was possibly associated with disturbances in retinoic acid metabolism, nuclear receptor signaling, and neuropeptide activity. When compared to TBT, TPT exhibited a more pronounced endocrine-disrupting effect, attributable to its higher bioaccumulation and substantial interruption of transcriptional regulation, OT detoxification, and biosynthesis of retinoic acids in R. clavigera. Our results, therefore, highlight the importance of considering the differences in bioaccumulation and molecular toxicity between TBT and TPT in future risk assessments of these contaminants. Overall, our study provided molecular insights into the toxicity and transcriptome profiles in R. clavigera exposed to TBT and TPT, shedding light on the endocrine-disrupting effects and reproductive impairment in female gastropods.

Curcumin protects against cadmium-induced germ cell death in the testis of rats.

Introduction: Cadmium (Cd) has been shown to disrupt the reproductive system. In this study, we evaluated the protective effects of Curcumin (Cur) against Cd-induced reproductive toxicity. Methods: Exploring the role of Cur in Cd-treated rat models. Results: The study demonstrated that Cd treatment impaired the seminiferous epithelium, leading to increased apoptosis of germ cells. Interestingly, pretreatment with Cur ameliorated the histological damage and decreased the germ cell apoptosis induced by Cd. Furthermore, after Cd exposure, B-cell lymphoma-2 expression was significantly decreased while Bax expression was increased. Pretreatment of rats with Cur protected against germ cell apoptosis by improving the expression of B-cell lymphoma-2 and reducing Bax. Additionally, Cd treatment increased reactive oxygen species, resulting in a decrease in antioxidant enzymes. However, pretreatment of rats with Cur followed by Cd administration led to a substantial decrease in reactive oxygen species levels and increased activities of antioxidant enzymes. Ultrastructural investigations revealed that damage to the mitochondrial structure was significantly ameliorated by Cur pretreatment in Cd-treated rats. Notably, Cur significantly activated the peroxisome proliferator-activated receptor gamma coactivator 1a/Sirtuins-3 signaling pathway. Conclusions: Overall, our data suggest that Cd induces germ cell apoptosis through mitochondrial-induced oxidative stress, but Cur pretreatment offers strong protection against Cd-induced reproductive toxicity.

Radiation and male reproductive system: Damage and protection.

Male fertility has been declining in recent decades, and a growing body of research points to environmental and lifestyle factors as the cause. The widespread use of radiation technology may result in more people affected by male infertility, as it is well established that radiation can cause reproductive impairment in men. This article provides a review of radiation-induced damage to male reproduction, and the effects of damage mechanisms and pharmacotherapy. It is hoped that this review will contribute to the understanding of the effects of radiation on male reproduction, and provide information for research into drugs that can protect the reproductive health of males.

Pesticides exposure and compromised fitness in wild birds: Focusing on the reproductive endocrine disruption.

Exposure of pesticides to wildlife species, especially on the aspect of endocrine disruption is of great concern. Wildlife species are more at risk to harmful exposures to the pesticides in their natural habitat through diet and several other means. Species at a higher tropic level in the food chain are more susceptible to the deleterious effects due to sequential biomagnifications of the pesticides/metabolites. Pesticides directly affect fitness of the species in the wild causing reproductive endocrine disruption impairing the hormones of the gonads and thyroid glands as reproduction is under the influence of cross regulations of these hormones. This review presents a comprehensive compilation of important literatures on the impact of the current use pesticides in disruption of both the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-thyroid axes particularly in birds addressing impacts on the reproductive impairments and overall fitness. In addition to the epidemiological studies, laboratory investigations those provide supportive evidences of the probable mechanisms of disruption in the wild also have been incorporated in this review. To accurately predict the endocrine-disruption of the pesticides as well as to delineate the risk associated with potential cumulative effects, studies are to be more focused on the environmentally realistic exposure dose, mixture pesticide exposures and transgenerational effects. In addition, strategic screening/appropriate methodologies have to be developed to reveal the endocrine disruption potential of the contemporary use pesticides. Demand for adequate quantitative structure-activity relationships and insilico molecular docking studies for timely validation have been highlighted.

D-ribose-L-cysteine exhibits restorative neurobehavioral functions through modulation of neurochemical activities and inhibition oxido-inflammatory perturbations in rats exposed to polychlorinated biphenyl.

Polychlorinated biphenyl (PCB) is potentially harmful environmental toxicant causing cognitive decline with depressive features. PCB-induced behavioral deficits are associated with neurochemical dysfunctions, immune changes, and oxidative stress. This study investigated the neuroprotective effects of D-ribose-L-cysteine (DRLC), a neuroprotective precursor element of glutathione on PCB-induced neurobehavioral impairments. Following the initial 15 days of PCB (2 mg/kg) exposure to rats, DRLC (50 mg/kg) was given orally for an additional 15 days, from days 16 to 30. Animals were assessed for behavioral effect such as changes in locomotion, cognition, and depression. Oxidative/nitrergic stress markers; antioxidant regulatory proteins paraoxonase-1 (PON-1), heme oxygenase-1 (HO-1), nuclear factor erythroid 2-related factor 2 (Nfr2), NADPH oxidase-1 (NOX-1), NAD(P)H quinone oxidoreductase 1 (NQO1), and neuroinflammation (NF-kß, and TNF-α); and neurochemical metabolizing enzymes (acetylcholinesterase (AChE), monoamine oxidase-A and -B (MAO-A, MAO-B)) were carried out. The PCB-induced decline in locomotion, cognitive performance, and depressive-like features were reversed by DRLC. More specifically, PCB-induced oxidative and nitrergic stress, typified by reduced levels GSH, CAT, and SOD, accompanied by elevated MDA and nitrite were attenuated by DRLC. Additionally, DRLC restored the neuroinflammatory milieu indicated by decreased NF-kß and TNF-α levels toward normal. Hyperactivities of AChE, MAO-A, MAO-B, PON-1, and NOX-1 levels as well as Nfr2, NQO1, and PON-1 due to PCB exposure were mitigated by DLRC. Our results suggest DRLC as a prospective neurotherapeutic agent against PCB-induced neurobehavioral impairments such as cognitive deficit and depressive-like feature through antioxidative and anti-nitrergic stress, anti-neuroinflammation, inhibition of brain metabolizing enzymes, and normalization of neurochemical homeostasis.

Zinc Ameliorates Tripterygium Glycosides-Induced Reproductive Impairment in Male Rats by Regulating Zinc Homeostasis and Expression of Oxidative Stress-Related Genes.

Tripterygium glycosides (TG) can seriously damage male reproductive function, and the reproductive system is difficult to restore after stopping the administration of TG in male rats. Zinc (Zn) is one of the most important trace elements in the human body and plays an important role in maintaining male fertility. The aim of this study was to investigate whether zinc supplementation could improve the testicular reproductive damage induced by TG toxicity in rats and to investigate its mechanism of action. The results showed that zinc sulfate (ZnSO4) could improve testicular tissue structure and semen parameters, promote testosterone synthesis, increase zinc-containing enzyme activity, increase zinc concentration in serum and testicular tissues, and maintain zinc homeostasis in male rats induced by TG toxicity. Zinc supplementation activated relevant signalling molecules in the KEAP1-NRF2/ARE pathway and alleviated TG-induced oxidative stress. Therefore, this study concluded that zinc supplementation could improve reproductive damage by regulating zinc homeostasis and the expression of genes related to oxidative stress.

Extended exposure to tetrabromobisphenol A-bis(2,3-dibromopropyl ether) leads to subfertility in male mice at the late reproductive age.

Tetrabromobisphenol A-bis(2,3-dibromopropyl ether) (TBBPA-BDBPE), a commonly used brominated flame retardant as a decabromodiphenyl ether substitute, has been detected in various environmental compartments, but its health hazards remain largely unknown. Our recent study showed that low-dose exposure of male mice to TBBPA-BDBPE from postnatal day (PND) 0 to 56 caused remarkable damage to the microtubule skeleton in Sertoli cells and the blood-testis barrier (BTB) but exerted little effect on conventional reproductive endpoints in adulthood. To investigate whether TBBPA-BDBPE may cause severe reproductive impairments at late reproductive age, here, we extended exposure of historically administrated male mice to 8-month age and allowed them to mate with non-treated females for the evaluation of fertility, followed by a general examination for the reproductive system. As expected, we found that 8-month exposure to 50 µg/kg/d as well as 1000 µg/kg/d TBBPA-BDBPE caused severe damage to the reproductive system, including reduced sperm counts, increased sperm abnormality, histological alterations of testes. Moreover, microtubule damage and BTB-related impairment were still observed following 8-month exposure. Noticeably, high-dose TBBPA-BDBPE-treated mice had fewer offspring with a female-biased sex ratio. All results show that long-term exposure to TBBPA-BDBPE caused severe reproductive impairment, including poor fertility at late reproductive age. It is therefore concluded that slight testicular injuries in early life can contribute to reproductive impairment at late reproductive age, highlighting that alterations in certain non-conventional endpoints should be noticed as well as conventional endpoints in future reproductive toxicity studies.

Reproductive toxicity in marine medaka (Oryzias melastigma) due to embryonic exposure to PCB 28 or 4'-OH-PCB 65.

Previous studies have shown that juvenile or adult exposure to polychlorinated biphenyls (PCBs) induces alterations in reproductive functions (e.g., reduced fertilization rate) and behavior (e.g., reduced nest maintenance) in fish. Embryonic exposures to other endocrine disrupting chemicals have been reported to induce long-term reproductive toxicity in fish. However, the effects of embryonic exposure to PCBs or their metabolites, OH-PCBs, on long-term reproductive function in fish are unknown. In the present study, we used the marine medaka fish (Oryzias melastigma) as a model to assess the reproductive endpoints in response to embryonic exposure to either PCB 28 or 4'-OH-PCB 65. Our results showed that the sex ratio of marine medaka was feminized by exposure to 4'-OH-PCB 65. Fecundity was decreased in the medaka treated with either PCB 28 or 4'-OH-PCB 65, whereas the medaka from embryonic exposure to 4'-OH-PCB 65 additionally exhibited reduced fertilization and a reduction in the hatching success rate of offspring, as well as decreased sperm motility. Serum 11-KT concentrations were reduced in the PCB 28-treated medaka, and serum estradiol (E2)/testosterone (T) and E2/11-ketotestosterone (11-KT) ratios were decreased in the 4'-OH-PCB 65-treated medaka. To explain these observations at the molecular level, transcriptomic analysis of the gonads was performed. Bioinformatic analysis using Gene Ontology and Ingenuity Pathway Analysis revealed that genes involved in various pathways potentially involved in reproductive functions (e.g., steroid metabolism and cholesterol homeostasis) were differentially expressed in the testes and ovaries of either PCB- or OH-PCB-treated medaka. Thus, the long-term reproductive toxicity in fish due to embryonic exposure to PCB or OH-PCB should be considered for environmental risk assessment.

Timing and magnitude of net methylmercury effects on waterbird reproductive output are dependent on food availability.

Mercury (Hg) is a globally distributed pollutant. Its sub-lethal effects on reproduction of birds have been used as indicators of contamination and of potential demographic effects. However, studies typically used single endpoints that might not be representative of entire reproductive cycle. To estimate timing and net cumulative effects of Hg exposure under field conditions, we used observational data over 11 years from >1200 nests of great egrets breeding under temporally and spatially varying food availability and Hg exposures in the Florida Everglades. We collected measures of fish biomass and availability (>100 locations annually) and used four avian reproductive endpoints that represented the entire breeding cycle. We calculated net reproductive loss by adding estimated Hg effects on failures prior to egg laying, clutch size, hatching success and nestling survival in response to food availability and Hg exposure. To validate and assess results of the observational egret study, we ran the same analyses with data of captive breeding white ibises experimentally exposed to Hg with ad libitum food over 3 years. We found large (>50 %) reductions in great egret offspring with high Hg exposure (18 µg/g dw THg nestling feather, ~0.7 µg/g ww whole egg THg) and high food availability, and even larger reductions (up to 100 %) with high Hg exposure and low food. Timing and the relative contribution of different endpoints to overall reproductive failure varied with food availability. Failures prior to egg laying were relevant at all food availabilities and proportionally most important during high food availability (~70 % of total losses). Under high food, post-hatching failures increased moderately with increasing exposure (~10 % of total losses), and under low food, hatching failures became dominant (~50 % of total losses). Patterns of failure of captive white ibis fed ad libitum resembled those of great egrets under high food availability but differed in total magnitude. We suggest that, a) net reproductive effects of Hg in free-ranging animals are probably much higher than generally reported in studies using single endpoints, b) Hg effect sizes vary considerably among different endpoints and c) food availability is a strong driver of timing and net effects of Hg exposure.

Inhibition of Oocyte Maturation by Malathion and Structurally Related Chemicals in Zebrafish (Danio rerio) After In Vitro and In Vivo Exposure.

Oogenesis is the process by which a primary oocyte develops into a fertilizable oocyte, making it critical to successful reproduction in fish. In zebrafish (Danio rerio), there are five stages of oogenesis. During the final step (oocyte maturation), the maturation-inducing hormone 17α,20ß-dihydroxy-4-pregnen-3-one (MIH) activates the membrane progestin receptor, inducing germinal vesicle breakdown. Using in vitro assays, it has been shown that anthropogenic stressors can dysregulate MIH-induced oocyte maturation. However, it is unknown whether the in vitro assay is predictive of reproductive performance after in vivo exposure. We demonstrate that a known inhibitor of oocyte maturation, malathion, and a structurally related chemical, dimethoate, inhibit oocyte maturation. However, malaoxon and omethoate, which are metabolites of malathion and dimethoate, did not inhibit oocyte maturation. Malathion and dimethoate inhibited maturation to a similar magnitude when oocytes were exposed for 4 h in vitro or 10 days in vivo, suggesting that the in vitro zebrafish oocyte maturation assay might be predictive of alterations to reproductive performance. However, when adult zebrafish were exposed to malathion for 21 days, there was no alteration in fecundity or fertility in comparison with control fish. Our study supports the oocyte maturation assay as being predictive of the success of in vitro oocyte maturation after in vivo exposure, but it remains unclear whether inhibition of MIH-induced oocyte maturation in vitro correlates to decreases in reproductive performance. Environ Toxicol Chem 2022;41:1381-1389. © 2022 SETAC.

Toxic and carcinogenic effects of hexavalent chromium in mammalian cells in vivo and in vitro: a recent update.

Chromium VI (Cr (VI)) can cross cell membranes readily and causes the formation of Cr-DNA adducts, genomic damages, elevation of reactive oxygen species (ROS) and alteration of survival signaling pathways, as evidenced by the modulation in p53 signaling pathway. Mammals, including humans are exposed to Cr, including Cr (VI), frequently through inhalation, drinking water, and food. Several studies demonstrated that Cr (VI) induces cellular death through apoptosis and autophagy, genotoxicity, functional alteration of mitochondria, endocrine and reproductive impairments. In the present review, studies on deleterious effects of Cr (VI) exposure to mammalian cells (in vivo and in vitro) have been documented. Special attention is paid to the underlying molecular mechanism of Cr (VI) toxicity.

Potential toxic effects produced by L-mimosine in the thyroid and reproductive systems. Evaluation in male rats.

Leucaena leucocephala is a worldwide plant used as forage; however, its use in animal production has been limited because of the presence of a toxic nonprotein amino acid, L-mimosine. L-mimosine exhibits negative effects not only in ruminants but also in monogastric animals; however, there is little information available on the effect of this amino acid in monogastric species. Thus, this study aimed to evaluate the general toxicity of L-mimosine in rats, as well as its effects on the endocrine and reproductive systems. L-mimosine was extracted from seeds of L. leucocephala that were administered orally by gavage to adult Wistar rats at different doses of 25, 40 and 60 mg/kg body weight/day for 28 days. The following parameters were evaluated: weight gain, feed intake, serum enzymes, histopathology (liver, kidney, thyroid, thymus, and spleen), serum hormones (testosterone, corticosterone, T3 and T4) and sexual behavior. No clinical signs of toxicity were observed in animals, but histopathology revealed consistent lesions in the thyroids. Additionally, rats exposed to L-mimosine presented low serum levels of testosterone, decreased mount numbers and increased mount intervals. Therefore, our study reinforces the assumption that L-mimosine has goitrogenic potential and causes impairment in male reproductive performance.

Accounting for food availability reveals contaminant-induced breeding impairment, food-modulated contaminant effects, and endpoint-specificity of exposure indicators in free ranging avian populations.

It remains unclear how sub-lethal effects of contaminants play out in relation to other stressors encountered by free-ranging populations. Effects may be masked or influenced by interactions with field stressors such as food availability. We predicted that (1) including food availability, and particularly its interaction with Hg, would reveal or enhance associations between Hg and breeding endpoints. We further predicted that (2) breeding impairment associated with Hg would be higher under food stress conditions. We monitored Hg and nest success of great egrets (Ardea alba) in eight breeding colonies in the Florida Everglades over 11 years. We characterized variation in local food availability among colonies and years using fish biomass and recession range -a proxy to fish vulnerability. We used two Hg exposure indicators (egg albumen Hg and nestling feather Hg) and six breeding endpoints (clutch-size, brood-size, fledged-size, hatching success, post-hatching success and fledglings per egg) to assess whether variation in food availability influenced associations between Hg and these endpoints. Accounting for interactions between Hg and food availability, we identified statistically significant associations in all 12 indicator-endpoint combinations, while only three were detectable without food. Further, 10 combinations showed interactions between Hg and components of food availability. Our results also indicated an endpoint-specific affinity, with albumen [Hg] explaining more variation in hatching success while nestling feather [Hg] explained more variation in post-hatching survival. Both Hg indicators accounted for relevant (6-10%) amounts of variation in fledglings produced per egg laid, an integrative endpoint. Increased Hg exposure resulted in overall reduced reproductive success when food availability was low, but our models predicted low or no effects of increasing Hg exposure when food availability was high. Our results indicate that Hg induced impairment is strongly driven by food availability, providing a framework that accommodates previously contradictory results in the literature.

Review on Bee Products as Potential Protective and Therapeutic Agents in Male Reproductive Impairment.

Bee products are sources of functional food that have been used in complementary medicine to treat a variety of acute and chronic illnesses in many parts of the world. The products vary from location to location as well as country to country. Therefore, the aim of this review was to identify various bee products with potential preventive and therapeutic values used in the treatment of male reproductive impairment. We undertook a vigorous search for bee products with preventive and therapeutic values for the male reproductive system. These products included honey, royal jelly, bee pollen, bee brood, apilarnil, bee bread, bee wax, and bee venom. We also explained the mechanisms involved in testicular steroidogenesis, reactive oxygen species, oxidative stress, inflammation, and apoptosis, which may cumulatively lead to male reproductive impairment. The effects of bee pollen, bee venom, honey, propolis, royal jelly, and bee bread on male reproductive parameters were examined. Conclusively, these bee products showed positive effects on the steroidogenic, spermatogenic, oxidative stress, inflammatory, and apoptotic parameters, thereby making them a promising possible preventive and therapeutic treatment of male sub/infertility.

Biomonitoring the effects of urban-stream waters on the health status of pale chub (Zacco platypus): A comparative analysis of biological indexes and biomarker levels.

The objective of this study was to biomonitor the effects of potential environmental pollutants in urban-stream waters, on fish health. Pale chub (Zacco platypus), a dominant species in the Korea urban stream waters, was chosen and biomonitoring indicators for the different spatial characteristics were tailored in an urban watershed. Biological responses including biotic-somatic index as well as gonadal development phase and plasma steroids levels, and the biochemical responses, ethoxyresorufin-o-deethylase (EROD) and acetylcholinesterase (AChE) activities, were measured. No significant difference was observed in the length-weight relationship between the up-stream waters and the down-stream waters. However, changes in the gonad-somatic index (GSI) levels, plasma 17ß-estradiol (E2) levels, and mature oocyte frequencies in the female fish collected during the spawning season were observed in the down-stream waters at each monitoring site. Moreover, intersex condition (testis-ova) in the male fish in down-stream waters was recorded, even if it was just one fish. Although no significant difference was observed in the EROD and AChE activities between the up-stream waters and the down-stream waters, changes in the reproductive biomarker levels, including the GSI levels, plasma E2 levels, and gonadal maturation, lead to variable biomonitoring endpoints between the spatial different sites. These results imply that exposure to the down-stream waters can cause reproductive impairment in wild Z. platypus, individual variability in the biological responses further indicate the reproductive health was affected more by the down-stream waters than the up-stream waters. The finding from this study can provide the biomonitoring endpoint on the wild fish health in urban watershed that is crucial to the early risk assessment of its biological impacts. More multi-biomarkers studies reflecting the variation in the biological organization of wild fish and, therefore, the effects of urban-stream waters in the fish health are warranted.

Contrasting reproductive health of female clams Megapitaria squalida from two nearby metal-polluted sites in the Gulf of California: Potential effects of copper, lead, and cobalt.

We studied the effects of chronic exposure to metals on energy reserves and reproduction in the clam Megapitaria squalida in two nearby populations exposed to different levels of pollution from mining operations in the Gulf of California, Mexico. Female M. squalida from San Lucas beach had good reproductive health status, whereas Santa Rosalia specimens consistently showed low energy reserves, massive oocyte resorption throughout the year, high frequencies of undifferentiated individuals, low proportions of ripe and spawning organisms, smaller and fewer oocytes per follicle, and significantly lower follicular areas. Ovarian levels of Co, Cu, Pb, Mn, and Zn were consistently higher in clams from Santa Rosalia. The poor reproductive health of clams inhabiting this site may be attributed to their long-term exposure to high Co, Cu, and Pb concentrations, as these have been shown to cause toxicity and reproductive impairments in other marine organisms.

Effects of elevated temperatures and cadmium exposure on stress biomarkers at different biological complexity levels in Eisenia fetida earthworms.

Several ecotoxicological studies assessed metal toxicity upon soil biota and other communities but were mainly focused on the study of a single chemical and usually under optimal conditions of temperature. Meanwhile an increasing global warming is leading to new scenarios by combining different stress factors; chemical stress and thermal stress. Presently, this study aims to assess the joint effects produced by cadmium and elevated temperature on earthworms different levels of biological complexity. Eisenia fetida earthworms were maintained at 19 °C and 26 °C and simultaneously exposed to four Cd concentrations (1.25, 2.5, 25 and 125 mg Cd/Kg soil) for 14 (Short term exposure) and 56 days (reproduction test). Endpoints were addressed at different levels of biological complexity: reproductive impairment (cocoons and juvenile productions), Cd tissue accumulation, mortality of adults, weight loss and cytotoxic effects (coelomocyte viability). In the Short term exposure, increase in temperature produced a larger accumulation of Cd. Hence, earthworms exposed to 125 mg Cd/kg soil under heat stress (26 °C) showed a two fold higher Cd accumulation comparing to those at 19 °C. Earthworms exposed to moderate-high concentrations of Cd (2.5-125 mg Cd/kg) and maintained at 26 °C showed severe weight loss and high mortality rates. The neutral red uptake capacity of coelomocytes extruded from earthworms exposed to the highest Cd concentration decreased after 14 d at 19 °C, and more markedly at 26 °C. The reproduction impairment (decreased number of cocoons) was enhanced after exposure to concentrations higher than 2.5 mg Cd/kg at 26 °C, and after exposure to 125 mg Cd/kg at 19 °C. Earthworm reproduction capability is highly vulnerable to the effect of toxicants at elevated temperatures and sublethal concentrations.

Transcriptomic analysis of reproductive damage in the epididymis of male Kunming mice induced by chronic infection of Toxoplasma gondii PRU strain.

BACKGROUND: Some researchers have reported that Toxoplasma gondii can cause serious reproductive impairment in male animals. Specifically, T. gondii destroy the quality of sperm in the epididymis, which affects their sexual ability. However, among such studies, none have investigated the male reproductive transcriptome. Therefore, to investigate the relationship between T. gondii and sperm maturation, we infected mice with T. gondii prugniaud (PRU) strain and performed transcriptome sequencing of the epididymis. RESULTS: Compared with the control group, 431 upregulated and 229 downregulated differentially expressed genes (DEGs) were found (P-value < 0.05, false discovery rate (FDR) < 0.05 and |log2 (fold change)| ≥ 1). According to results of a bioinformatics analysis, Gene Ontology (GO) function is divided into three categories: cellular component, molecular function and biological process. Upon performing GO analysis, we found that some DEGs correlated with an integral part of membrane, protein complex, cell surface, ATP binding, immune system process, signal transduction and metabolic process which are responsible for the epididymal injury. DEGs were mapped to 101 unique KEGG pathways. Pathways such as cytokine-cytokine receptor interaction, glycolysis/gluconeogenesis and apoptosis are closely related to sperm quality. Moreover, Tnfsf10 and spata18 can damage the mitochondria in sperm, which decreases sperm motility and morphology. CONCLUSIONS: We sequenced the reproductive system of male mice chronically infected with T. gondii, which provides a new direction for research into male sterility caused by Toxoplasma infection. This work provides valuable information and a comprehensive database for future studies of the interaction between T. gondii infection and the male reproductive system.

African star apple fruit pulp-supplemented diet modulates fertility-related biomolecules in the testis and epididymis of high-fat diet/streptozotocin-induced diabetic rats.

This study evaluated the modulatory effect of African star apple fruit (ASAF) pulp inclusive diet on biomolecules associated with reproductive function in the testis and epididymis of high-fat diet/streptozotocin-induced diabetic male rats. The rats were divided into seven groups: control, diabetic control, diabetic rats treated with metformin, diabetic rats served with diet having 5 and 10% ASAF, respectively, and control rats served with diet containing 5%, and 10% ASAF respectively for 14 days. There were noticeable decrease in sperm parameters, reproductive hormone, glycogen, nitric oxide, total thiol, nonprotein thiol levels, and testicular 3ß- and 17ß-hydroxysteroid dehydrogenase activities and concomitant increase in cholesterol, reactive oxygen species, malondialdehyde levels, and arginase activity compared to the control. Nevertheless, ASAFs reversed all these parameters toward the control levels. Therefore, these findings suggest that ASAF pulp-supplemented diet might be an active approach in controlling male reproductive dysfunction induced by diabetes. PRACTICAL APPLICATIONS: The results suggest that ASAF pulp-supplemented diet might be an active approach in controlling male reproductive dysfunction induced by diabetes through alterations in the levels of blood glucose, glycogen, cholesterol, nitric oxide, reproductive hormones, activities of steroidogenic enzymes, arginase, and sperm characteristics as well as the antioxidant status in the testes and epididymis.

Physiological impacts of pollution exposure in seabird's progeny nesting in a Mediterranean contaminated area.

Aquatic wildlife is exposed through trophic transfer of hazardous substances to several threats inducing physiological impairments. We aimed at assessing the impact of contamination in one of the hot spots of pollution along Mediterranean coasts, the gulf of Gabes in Tunisia, on Common tern Sterna hirundo, a piscivorous top predator bird. Firstly, we compared the reproductive effort of breeding adults through clutch size distribution in three sites with different levels of pollution. Then, a battery of genotoxicity and oxidative stress biomarkers was carried out to assess physiological impairments in chicks. While defense mechanisms showed a depletion, lipid peroxidation and genotoxicity increased significantly according to pollution level. The multi-biomarker approach used here, discriminated chicks according to contamination degree of their nesting sites. Increases in genotoxicity and oxidative stress were correlated to a decrease in chick body mass known to lead to long-term impacts on juvenile survival and recruitment in birds.