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The present study has investigated the effects of Metro Vancouver's wastewater treatment plant (WWTP) effluents on English sole (Parophrys vetulus) hepatic gene expression using novel targeted gene expression assays to complement the 2017 Burrard Inlet Ambient Monitoring Program conducted by Metro Vancouver. Seven locations of varying distance to the WWTPs were included. Twelve genes involved in xenobiotic defense (CYP1A, HSP70), thyroid function (DIO1), lipid and glucose metabolism (FABP1, FASN, GLUT2, PPAR δ , PPAR γ), protein synthesis (18S rRNA, RPS4X), and reproduction (ER α , VTG) revealed several differences between these impacted sites. A key finding of the present study was that males exhibited VTG transcript levels either equivalent or exceeding female levels of this gene at all sites investigated, indicating widespread exposure of estrogenic contaminants throughout Burrard Inlet. Furthermore, the induction of hepatic CYP1A was observed due to possible downstream sites being subjected to a larger influx of certain planar halogenated and non-halogenated hydrocarbons from multiple industrial contributors. This study also revealed significant differences between the sites examined and in genes involved in transcriptional regulation and synthesis of proteins, lipids and glucose metabolism, and thyroid hormone metabolism. Collectively, this study demonstrates the potential of molecular biomarkers of urban contaminant exposure in wild caught English sole for use in diagnosing a broader range of adverse health effects when combined with conventional whole organism health indicators. [ABSTRACT FROM AUTHOR]

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent environmental contaminant, is an endocrine disrupter with a proven reproductive toxicity in mammals. However, its effects on male fertility across generations are still elusive. The current work evaluates the toxicity of dioxin on male reproductive system in two separate groups of BALB/C mice; a group of pubertal males directly exposed to TCDD (referred to as DEmG), and a group of indirectly exposed males (referred to as IDEmG) comprises of F1, F2 and F3 males born from TCDD-exposed pregnant females. Both groups were exposed to 25 μg TCDD/kg body weight for a week. Our data show that males of TCDD-DEmG exhibited significant alterations in the expression of certain genes involved in the detoxification of TCDD and the biosynthesis of testosterone. This was accompanied with testicular pathological symptoms, including a sloughing in the germinal epithelium and a congestion of blood vessels in interstitial tissue with the presence of multinuclear cells into seminiferous tubule, with a 4-fold decline in the level of serum testosterone and reduced sperm count. Otherwise, the male reproductive toxicity across F1, F2 and F3 generations from TCDD-IDEmG was mainly characterized by: i) a reduce in body and testis weight. ii) a decrease in gene expression of steriodogenesis enzyme, e.g., AhR, CYP1A1, CYP11A1, COX1, COX2, LOX5 and LOX12. iii) a remarked and similar testicular histopathology that found for DEmG, iv) a serious decline in serum testosterone. v) a decreased male-to-female ratio. vi) a low sperm count with increasing abnormalities. Thus, pubertal or maternal exposure to TCDD provokes multigenerational male reproductive toxicity in mice, ultimately affecting the spermatogenesis and suggesting that the hormonal alternation and sperm abnormality are the most marked effects of the indirect exposure of mammalian male to TCDD.

Summary: As 3,3′,5-triiodothyroacetic acid (TRIAC), a metabolite of thyroid hormones (THs), was previously detected in sewage effluent, we aimed to investigate exogenous TRIAC’s potential for endocrine disruption. We administered either TRIAC or 3,3′,5-triiodo-L-thyronine (LT3) to euthyroid mice and 6-propyl-2-thiouracil-induced hypothyroid mice. In hypothyroid mice, TRIAC administration suppressed the hypothalamus-pituitary-thyroid (HPT) axis and upregulated TH-responsive genes in the pituitary gland, the liver, and the heart. We observed that, unlike LT3, TRIAC administration did not upregulate cerebral TH-responsive genes. Measurement of TRIAC contents suggested that TRIAC was not efficiently trafficked into the cerebrum. By analyzing euthyroid mice, we found that cerebral TRIAC content did not increase despite TRIAC administration at higher concentrations, whereas serum levels and cerebral contents of THs were substantially decreased. Disruption by TRIAC is due to the additive effects of circulating endogenous THs being depleted via a negative feedback loop involving the HPT axis and heterogeneous distribution of TRIAC among different organs.

We studied features of age-related changes in the thymus of mature male Wistar rats developmentally exposed to the endocrine disruptor dichlorodiphenyltrichloroethane (DDT). The study was carried out at the stage of early thymus involution. Differences in the thymus morphology associated with imbalance of morphogenetic processes in the cortex and medulla were observed after puberty in rats developmentally exposed to DDT. Increased proliferation of thymocytes, higher content of lymphoblasts, and concomitant decrease in T-cell migration in comparison with the control were found. Our findings indicate lower functional maturity of the thymus and prolonged disorders in the program of postnatal thymus development induced by the endocrine disruptor DDT. [ABSTRACT FROM AUTHOR]

Last years researches focused on several natural and synthetic compounds that may interfere with the major functions of the endocrine system and were termed endocrine disrupters. Endocrine disrupters are defined as chemical substances with either agonist or antagonist endocrine effects in human and animals. These effects may be achieved by interferences with the biosynthesis or activity of several endogenous hormones. Recently, it was demonstrated that heavy metals such as cadmium (Cd), arsen (As), mercury (Hg), nickel (Ni), lead (Pb) and zinc (Zn) may exhibit endocrine-disrupting activity in animal experiments. Emerging evidence of the intimate mechanisms of action of these heavy metals is accumulating. It was revealed, for example, that the Zn atom from the Zn fingers of the estrogen receptor can be replaced by several heavy metal molecules such as copper, cobalt, Ni and Cd. By replacing the Zn atom with Ni or copper, binding of the estrogen receptor to the DNA hormone responsive elements in the cell nucleus is prevented. In both males and females, low-level exposure to Cd interferes with the biological effects of steroid hormones in reproductive organs. Arsen has the property to bind to the glucocorticoid receptor thus disturbing glucocorticoids biological effects. With regard to Hg, this may induce alterations in male and female fertility, may affect the function of the hypothalamo-pituitary-thyroid axis or the hypothalamo-pituitary-adrenal axis, and disrupt biosynthesis of steroid hormones.

The male reproductive system is especially affected by dioxins, a group of persistent environmental pollutants, resulting in irreversible abnormalities including effects on sexual function and fertility in adult males and possibly on the development of male offspring. The reproductive toxicity caused by dioxins is mostly mediated by an aryl hydrocarbon receptor (AhR). In animals, spermatogenesis is a highly sensitive and dynamic process that includes proliferation and maturation of germ cells. Spermatogenesis is subject to multiple endogenous and exogenous regulatory factors, including a wide range of environmental toxicants such as dioxins. This review discusses the toxicological effects of dioxins on spermatogenesis and their relevance to male infertility. After a detailed categorization of the environmental contaminants affecting the spermatogenesis, the exposure pathways and bioavailability of dioxins in animals was briefly reviewed. The effects of dioxins on spermatogenesis are then outlined in detail. The endocrine-disrupting effects of dioxins in animals and humans are discussed with a particular focus on their effects on the expression of spermatogenesis-related genes. Finally, the impacts of dioxins on the ratio of X and Y chromosomes, the status of serum sex hormones, the quality and fertility of sperm, and the transgenerational effects of dioxins on male reproduction are reviewed. [ABSTRACT FROM AUTHOR]

Emerging contaminants (ECs) are synthetic or naturally occurring chemicals or any microorganisms that are not commonly monitored in the environment but have the potential to enter the environment and cause known or suspected adverse ecological or human health effects. The issue of ECs persistent in the environment and can disrupt the physiology of target receptors, they are recognized as Contaminants of emerging environmental concerns. The prominent classes of ECs include pharmaceuticals and personal care products (PPCPs), plasticizers, surfactants, fire retardants, nanomaterials, and pesticides. Several ECs have been recognized as endocrine disruptive compounds (EDCs) due to their deleterious effects on endocrine systems (EDCs). The contaminants present in the aquatic environment resources are a major cause of concern for human health and the environment and safety concern. These contaminations have risen into a major threat to the water distribution system. The impact of emerging contaminants (ECs) such as medicines, x-ray media, endocrine disruptors, insecticides, and personal care items has been reported in surface water, wastewater, and groundwater sources worldwide in recent years. Various techniques have been explored for ECs degradation and removal to mitigate their harmful effect. Numerous prior or continuing investigations have focused on the degradation and removal of contaminants using a variety of treatment techniques, including (1) physical, (2) chemical, and (3) biological. However, experimental data is insufficient to provide precise predictions regarding the mechanistic degradation and removal fate of ECs across various in-practice systems. The membrane technology can remove particles as fine as 10 μm and colloidal particles, It can be effectively eliminated by up to 99% through the use of MBR and treatment technologies such as reverse osmosis, ultrafiltration, or nanofiltration at concentrations up to 5 g/liter. In this paper, the emerging contaminants overview, their sources, and their removal by application of various treatments based on recent studies have been presented.

The male reproductive system is especially affected by dioxins, a group of persistent environmental pollutants, resulting in irreversible abnormalities including effects on sexual function and fertility in adult males and possibly on the development of male offspring. The reproductive toxicity caused by dioxins is mostly mediated by an aryl hydrocarbon receptor (AhR). In animals, spermatogenesis is a highly sensitive and dynamic process that includes proliferation and maturation of germ cells. Spermatogenesis is subject to multiple endogenous and exogenous regulatory factors, including a wide range of environmental toxicants such as dioxins. This review discusses the toxicological effects of dioxins on spermatogenesis and their relevance to male infertility. After a detailed categorization of the environmental contaminants affecting the spermatogenesis, the exposure pathways and bioavailability of dioxins in animals was briefly reviewed. The effects of dioxins on spermatogenesis are then outlined in detail. The endocrine-disrupting effects of dioxins in animals and humans are discussed with a particular focus on their effects on the expression of spermatogenesis-related genes. Finally, the impacts of dioxins on the ratio of X and Y chromosomes, the status of serum sex hormones, the quality and fertility of sperm, and the transgenerational effects of dioxins on male reproduction are reviewed.

The present study has investigated the effects of Metro Vancouver’s wastewater treatment plant (WWTP) effluents on English sole (Parophrys vetulus) hepatic gene expression using novel targeted gene expression assays to complement the 2017 Burrard Inlet Ambient Monitoring Program conducted by Metro Vancouver. Seven locations of varying distance to the WWTPs were included. Twelve genes involved in xenobiotic defense (CYP1A, HSP70), thyroid function (DIO1), lipid and glucose metabolism (FABP1, FASN, GLUT2, PPARδ, PPARγ), protein synthesis (18S rRNA, RPS4X), and reproduction (ERα, VTG) revealed several differences between these impacted sites. A key finding of the present study was that males exhibited VTG transcript levels either equivalent or exceeding female levels of this gene at all sites investigated, indicating widespread exposure of estrogenic contaminants throughout Burrard Inlet. Furthermore, the induction of hepatic CYP1A was observed due to possible downstream sites being subjected to a larger influx of certain planar halogenated and non-halogenated hydrocarbons from multiple industrial contributors. This study also revealed significant differences between the sites examined and in genes involved in transcriptional regulation and synthesis of proteins, lipids and glucose metabolism, and thyroid hormone metabolism. Collectively, this study demonstrates the potential of molecular biomarkers of urban contaminant exposure in wild caught English sole for use in diagnosing a broader range of adverse health effects when combined with conventional whole organism health indicators.

Background: Exposure of children and adolescents to endocrine disrupting chemicals (EDCs) causes the development of non-communicable diseases. Triclosan (TCS) is a fat-soluble antimicrobial agent, and methyl-triclosan (MTCS) is the predominant metabolite of TCS. The increasing use of consumables TCS (toothpaste, mouthwash, personal care products) in human has raised concerns about human health. Methods: The urinary concentrations of TCS and MTCS were measured by GC/MS. Lipid profiles (TG, TC, LDL, and HDL), anthropometric parameters (WC, BMI z-score, and BMI), FBS, SBP, and DBP tests were performed on 79 children and adolescents. Results: Of 79 people included as the study population, 42 subjects (53.16%) were males. Most of the study population as 32 subjects (40.50%) were obese. The mean concentrations of TCS and MTCS in the obese population were 5.47 ± 2.99 and 2.32 ± 1.04 μg/L, respectively. After adjusting for possible confounding factors, the results showed that a one-unit increase in DBP caused a 0.03 units increase in TCS levels in male subjects (P = 0.01). A one-unit increase in DBP also caused a 0.02 units increase in MTCS (P = 0.001). There was a significant relationship between TCS and HDL (OR = 0.90, P = 0.005), LDL (OR = 1.13, P = 0.01), and TG (OR =1.05, P < 0.0001). There was also a significant relationship between MTCS and HDL (OR = 0.88, P = 0.001), LDL (OR = 1.03, P = 0.009), and TG (OR = 1.04, P < 0.0001). Conclusion: According to the results, there is a relationship between TCS, MTCS, and predictive indicators of cardiovascular diseases and obesity.

Paracetamol is suggested to have endocrine disrupting properties possibly affecting fetal programming of reproductive health that might lead to impaired semen quality and changes in reproductive hormones. In this longitudinal study, we included 1058 young adult men born 1998–2000 into the Danish National Birth Cohort with follow-up at 18–21 years of age. The exposure, maternal intake of paracetamol, was modelled in three ways: dichotomized, trimester-specific, and as duration of exposure categorized into: short (1–2 weeks), medium (3–9 weeks) or long duration (>9 weeks) vs. no intake. Outcomes included semen characteristics, self-measured testis volume, and reproductive hormone levels. We used negative binominal regression to estimate the percentage difference and 95% confidence interval (CI) for each outcome. In total, 547 (48%) sons were prenatally exposed to paracetamol due to maternal intake at least once. Maternal intake of paracetamol during pregnancy was not associated with any of the biomarkers in the dichotomized or trimester-specific exposure models. For duration of exposure, sons of mothers with long duration of maternal intake of paracetamol showed tendencies towards lower semen concentration (-14% [95% CI: -31%; 8%]), a higher proportion of nonprogressive and immotile spermatozoa (8% [95% CI: -4%; 21%]) and higher DNA Fragmentation Index (16% [95% CI: -1%; 36%]) compared to son of mothers with no intake. Maternal intake of paracetamol during pregnancy was not clearly associated with biomarkers of male fecundity in adult sons. However, it cannot be ruled out that long duration of maternal intake of paracetamol might be associated with impaired semen characteristics. • Paracetamol in utero might affect reproductive health through endocrine disruption. • This large cohort study found no clear effect on biomarkers of fecundity in sons. • It cannot be excluded that prolonged intake might impair semen quality. [ABSTRACT FROM AUTHOR]

Endocrine disruptors (EDs) are chemical substances that interfere with the endocrine system, adversely affecting human health and environment. Legislation with aim to eliminate and ban EDs have been introduced in EU, but the identification of EDs remains challenging and crucial step towards regulation and risk management. A guidance for ED assessment has been recently established for pesticides and biocides in the EU, which heavily relies on traditional toxicological testing in vivo. Most notably lacking mechanistic methods for some ED modalities and not covering many other modalities that might be affected by EDs. In this project, we focus on the ED assessment according to the valid legislation and explore the possibility to employ alternative methods to bolster the mechanistic understanding of the ED effects and eventually decrease the need for in vivo testing. We selected a well‐studied industrial chemical perfluorooctanesulfonic acid (PFOS) to be a model compound in a case study for ED assessment where the EU criteria were applied in the frame of human health risk assessment with focus on thyroid disruption and developmental neurotoxicity. A systematic literature review has been conducted for these effects (Scopus, Pubmed, Embase), and relevant studies were selected by title/abstract screening (RAYYAN) and full‐text examination. Selected studies were assessed for reliability (SciRAP), and all relevant data were extracted into a database and assessed by Weight of Evidence (WoE) approach. The initial analysis showed potential endocrine adverse effects and endocrine activity, meeting the ED criteria. The use of mechanistic and alternative methods enhanced the outcomes of WoE assessment. Also, the study provides a great hands‐on experience with the most up‐to‐date development in the area of risk assessment and EDs. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA), an endocrine-disrupting chemical (EDC), has strong potential for daily exposure to humans and animals due to its persistence and widespread in the environment, so its effects directly concern public health. Although invertebrates represent important components of aquatic ecosystems and are at significant risk of exposure, there is little information about the biological effects of EDCs in these organisms. Astacus leptodactylus used in this study is one of the most consumed and exported freshwater species in Europe. In this study, the 96-h effect of BPA on A. leptodactylus was examined using various biomarkers. The LC50 value of BPA was determined as 96.45 mg L−1. After 96 h of exposure to BPA, there were increases in superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) activities and levels of malondialdehyde (MDA), and total oxidant status context (TOSC), and there were decreases in the activity of glutathione reductase (GR), carboxylesterase (CaE), acetylcholinesterase (AChE), Na+/K+ ATPase, Mg2+ ATPase, Ca2+ ATPase, and total ATPase and the total antioxidant context (TAC). From the results of this study, it can be concluded that BPA has significant toxic effects on A. leptodactylus based on the selected biochemical parameters of antioxidant, cholinergic, detoxification, and metabolic systems in crayfish even at low doses. Thus, it can be said that BPA can seriously threaten the aquatic ecosystem and public health. [ABSTRACT FROM AUTHOR]

Abstract Endocrine disruptors (EDs) are chemical substances that interfere with the endocrine system, adversely affecting human health and environment. Legislation with aim to eliminate and ban EDs have been introduced in EU, but the identification of EDs remains challenging and crucial step towards regulation and risk management. A guidance for ED assessment has been recently established for pesticides and biocides in the EU, which heavily relies on traditional toxicological testing in vivo. Most notably lacking mechanistic methods for some ED modalities and not covering many other modalities that might be affected by EDs. In this project, we focus on the ED assessment according to the valid legislation and explore the possibility to employ alternative methods to bolster the mechanistic understanding of the ED effects and eventually decrease the need for in vivo testing. We selected a well‐studied industrial chemical perfluorooctanesulfonic acid (PFOS) to be a model compound in a case study for ED assessment where the EU criteria were applied in the frame of human health risk assessment with focus on thyroid disruption and developmental neurotoxicity. A systematic literature review has been conducted for these effects (Scopus, Pubmed, Embase), and relevant studies were selected by title/abstract screening (RAYYAN) and full‐text examination. Selected studies were assessed for reliability (SciRAP), and all relevant data were extracted into a database and assessed by Weight of Evidence (WoE) approach. The initial analysis showed potential endocrine adverse effects and endocrine activity, meeting the ED criteria. The use of mechanistic and alternative methods enhanced the outcomes of WoE assessment. Also, the study provides a great hands‐on experience with the most up‐to‐date development in the area of risk assessment and EDs.

Objective:We aimed to investigate a possible role of the endocrine disruptors phthalates, di-2-ethylhexyl phthalate (DEHP) and mono (2-ethylhexyl) phthalate (MEHP), in polycystic ovary syndrome (PCOS) aetiopathogenesis. We also wished to evaluate the relationship between phthalates and metabolic disturbances in adolescents with PCOS.Methods:A total of 124 adolescents were included. Serum MEHP and DEHP levels were determined by high-performance liquid chromatography. Insulin resistance was evaluated using homeostasis model assessment-insulin resistance, quantitative Insulin Sensitivity Check Index, fasting glucose/insulin ratio, Matsuda index, and total insulin levels during oral glucose tolerance test. Participants were further subdivided into lean and obese subgroups according to body mass index (BMI).Results:Sixty-three PCOS and 61 controls, (mean age 15.2±1.5; range: 13-19 years) were enrolled. Serum DEHP and MEHP concentrations were not significantly different between PCOS and control groups. The mean (95% confidence interval) values of DEHP and MEHP were 2.62 (2.50-2.75) μg/mL vs 2.71 (2.52-2.90) μg/mL and 0.23 (0.19-0.29) μg/mL vs 0.36 (0.18-0.54) μg/mL in PCOS and the control groups respectively, p>0.05. Correlation analysis, adjusted for BMI, showed that both phthalates significantly correlated with insulin resistance indices and serum triglycerides in adolescents with PCOS.Conclusion:Serum DEHP and MEHP concentrations were not different between adolescents with or without PCOS. However, these phthalates are associated with metabolic disturbances such as dyslipidemia and insulin resistance, independently of obesity, in girls with PCOS.

Endocrine disrupting chemicals (EDCs) can impair hippocampus-dependent behaviors in rat offspring and in children. In search for key processes underlying this effect, we compared the transcriptomes of rat hippocampus on postnatal day 6 after gestational and lactational exposure to three different EDCs at doses known to impair development of learning and memory. Aroclor 1254, a commercial PCB mixture (5 mg/kg or 0.5 mg/kg), or bisphenol A (5 mg/kg or 0.5 mg/kg) were administered in chow, chlorpyrifos (3 mg/kg or 1 mg/kg) was injected subcutaneously. Male hippocampus exhibited a common effect of all three chemicals on genes involved in cell-autonomous processes, Sox6, Sox11, Pou2f2/Oct2, and Pou3f2/Brn2, all upregulated at the high dose. Additional genes of the Sox and Pou families were affected by only one or two of the chemicals. Real time RT PCR showed a comparable expression change for bisphenol A also at the lower dose. Female hippocampus exhibited much fewer genes with expression changes (almost none with false discovery rate <0.05), and none of the genes of the Sox and Pou families was affected. Since gene network analyses in male hippocampus suggested a link between Sox6 and miR-24, known to be repressed by activation of ER-alpha and to repress Sox6 in other tissues, this microRNA was measured. miR-24 was downregulated by all chemicals at the high dose in males. Values of Sox6 mRNA and miR-24 were inversely correlated in individual male hippocampus samples, supporting the hypothesis that the change in Sox6 expression resulted from an action of miR-24. In contrast, miR-24 levels remained unchanged in hippocampus of females. A sexually dimorphic response of miR-24 may thus be at the basis of the sex difference in Sox6 expression changes following exposure to the three chemicals. ER-alpha expression was also sex-dependent, but the expression changes did not parallel those of potential downstream genes such as Sox6. Sox6 is known to suppress differentiation of Parvalbumin (Pvalb)-expressing interneurons. Individual Sox6 levels (FPKM) were inversely correlated with levels of Pvalb, but not with markers of Sox6-independent interneuron subpopulations, Nos1 and 5HT3aR. Effects on interneuron development are further suggested, in males, by expression changes of Nrg1 and its receptor Erbb4, controlling interneuron migration. Our study disclosed new types of EDC-responsive morphogenetic genes, and illustrated the potential relevance of microRNAs in sexually dimorphic EDC actions. [ABSTRACT FROM AUTHOR]

Endocrine disrupting chemicals (EDCs) can impair hippocampus-dependent behaviors in rat offspring and in children. In search for key processes underlying this effect, we compared the transcriptomes of rat hippocampus on postnatal day 6 after gestational and lactational exposure to three different EDCs at doses known to impair development of learning and memory. Aroclor 1254, a commercial PCB mixture (5 mg/kg or 0.5 mg/kg), or bisphenol A (5 mg/kg or 0.5 mg/kg) were administered in chow, chlorpyrifos (3 mg/kg or 1 mg/kg) was injected subcutaneously. Male hippocampus exhibited a common effect of all three chemicals on genes involved in cell-autonomous processes, Sox6, Sox11, Pou2f2/Oct2, and Pou3f2/Brn2, all upregulated at the high dose. Additional genes of the Sox and Pou families were affected by only one or two of the chemicals. Real time RT PCR showed a comparable expression change for bisphenol A also at the lower dose. Female hippocampus exhibited much fewer genes with expression changes (almost none with false discovery rate

Alkylphenol polyethoxylates (APEOn) are the second-largest category of commercial nonionic surfactants, which are difficult to degrade naturally in the environment. This study examined the degradation of octylphenol polyethoxylate (OPEOn) by laccase and its laccase-mediated systems. The results showed that OPEOn was poorly degraded by laccase alone. 2, 2′-azino-bis [3-ethylbenzothiazoline-6-sulphonic acid] (ABTS), 1-hydroxybenzotriazole (HBT), and 2, 2, 6, 6-tetramethylpiperidine-1-oxyl (TEMPO) were selected as the redox mediators. Experimental results also indicated that 52.4% of the initial OPEOn amount was degraded by laccase in the presence of TEMPO. The degradation efficiency was analyzed using high-performance liquid chromatography. Furthermore, the structural characteristics of the degradation products were measured using matrix-assisted laser desorption/ionization-time of flight mass spectrometry and nuclear magnetic resonance spectroscopy, and it could be found that the laccase-TEMPO system could gradually shorten the ethoxylate chain by oxidizing the primary hydroxyl group of OPEOn, thereby degrading the OPEOn of the macromolecule into small molecules. The maximum of the ion peak distributions of OPEOn decreased from n = 8 finally down to 3. The novel enzymatic system introduced by this study will become a promising alternative method for high-efficiency APEOn conversion and had great potential value in wastewater treatment. [ABSTRACT FROM AUTHOR]

• Neurodevelopmental disorders are highly prevalent. • Reducing exposure to environmental factors can reduce their prevalence. • Comprehensive review: endocrine disruptors and pesticides in neurodevelopmental disorders. • Pesticides and endocrine disruptors are associated with neurodevelopmental disorders. • Preventive actions are urgently needed. In recent years, environmental epidemiology and toxicology have seen a growing interest in the environmental factors that contribute to the increased prevalence of neurodevelopmental disorders, with the purpose of establishing appropriate prevention strategies. A literature review was performed, and 192 articles covering the topic of endocrine disruptors and neurodevelopmental disorders were found, focusing on polychlorinated biphenyls, polybrominated diphenyl ethers, bisphenol A, and pesticides. This study contributes to analyzing their effect on the molecular mechanism in maternal and infant thyroid function, essential for infant neurodevelopment, and whose alteration has been associated with various neurodevelopmental disorders. The results provide scientific evidence of the association that exists between the environmental neurotoxins and various neurodevelopmental disorders. In addition, other possible molecular mechanisms by which pesticides and endocrine disruptors may be associated with neurodevelopmental disorders are being discussed. [ABSTRACT FROM AUTHOR]

Purpose: Bisphenol-A (BPA) is an endocrine-disrupting chemical that may affect the hormones and their receptors. The aim of this study is to determine whether BPA has an effect on the development of nonfunctional adrenal incidentaloma (NFAI). Methods: Fifty patients who were admitted to endocrinology outpatient clinics and diagnosed as NFAI were included in the study. Fifty healthy people without adrenal mass and adrenal pathology in the upper abdominal computerized tomography or magnetic resonance imaging were also included as control group. Age, gender and body mass index of the study groups were similar. The serum samples for BPA were stored at −80 °C in refrigerator until working in the lab. Serum BPA levels were measured using ELISA technique. Results: Mean serum BPA level was 7.06 ± 3.96 ng/ml in NFAI patients and 4.79 ± 3.01 ng/ml in control group. Serum BPA level was significantly higher in NFAI group than control group (p = 0.001). Serum BPA levels were also found to be significantly higher in women with NFAI than in men with NFAI (p = 0.019). Conclusions: The mechanisms of NFAI development have not been clarified yet. Increased BPA exposure with developed industrialization may play a role in NFAI formation. For the reduction of BPA exposure, the use of plastic prepacked products, plastic containers, and safety measures are essential for public health. [ABSTRACT FROM AUTHOR]

The aim of the research was to study formation of thymic lymphocytes proliferative response to T cell mitogen Concanavalin A in 7, 42, and 70 days-old male Wistar rats developmentally exposed to low doses of endocrine disruptor dichlorodiphenyltrichloroethane (2.90 ± 0.13 μg/kg body weight). The thymus of the exposed rats did not show morphological abnormalities. Exposure to the endocrine disrupter was found to alter age-dependent changes of thymic lymphocyte proliferative activity and attenuate proliferative response to Concanavalin A in puberty and adulthood. Insufficient response to mitogen was mediated by higher content of actively proliferating Ki-67-positive lymphoblasts compared to the control values. Insufficient proliferative response to mitogen in developmentally exposed to the endocrine disruptor rats may provide higher risk of impaired cellular immune reactions.

Objective: We aimed to investigate a possible role of the endocrine disruptors phthalates, di-2-ethylhexyl phthalate (DEHP) and mono (2-ethylhexyl) phthalate (MEHP), in polycystic ovary syndrome (PCOS) aetiopathogenesis. We also wished to evaluate the relationship between phthalates and metabolic disturbances in adolescents with PCOS. Methods: A total of 124 adolescents were included. Serum MEHP and DEHP levels were determined by high-performance liquid chromatography. Insulin resistance was evaluated using homeostasis model assessment-insulin resistance, quantitative Insulin Sensitivity Check Index, fasting glucose/insulin ratio, Matsuda index, and total insulin levels during oral glucose tolerance test. Participants were further subdivided into lean and obese subgroups according to body mass index (BMI). Results: Sixty-three PCOS and 61 controls, (mean age 15.2±1.5; range: 13-19 years) were enrolled. Serum DEHP and MEHP concentrations were not significantly different between PCOS and control groups. The mean (95% confidence interval) values of DEHP and MEHP were 2.62 (2.50-2.75) μg/mL vs 2.71 (2.52-2.90) μg/mL and 0.23 (0.19-0.29) μg/mL vs 0.36 (0.18-0.54) μg/mL in PCOS and the control groups respectively, p>0.05. Correlation analysis, adjusted for BMI, showed that both phthalates significantly correlated with insulin resistance indices and serum triglycerides in adolescents with PCOS. Conclusion: Serum DEHP and MEHP concentrations were not different between adolescents with or without PCOS. However, these phthalates are associated with metabolic disturbances such as dyslipidemia and insulin resistance, independently of obesity, in girls with PCOS. [ABSTRACT FROM AUTHOR]

The study is aimed at elucidation of ultrastructural mechanisms underlying impaired aldosterone synthesis by glomerulosa cells in Wistar rats exposed to low doses of endocrine disrupter DDT during prenatal and postnatal development. Analysis of rat zona glomerulosa histology and function during the pubertal and postpubertal periods showed that exposure to endocrine disrupter DDT disturbs its development and reduced the production of aldosterone. Electron microscopy showed that changes in the aldosterone synthesis are related to impaired reorganization of the mitochondrial apparatus, one of the leading factors in the regulation of steroidogenesis, in glomerulosa cells in DDT-exposed rats during puberty. [ABSTRACT FROM AUTHOR]

Endocrine disrupting compounds (EDCs) are commonly detected in aquatic environments and can endanger aquatic life. The responses of enzymatic biomarkers in asexual freshwater planarians (lactate dehydrogenase, glutathione S-transferase, glucose-6-phosphate dehydrogenase, and isocitric dehydrogenase) were evaluated after 7-day exposure to endocrine disruptors (bisphenol A [BPA], diethylstil-bestrol [DES], 17a-ethinylestradiol [EE2], and 17(3-estradiol [E2]). These biomarkers are ubiquitous enzymes and play crucial physiological roles in living organisms. In this study, EDCs influenced the non-specific enzyme activities of asexual planarians. However, the effects of EDCs on enzymatic biomarkers did not correspond with the order of their estrogenic potencies. Furthermore, exposure to EDCs for 7 days mostly slightly or significantly reduced the enzyme activities of planarians compared with those of their respective controls. Alterations in enzyme activities can affect the energy metabolism and health status of organisms. The environmental levels of E2, EE2, and DES can range from lower than their detectable limits to tens of ng L-1, and BPA levels in river water can be several μg L-1. These findings suggest that some aquatic animals might be affected by the current levels of BPA in hotspot pollution scenarios. [ABSTRACT FROM AUTHOR]

One of the most important environmental problems in the world is micro-pollutants. The aim of this study was to investigate the antioxidant responses of Gammarus pulex to Bisphenol A (BPA), an endocrine-disrupting agent. For this purpose, sublethal concentrations of BPA were applied to G. pulex and biochemical responses were studied. Enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) activities and nonenzymatic antioxidants glutathione (GSH) and thiobarbituric acid reagents (TBARS) levels in G. pulex were determined in four different groups during 24 and 96 h. Biochemical biomarkers were measured using commercial kits in a microplate reader. When we compared with control, SOD enzyme activity increased in all groups during both administration periods and CAT enzyme activity decreased in all groups. GSH and TBARS levels were increased after 24 and 96 h of application periods in all groups when compared with control. For changes in SOD and CAT activities and GSH, TBARS levels have been determined to be useful as biomarkers against BPA in G. pulex tissues. It has also been proven that G. pulex is an effective bioindicator that shows BPA pollution in water. The different results of biochemical biomarkers can be evaluated as a marker of possible metabolic processes, and the biochemical response of G. pulex can reveal to some extent the environmental consequences of BPA pollution resulting from industrial waters. [ABSTRACT FROM AUTHOR]

The common steroid hormones are estrone (E1), 17β-estradiol (E2), estriol (E3), 17α-ethinylestradiol (EE2), and testosterone (T). These steroids are reported to contaminate the environment through wastewater treatment plants. Steroid estrogens are widespread in the aquatic environment and therefore pose a potential risk, as exposure to these compounds has adverse impacts on vertebrates. Excessive exposure to steroid estrogens causes endocrine disruption in aquatic vertebrates, which affects the normal sexual life of these animals. Steroid pollutants also cause several health problems in humans and other animals. Microbial degradation is an efficient method for removing hormone pollutants from the environment by remediation. Over the last two decades, microbial metabolism of steroids has gained considerable attention due to its higher efficiency to reduce pollutants from the environment. The present review is focused on the major causes of steroid pollution, concentrations of these pollutants in surface water, groundwater, drinking water, and wastewater, their effect on humans and aquatic animals, as well as recent efforts by various research groups that seek better ways to degrade steroids by aerobic and anaerobic microbial systems. Detailed overview of aerobic and anaerobic microbial biotransformation of steroid estrogens and testosterone present in the environment along with the active enzyme systems involved in these biotransformation reactions is described in the review article, which helps readers to understand the biotransformation mechanism of steroids in depth. Other measures such as co-metabolic degradation, consortia degradation, algal, and fungal steroid biotransformation are also discussed in detail. [ABSTRACT FROM AUTHOR]

Nonylphenol, an endocrine disrupter, is widely released to the aquatic environment, which is accumulative and extremely toxic to aquatic organisms. Here, we report a simple and cost-effective large-scale green synthesis of water-soluble highly fluorescent carbon quantum dots (CQDs) from marine biowaste (offshore washed algae) which gets quenched strongly in the presence of nonylphenol. These CQDs were around 20–40 nm in size and exhibit fluorescence constantly at 360 nm. The XRD profile depicted the interlayer spacing in the particle as 0.284 nm with a humped peak around 14 degrees showing the amorphous nature of the CQDs. FTIR spectra showed the stretching vibration of the hydroxyl groups (OH), asymmetric and symmetric stretching vibrations of the carboxylate anions (COO–). The fluorescence quantum yield of the CQDs is up to 68% and nonyl phenol detection limit is less than 0.1 µM. Furthermore, the CQDs were found to be stable at a wide pH range which makes it a suitable nonylphenol sensor for a variety of environmental samples. We functionalized these CQDs on an agarose gel matrix to develop a convenient sensor for the rapid detection of nonylphenol. [ABSTRACT FROM AUTHOR]

Exposure to environmental pollutants may lead to early kidney injury, chronic kidney disease (CKD) and end-stage renal disease (ESRD). This study investigated the early renal effects associated with exposure to endocrine-disrupting chemicals (EDCs) and heavy metals using general Korean population data. We used data from the Second Korean National Environmental Health Survey (2012–2014). As exposure markers, the concentrations of EDCs, such as triclosan (TCS), bisphenol A (BPA) and phthalate metabolites (DEHP, MnBP and MBzP), and heavy metals, such as cadmium, lead and mercury were analyzed. As an early kidney injury marker, the urinary concentration of β 2 -microglobulin (β 2 M) was measured. Multiple linear regression was used to analyze the relationship between environmental pollutants and β 2 M. A total of 5489 people (male: 2538, female: 2951) aged 19 years and older were enrolled. The geometric mean (GM) concentration of β 2 M in the total population was 1.88 μg/g creatinine (95% confidence interval (CI) 1.85–1.91). The β 2 M concentrations were significantly higher in cases of female, old age, low income, and presence of a history of diabetes mellitus or hypertension. The GM concentrations of urinary TCS and cadmium were 1.16 μg/g creatinine (95% CI 1.11–1.21) and 0.57 μg/g creatinine (95% CI 0.57–0.59), respectively. TCS, DEHP, cadmium, lead, and mercury exposure was significantly positively related to urinary β 2 M in the multiple regression analysis. β 2 M levels increased significantly with increases in the cadmium, mercury, and lead levels (p for trend <0.0001). The higher the DEHP, MnBP, and TCS concentrations, the higher the β 2 M level (p for trend <0.01). Environmental pollutants exposure significantly increased urinary β 2 M levels in the general Korean population. To prevent the development of early kidney injury and CKD, it is important to reduce environmental pollutants exposure through regulatory measures, and cooperation between related bodies in both developing and developed countries. Unlabelled Image • Endocrone disrupting chemicals and heavy metals were related to increases in the levels of urinary β2-microglobulin • Particularly, triclosan, phthalate, lead, mercury, cadmium show dose response relationship to early renal damage. [ABSTRACT FROM AUTHOR]

The effects of endocrine disrupters of transcriptional control of morphogenesis are poorly studied. Changes in the expression of transcriptional factor PRH and proliferation of adrenal cortical cells were analyzed in pubertal and postpubertal rats exposed prenatally and postnatally to low doses of endocrine disrupter DDT. In rats exposed to DDT, the expression of PRH and proliferation of adrenal cortical cells differed from those in control rats. Association between these parameters was weakened in the zona glomerulosa and zona reticularis and was absent in the zona fasciculata. These findings suggest that exposure to DDT in pre- and postnatal periods impairs the regulation of proliferative processes by transcriptional factor PRH in all zones of rat adrenal cortex, which can be a mechanism of the disruptive action of DDT. [ABSTRACT FROM AUTHOR]

Laccase extract (LE) from Pycnoporus sanguineus was immobilized on calcium and copper alginate–chitosan beads and applied for the removal of 17α-ethinylestradiol (EE2). Effects of immobilization conditions such as: sodium alginate (SA) concentration; LE/SA ratio and chitosan/ion (Ca+2 or Cu+2) ratio on the immobilization yield were investigated. Immobilized LE on Ca-beads and Cu-beads was then used to degrade an EE2 solution. The optimal conditions for LE immobilization on Ca-beads were: 1.5% (w/v) SA, 1:5 (v/v) LE/SA and 3:7 (v/v) chitosan/ion (Ca+2). The optimal conditions for immobilization on Cu-beads were 2.0% (w/v) SA, 0.5:5 (v/v) LE/SA and 3:7 (v/v) chitosan/ion (Cu+2). The best result was obtained for immobilized LE on Ca-beads in buffer-absent medium. Furthermore, the immobilized enzyme was reused in five cycles for EE2 removal. The formation of EE2 dimers by LE treatment has been demonstrated by electrospray ionization coupled to time of flight mass spectrometer (ESI–TOF–MS). The results evidenced that immobilized LE in alginate–chitosan–divalent cation bead is an effective alternative for EE2 removal. [ABSTRACT FROM AUTHOR]

Seasonal variations of bisphenol A (BPA) were investigated in the Danube along the Novi Sad bank, Serbia using solid-phase extraction followed by gas chromatographic mass spectrometric method. The obtained results confirmed the presence of BPA above the limit of quantification (6 ng/L) in 22 out of 32 water samples at all eight sampling sites. Тhe BPA concentration varied from 1) for autumn, spring and summer. The high potential risk which is attributed to the elevated summer concentrations is probably the result of the increased human activates and weather conditions. [Projekat Ministarstva nauke Republike Srbije, br. III46009]

Phthalates are ubiquitous environmental endocrine-disrupting chemicals suspected to interfere with developmental androgen action leading to adverse effects on male reproductive function. Prenatal exposure studies in rodents show cryptorchidism, hypospadias and reduced testicular volume (TV), testosterone and anogenital distance in males. It is postulated that there is a developmental window in utero when phthalate exposure has the most potent adverse effects. Some human studies show associations between prenatal phthalate exposure and reduced calculated “free” serum testosterone in infant boys and shorter anogenital distance. However, there are no data available yet which link antenatal exposure to long-term effects in men. We aimed to correlate antenatal phthalate exposure with adult TV, semen parameters and serum reproductive hormone concentrations. 913 men from the Western Australian (Raine) Pregnancy Cohort were contacted aged 20–22 years. 423 (56%) agreed to participate; 404 underwent testicular ultrasound examination; 365 provided semen samples, and reproductive hormones were measured in 384. Maternal antenatal serum phthalate metabolite measurements were available for 185 and 111 men, who provided serum and semen, respectively. Maternal serum collected at 18 and 34 weeks gestation, stored at −80°C, was pooled and analyzed for 32 phthalate metabolites by liquid chromatography-tandem mass spectrometry. TV was calculated, semen analysis performed by WHO approved methods, and serum concentrations of gonadotrophins, inhibin B, and testosterone measured. Eleven phthalate metabolites were detected. Primary and secondary metabolites of di-(2-ethyl-hexyl) phthalate (DEHP) and di-iso-nonyl phthalate (DiNP) were positively correlated. After correction for adult height, BMI, presence of a varicocele and exposure to maternal smoking mono-iso-nonyl phthalate (MiNP) (r = −0.22) and sums of DEHP and DiNP metabolites (r = −0.24) and the sum of the metabolites of the high molecular weight phthalates (r = −0.21) were negatively correlated with TV (all p

The polished silver solid amalgam electrode (p-AgSAE) combined with square wave voltammetry (SWV) was used in the development of an analytical procedure to Methomyl determination in natural water samples. The experimental and voltammetric parameters were optimized and the use of cationic surfactant cetyltrimethyl ammonium bromide promoted a considerable change in the kinetic and mechanism of the Methomyl reaction. Was observed the presence one-single reduction peak, related to a totally irreversible two-electrons transfer, followed by chemical reaction involving two protons. Analytical parameters (linearity range, analytical curve equations, correlation coefficient, detection and quantification limits, recovery efficiency, and relative standard deviation for intraday and interday experiments) were evaluated indicating that the proposed voltammetric procedure is suitable for determination of Methomyl. The application of the proposed procedure in natural water analysis indicated high robustness with only simple filtration, without pre-concentration steps, good stability and suitable sensitivity to determination of Methomyl in natural water samples. [ABSTRACT FROM AUTHOR]

Phthalates are ubiquitous environmental endocrine-disrupting chemicals suspected to interfere with developmental androgen action leading to adverse effects on male reproductive function. Prenatal exposure studies in rodents show cryptorchidism, hypospadias and reduced testicular volume (TV), testosterone and anogenital distance in males. It is postulated that there is a developmental window in utero when phthalate exposure has the most potent adverse effects. Some human studies show associations between prenatal phthalate exposure and reduced calculated "free" serum testosterone in infant boys and shorter anogenital distance. However, there are no data available yet which link antenatal exposure to long-term effects in men. We aimed to correlate antenatal phthalate exposure with adult TV, semen parameters and serum reproductive hormone concentrations. 913 men from the Western Australian (Raine) Pregnancy Cohort were contacted aged 20-22 years. 423 (56%) agreed to participate; 404 underwent testicular ultrasound examination; 365 provided semen samples, and reproductive hormones were measured in 384. Maternal antenatal serum phthalate metabolite measurements were available for 185 and 111 men, who provided serum and semen, respectively. Maternal serum collected at 18 and 34 weeks gestation, stored at -80°C, was pooled and analyzed for 32 phthalate metabolites by liquid chromatography-tandem mass spectrometry. TV was calculated, semen analysis performed by WHO approved methods, and serum concentrations of gonadotrophins, inhibin B, and testosterone measured. Eleven phthalate metabolites were detected. Primary and secondary metabolites of di-(2-ethyl-hexyl) phthalate (DEHP) and di-iso-nonyl phthalate (DiNP) were positively correlated. After correction for adult height, BMI, presence of a varicocele and exposure to maternal smoking mono-iso-nonyl phthalate (MiNP) (r = -0.22) and sums of DEHP and DiNP metabolites (r = -0.24) and the sum of the metabolites of the high molecular weight phthalates (r = -0.21) were negatively correlated with TV (all p < 0.05). After adjustment for BMI adult serum total testosterone was positively associated with exposure to the following antenatal serum phthalate metabolites: mono-(2-ethylhexyl) phthalate (r = 0.26), MiNP (r = 0.18), the sum of metabolites for DEHP (r = 0.21) and DiNP (r = 0.18), and the sum of high molecular phthalates (r = 0.20) (p = 0.0005 to p = 0.02). Given sample size, storage duration and confounding through postnatal exposures, further studies are required. [ABSTRACT FROM AUTHOR]

Bisphenol A (BPA) is a ubiquitous chemical suspected to possess oestrogenic hormonal activities. Male population studies suggest a negative impact on testicular function. As Sertoli cell proliferation occurs during fetal or early postnatal life, it is speculated that oestrogenic environmental exposures may influence mature testicular function. Among 705 Western Australian Pregnancy Cohort (Raine) Study men aged 20–22 years, 404 underwent testicular ultrasound examination (149 had maternal serum available), and/or 365 provided semen (136 had maternal serum) and/or 609 serum samples for sex steroids, gonadotrophins and inhibin B analysis (244 had maternal serum). Maternal serum collected at 18 and 34 weeks' gestation was pooled and assayed for concentrations of total BPA (free plus conjugated) as an estimate of antenatal exposure. Testicular volume was calculated by ultrasonography, and semen analysis performed. Serum LH, FSH and inhibin B were measured by immunoassay; testosterone, oestradiol, oestrone andBPA were measured by liquid chromatography-mass spectrometry. BPA levels were detectable in most (89%) maternal serum samples. After adjustment for maternal smoking, abstinence and varicocele, sperm concentration and motility were significantly correlated to maternal serum BPA ( r = 0.18; P = 0.04 for both). No other associations of maternal serum BPA with testicular function were observed. [ABSTRACT FROM AUTHOR]

As bisphenol A (BPA) is characterized by a pronounced influence on human hormonal regulation, particular attention has been aimed at understanding its role in reproductive processes in males and females, as well as on fetal development. Owing to the increasing number of alarming reports on the negative consequences of the presence of BPA in human surroundings, more and more studies are being undertaken to clarify the negative effects of BPA on human reproductive processes. The aim of this work was to collect and summarize data on the influence of BPA exposure on reproductive health. Based on an analysis of selected publications it was stated that there is strong proof confirming that BPA is an ovarian, uterine and prostate toxicant at a level below the lowest observed adverse effect level (50 mg kg−1 bodyweight) as well as a level below the proposed safe level (4 μg kg−1 bodyweight). It seems there is also reliable evidence in relation to the negative effect of BPA on sperm quality and motility. Limited evidence also pertains to the case of the potential of BPA to affect polycystic ovary syndrome occurrence. Although in epidemiological studies this disease was common, in studies on animal models such results were still not confirmed. No unambiguous results of epidemiological studies and with animal models were obtained in relation to the evaluation of associations between BPA and implantation failure in women, evaluation of associations between BPA and sexual dysfunction in men, and impact of BPA on birth rate, birth weight and length of gestation. Copyright © 2017 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), a potent environmental contaminant, is an endocrine disrupter with a proven reproductive toxicity in mammals. However, its effects on male fertility across generations are still elusive. The current work evaluates the toxicity of dioxin on male reproductive system in two separate groups of BALB/C mice; a group of pubertal males directly exposed to TCDD (referred to as DEmG), and a group of indirectly exposed males (referred to as IDEmG) comprises of F1, F2 and F3 males born from TCDD-exposed pregnant females. Both groups were exposed to 25 μg TCDD/kg body weight for a week. Our data show that males of TCDD-DEmG exhibited significant alterations in the expression of certain genes involved in the detoxification of TCDD and the biosynthesis of testosterone. This was accompanied with testicular pathological symptoms, including a sloughing in the germinal epithelium and a congestion of blood vessels in interstitial tissue with the presence of multinuclear cells into seminiferous tubule, with a 4-fold decline in the level of serum testosterone and reduced sperm count. Otherwise, the male reproductive toxicity across F1, F2 and F3 generations from TCDD-IDEmG was mainly characterized by: i) a reduce in body and testis weight. ii) a decrease in gene expression of steriodogenesis enzyme, e.g., AhR , CYP1A1 , CYP11A1 , COX1 , COX2 , LOX5 and LOX12. iii) a remarked and similar testicular histopathology that found for DEmG, iv) a serious decline in serum testosterone. v) a decreased male-to-female ratio. vi) a low sperm count with increasing abnormalities. Thus, pubertal or maternal exposure to TCDD provokes multigenerational male reproductive toxicity in mice, ultimately affecting the spermatogenesis and suggesting that the hormonal alternation and sperm abnormality are the most marked effects of the indirect exposure of mammalian male to TCDD. • Pregnant mice on gestation day 13 were exposed to a single dose of TCDD. • Male fertility was evaluated by histomolecular approach across three generations. • Remarked histological alterations were revealed in the testes of F1, F2 and F3. • Serum testosterone was seriously declined in F1, F2 and F3 males as well. • Spermatogenesis was dramatically affected across generations by TCDD. [ABSTRACT FROM AUTHOR]