A systematic review and meta-analysis of the impact of triclosan exposure on human semen quality.

Introduction: Triclosan is an antibacterial and antifungal compound that is frequently found in personal care and consumer products, and its its impact on male reproductive health is a growing concern. Despite existing experimental studies demonstrating its potential threats to male fertility, reports on its effects on human semen quality remains limited and inconsistent. Therefore, this study presents a systematic review and meta-analysis assessing the relationship between triclosan exposure and semen quality. Methods: This study was registered with PROSPERO (CRD42024524192) and adhered to PRISMA guidelines. Results: The study analyzed 562 screened studies, out of which five articles including 1,312 male subjects were finally included in the study. The eligible studies were geographically diverse, with three from China, one from Belgium, and one from Poland. More so, the eligible studies were both case-control and cross-sectional. The meta-analysis revealed that triclosan exposure significantly reduced sperm concentration (Standard Mean Difference (SMD) -0.42 [95% CI: -0.75, -0.10], P = 0.01) and sperm total motility (SMD -1.30 [95% CI: -2.26, -0.34], P = 0.008). Mechanistic insights from animal and in vitro studies showed that oxidative stress may mediate the adverse effects of triclosan on semen quality. Discussion: This meta-analysis is the first comprehensive evaluation of the impact of triclosan on human semen quality, highlighting its potential to impair male fertility through reductions in sperm concentration and motility. However, the high heterogeneity among the included studies underscores the need for further high-quality research to establish more definitive conclusions regarding the effects of triclosan exposure on human reproductive health.

Protecting our future: environmental hazards and children's health in the face of environmental threats: a comprehensive overview.

Children face the excitement of a changing world but also encounter environmental threats to their health that were neither known nor suspected several decades ago. Children are at particu-lar risk of exposure to pollutants that are widely dispersed in the air, water, and food. Children and adolescents are exposed to chemical, physical, and biological risks at home, in school, and elsewhere. Actions are needed to reduce these risks for children exposed to a series of envi-ronmental hazards. Exposure to a number of persistent environmental pollutants including air pollutants, endocrine disruptors, noise, electromagnetic waves, tobacco and other noxious sub-stances, heavy metals, and microplastics, is linked to damage to the nervous and immune sys-tems and affects reproductive function and development. Exposure to environmental hazards is responsible for several acute and chronic diseases that have replaced infectious diseases as the principal cause of illnesses and death during childhood. Children are disproportionately ex-posed to environmental toxicities. Children drink more water, eat more food, and breathe more frequently than adults. As a result, children have a substantially heavier exposure to toxins pre-sent in water, food, or air than adults. In addition, their hand-to-mouth behaviors and the fact that they live and play close to the ground make them more vulnerable than adults. Children undergo rapid growth and development processes that are easily disrupted. These systems are very delicate and cannot adequately repair the damage caused by environmental toxins. The first international development in children's environmental health was the Declaration of the Environment Leaders of the Eight on Children's Environmental Health by the Group of Eight. In 2002, the World Health Organization launched an initiative to improve children's environ-mental protection effort. Here, we review major environmental pollutants and related hazards among children and adolescents.

Persistent effects of larval exposure to glyphosate in mangrove rivulus fish.

Glyphosate, a key ingredient in many herbicides, is increasingly present in aquatic systems due to agricultural runoff. High doses of glyphosate cause defects in organisms due to its ability to interfere with physiological processes as an endocrine disruptor. We used the mangrove rivulus fish (Kryptolebias marmoratus) to evaluate the effects of larval exposure to glyphosate on non-target species in aquatic environments. These fish produce genetically identical offspring, allowing us to evaluate phenotypic responses to toxicant exposure while controlling for genetics. We treated newly hatched larvae for 96 h with concentrations of glyphosate on the low and high end of what they would experience in the wild: control (0 mg/L), low (0.01 mg/L), and high (1.1 mg/L), and then measured behavior, morphology, and reproductive traits at 60 and 130 days. We predicted that these amphibious fish exposed to low, environmentally relevant doses would show adaptive emersion behavior to escape poor quality water conditions, and deficits in other traits would be greater with higher glyphosate dosages. We found that low doses (0.01 mg/L) of glyphosate led to lower anxiety (decreased thigmotaxis) and impaired jumping behaviors while high dose exposures to glyphosate resulted in lower activity and lower average egg yield per individual. None of these effects appeared to be adaptive at low or high doses of glyphosate. While deficits in reproductive output scaled with dosage, phenotypic effects were often dosage-specific for each trait. This study demonstrates that even environmentally relevant concentrations of herbicide may be harmful to aquatic organisms and have consequences that persist well into adulthood. Furthermore, given that environmentally relevant concentrations of glyphosate induced deficits in reproductive output, this suggests that glyphosate contamination in natural systems may have population level consequences.

Metal-oxide nanocatalysts for spontaneous sequestration of endocrine-disrupting compounds from wastewater.

The quest for a good life, urbanization, and industrialization have led to the widespread distribution of endocrine-disrupting chemicals (EDCs) in water bodies through anthropogenic activities. This poses an imminent threat to both human and environmental health. In recent years, the utilization of advance materials for the removal of EDCs from wastewater has attracted a lot of attention. Metal-oxide nanocatalysts have emerged as promising candidates due to their high surface area, reactivity, and tunable properties, as well as enhanced surface properties such as mesoporous structures and hierarchical morphologies that allow for increased adsorption capacity, improved photocatalytic activity, and enhanced selectivity towards specific EDCs. As a result, they have shown extraordinary efficacy in removing a wide range of EDCs from aqueous solutions, including pharmaceuticals, agrochemicals, personal care items, and industrial chemicals. This study give insight into the unique physicochemical characteristics of metal-oxide nanocatalysts to effectively and efficiently remove harmful endocrine-disrupting chemicals (EDCs) from wastewater. Focusing on the advances in the synthesis, and properties of metal-oxide nanocatalysts, and insight into understanding the fundamental mechanisms underlying the adsorption and degradation of EDCs on metal-oxide nanocatalysts using advanced characterization techniques such as spectroscopic analysis and electron microscopy. The findings of the study present metal-oxide nanocatalysts as a good candidate for the spontaneous sequestration of EDCs from wastewater is an intriguing approach to mitigating water pollution and safeguarding public health and the environment.

Altered Expression of Thyroid- and Calcium Ion Channels-Related Genes in Rat Testes by Short-Term Exposure to Commercial Herbicides Paraquat or 2,4-D.

Exposure to pesticides such as paraquat and 2,4-dichlorophenoxyacetic acid (2,4-D) has been linked to harmful health effects, including alterations in male reproduction. Both herbicides are widely used in developing countries and have been associated with reproductive alterations, such as disruption of spermatogenesis and steroidogenesis. The thyroid axis and Ca2+-permeable ion channels play a key role in these processes, and their disruption can lead to reproductive issues and even infertility. This study evaluated the short-term effects of exposure to commercial herbicides based on paraquat and 2,4-D on gene expression in rat testes. At the molecular level, exposure to paraquat increased the expression of the thyroid hormone transporters monocarboxylate transporter 8 (Mct8) and organic anion-transporting polypeptide 1C1 (Oatp1c1) and the thyroid receptor alpha (TRα), suggesting a possible endocrine disruption. However, it did not alter the expression of the sperm-associated cation channels (CatSper1-2) or vanilloid receptor-related osmotically activated channel (Trpv4) related to sperm motility. In contrast, exposure to 2,4-D reduced the expression of the Mct10 transporter, Dio2 deiodinase, and CatSper1, which could affect both the availability of T3 in testicular cells and sperm quality, consistent with previous studies. However, 2,4-D did not affect the expression of CatSper2 or Trpv4. Deregulation of gene expression could explain the alterations in male reproductive processes reported by exposure to paraquat and 2,4-D. These thyroid hormone-related genes can serve as molecular biomarkers to assess endocrine disruption due to exposure to these herbicides, aiding in evaluating the health risks of pesticides.

BPA induces testicular damage in male rodents via apoptosis, autophagy, and ferroptosis.

Bisphenol A (BPA), chemically known as 2,2-bis(4-hydroxyphenyl) propane, is one of the most common endocrine-disrupting chemicals in our environment. Long-term or high-dose exposure to BPA may lead to testicular damage and adversely affect male reproductive function. In vivo studies on rodents have demonstrated that BPA triggers apoptosis in testicular cells through both intrinsic and extrinsic pathways. Further in vitro studies on spermatogonia, Sertoli cells, and Leydig cells have all confirmed the pro-apoptotic effects of BPA. Given these findings, apoptosis is considered a primary mode of cell death induced by BPA in testicular tissue. In addition, BPA promotes autophagy by altering the activity of the Akt/mTOR pathway and upregulating the expression of autophagy-related genes and proteins. Recent studies have also identified ferroptosis as a significant contributing factor to BPA-induced testicular damage, further complicating the landscape of BPA's effects. This review summarizes natural substances that mitigate BPA-induced testicular damage by inhibiting these cell death pathways. These findings not only highlight potential therapeutic strategies but also underscore the need for further research into the underlying mechanisms of BPA-induced toxicity, particularly as it pertains to human health risk assessment and the development of more effective BPA management strategies.

Estrogen Regulated Genes Compel Apoptosis in Breast Cancer Cells, Whilst Stimulate Antitumor Activity in Peritumoral Immune Cells in a Janus-Faced Manner.

Background: Breast cancer incidence and mortality exhibit a rising trend globally among both premenopausal and postmenopausal women, suggesting that there are serious errors in our preventive and therapeutic measures. Purpose: Providing a series of valuable, but misunderstood inventions highlighting the role of increasing estrogen signaling in prevention and therapy of breast cancer instead of its inhibition. Results: 1. Breast cells and breast cancer cells with germline BRCA1/2 mutations similarly show defects in liganded estrogen receptor (ER) signaling, demonstrating its role in genomic instability and cancer initiation. 2. In breast tumors, the increased expression of special receptor family maybe an effort for self-directed improvement of genomic defects, while the weakness or loss of receptors indicates a defect requiring medical repair. 3. ER overexpression in breast cancer cells is capable of strengthening estrogen signaling and DNA repair, while in ER negative tumors, HER2 overexpression tries to upregulate unliganded ER activation and genome stabilization. 4. ER-positive breast cancers responsive to endocrine therapy may show a compensatory ER overexpression resulting in a transient tumor response. Breast cancers non-responsive to antiestrogen treatment exhibit HER2-overexpression for compensating the complete inhibition of hormonal ER activation. 5. In breast tumors, somatic mutations serve upregulation of ER activation via liganded or unliganded pathway helping genome stabilization and apoptotic death. 6. The mutual communication between breast cancer and its inflammatory environment is a wonderful partnership among cells fighting for genome stabilization and apoptotic death of tumor. 7. In breast cancers, there is no resistance to genotoxic or immune blocker therapies, but rather, the nonresponsive tumor cells exhaust all compensatory possibilities against therapeutic damages. Conclusions: Understanding the behavior and ambition of breast cancer cells may achieve a turn in therapy via applying supportive care instead of genotoxic measures.

Chronic bisphenol A induced neurotoxicity: Exposure risk, molecular fate within carp and its potential phytoremediation.

Bisphenol A (BPA) is an endocrine-disrupting toxicant commonly used in the plastics industry, as a result, it is present in large quantities in the environment. Therefore, current study was designed to assess BPA induced neurotoxicity and molecular fate within common carp (Cyprinus carpio), largely used edible fish. Following 6 weeks exposure to BPA 1/5th of 96 h LC50 (1.31 mg/L), brain exhibited oxidative damage, which was evidenced by compromised antioxidant system (CAT, SOD, GSH) and increased level of biomacromolecule peroxidation (MDA and 8-OHDG). Functional damage to the brain observed in the form of blood-brain barrier disruption (decreased tight junction gene expression) and nerve conduction impairment (reduced acetylcholinesterase activity). Mechanistically, apoptotic cell death indicated by characteristic alteration in key biomarkers (bcl-2, caspase, and p53-related gene family). Whereas, coadministration of powdered PP (pomegranate peel) (8 %) with BPA effectively mitigated the BPA toxicity, as evidenced by the restoration of the above-mentioned bioindicators. Thereby, BPA-induced neurotoxicity could be potentially detoxified by applying PP dietary enrichment.

The Role of 11-Oxygenated Androgens and Endocrine Disruptors in Androgen Excess Disorders in Women.

Polycystic ovary syndrome (PCOS) and idiopathic hirsutism (IH) are androgen excess disorders requiring the determination of classic androgen levels for diagnosis. 11-oxygenated androgens have high androgenic potential, yet their clinical value in those disorders is not clear. Additionally, the role of endocrine disruptors (EDs), particularly in IH, remains understudied. We analyzed 25 steroids and 18 EDs in plasma samples from women with IH, PCOS, and controls using LC-MS/MS. Cytokine levels and metabolic parameters were assessed. Comparisons included non-obese women with PCOS (n = 10), women with IH (n = 12) and controls (n = 20), and non-obese versus obese women with PCOS (n = 9). Higher levels of 11-oxygenated androgens were observed in women with PCOS compared to those with IH, but not controls. Conversely, 11-oxygenated androgen levels were lower in women with IH compared to controls. Cytokine levels did not differ between women with IH and controls. Bisphenol A (BPA) levels were higher in obese women with PCOS compared to non-obese women with PCOS. Bisphenol S occurrence was higher in women with PCOS (90%) compared to controls (65%) and IH (50%). Significant correlations were found between androgens (11-ketotestosterone, androstenedione, testosterone) and insulin and HOMA-IR, as well as between immunomodulatory 7-oxygenated metabolites of DHEA and nine interleukins. Our data confirms that PCOS is a multiendocrine gland disorder. Higher BPA levels in obese women might exacerbate metabolic abnormalities. IH was not confirmed as an inflammatory state, and no differences in BPA levels suggest BPA does not play a role in IH pathogenesis.

The Impact of Polychlorinated Biphenyls on the Development of Zebrafish (Danio rerio).

Polychlorinated biphenyls (PCBs) are a group of 209 highly stable molecules that were used extensively in industry. Although their commercial use ceased in 1979, they are still present in many aquatic ecosystems due to improper disposal, oceanic currents, atmospheric deposition, and hydrophobic nature. PCBs pose a significant and ongoing threat to the development and sustainability of aquatic organisms. In areas with PCB exposure high mortality rates of organisms inhabiting them are still seen today, posing a significant threat to local species. Zebrafish were exposed to a standard PCB mixture (Aroclor 1254) for the first 5 days post fertilization, as there is a gap in knowledge during this important developmental period for fish (i.e., organization of the body). This PCB mixture was formally available commercially and has a high prevalence in PCB-contaminated sites. We tested for the effects of PCB dosage (control (embryo water only; 0 mg/L), methanol (solvent control; 0 mg/L); PCB 1 (0.125 mg/L), PCB 2 (0.25 mg/L), PCB 3 (0.35 mg/L), and PCB 4 (0.40 mg/L)) on zebrafish survival, rate of metamorphosis, feeding efficiency, and growth. We found significant, dose-dependent effects of PCB exposure on mortality, feeding efficiency, and growth, but no clear effect of PCBs on the rate of zebrafish metamorphosis. We identified a concentration in which there were no observable effects (NOEC), PCB concentration above the NOEC had a significant impact on life-critical processes. This can further inform local management decisions in environments experiencing PCB contamination.

New insights about the toxicity of 2,4-D: Gene expression analysis reveals modulation on several subcellular responses in Chironomus riparius.

Herbicides are the main class of pesticides applied in crops and are capable of polluting the surrounding freshwater system; thus, understanding their impact on non-target species, whose mechanism of action is not described, helps to elucidate the real risks of these pollutants to the environment. 2,4-dichlorophenoxyacetic acid (2,4-D) is frequently detected in water and, due to its persistence, poses a risk to wildlife. In this way, the present work aimed to describe the implication of exposure to concentrations of 2,4-D already reported in aquatic environments in several physiological mechanisms of C. riparius at molecular and biochemical levels. To achieve this, bioassays were conducted with fourth instar larvae exposed to three concentrations of 2,4-D (0.1, 1.0, and 7.5 µg L-1). Larvae were collected after 24 and 96 h of exposure, and the expression of 42 genes, related to six subcellular mechanisms, was assessed by Real-Time PCR (RT-PCR). Besides, the activity of the enzymes catalase (CAT), glutathione S-transferase (GST), and acetylcholinesterase (AChE) was determined. The main metabolic route altered after exposure to 2,4-D was the endocrine system (mainly related to 20-hydroxyecdysone and juvenile hormone), confirming its endocrine disruptor potential. Four of the eleven stress response genes studied were down-regulated, and later exposure modulated DNA-repair genes suggesting genotoxic capacity. Moreover, only one gene from each detoxification phase was modulated at short exposure to 1.0 µg L-1. The molecular responses were not dose-dependent, and some early responses were not preserved after 96 h, indicating a transient response to the herbicide. Exposure to 2,4-D did not alter the activity of CAT, GST, and AChE enzymes. The responses described in this study reveal new mechanistic pathways of toxicity for 2,4-D in non-target organisms and highlight potential ecological consequences for chironomids in aquatic systems at the edges of agricultural fields.

Effects of hypoxia on the reproductive endocrine axis of the pejerrey (Odontesthes bonariensis).

Recently, hypoxic areas have been identified in water bodies of the Pampas region due to human activity. The objective of this work was to study the effect of low concentrations of dissolved oxygen (hypoxia) on the reproductive endocrine axis of a pampas fish (Odontesthes bonariensis). Groups of 8 males and 8 females were subjected to severe hypoxia (2-3 mg l-1) and normoxia (7-9 mg l-1) in 3000 l tanks by duplicate during the reproductive season (spring). After 21 days, 4 males and 4 females from each tank were sacrificed, and blood was drawn to measure estradiol (E2) and testosterone (T). The brain, pituitary gland and a portion of the gonads were extracted and processed to measure the expression of: gnrh1, cyp19a1b, fshß, lhß, fshr, lhcgr and cyp19a1a. From the second experimental week, no spawning was found in the hypoxic females, while at the end of the treatment period no male released sperm. Fish under hypoxic conditions showed signs of gonadal regression, reduction of GSI and plasma levels of sex steroids. Furthermore, the expression of gnrh1 in both sexes, cyp19a1b and fshr in males and only fshß and cyp19a1a in females decreased in comparison with normoxic fish. After 40 days under normal conditions, signs of reproductive recovery were observed in the treated fish. The results obtained demonstrated that hypoxia generated an inhibition of some components of the pejerrey's reproductive endocrine axis, but the effect was reversible.

Exposure to endocrine disruptor DEHP promotes the progression and radiotherapy resistance of pancreatic cancer cells by increasing BMI1 expression and properties of cancer stem cells.

Most patients diagnosed with pancreatic cancer are initially at an advanced stage, and radiotherapy resistance impact the effectiveness of treatment. This study aims to investigate the effects of endocrine disruptor Di-(2-ethylhexyl) phthalate (DEHP) on various biological behaviors and the radiotherapy sensitivity of pancreatic cancer cells, as well as its potential mechanisms. Our findings indicate that exposure to DEHP promotes the proliferation of various cancer cells, including those from the lung, breast, pancreas, and liver, in a time- and concentration-dependent manner. Furthermore, DEHP exposure could influence several biological behaviors of pancreatic cancer cells in vivo and vitro. These effects include reducing cell apoptosis, causing G0/G1 phase arrest, increasing migration capacity, enhancing tumorigenicity, elevating the proportion of cancer stem cells (CSCs), and upregulating expression levels of CSCs markers such as CD133 and BMI1. DEHP exposure can also increase radiation resistance, which can be reversed by downregulating BMI1 expression. In summary our research suggests that DEHP exposure can lead to pancreatic cancer progression and radiotherapy resistance, and the mechanism may be related to the upregulation of BMI1 expression, which leads to the increase of CSCs properties.

Prenatal exposure to dibutyl phthalate contributes to erectile dysfunction in offspring male rats by activating the RhoA/ROCK signalling pathway.

Prenatal exposure to dibutyl phthalate (DBP) has been reported to cause erectile dysfunction (ED) in adult offspring rats. However, its underlying mechanisms are not fully understood. Previously, we found that DBP activates the RhoA/ROCK pathway in the male reproductive system. This study investigated how prenatal exposure to DBP activates the RhoA/ROCK signalling pathway, leading to ED in male rat offspring. Pregnant rats were stratified into DBP-exposed and NC groups, with the exposed group receiving 750 milligrams per kilogram per day (mg/kg/day) of DBP through gavage from days 14-18 of gestation. DBP exposure activated the RhoA/ROCK pathway in the penile corpus cavernosum (CC) of descendants, causing smooth muscle cell contraction, fibrosis, and apoptosis, all of which contribute to ED. In vitro experiments confirmed that DBP induces apoptosis and RhoA/ROCK pathway activation in CC smooth muscle cells. Treatment of DBP-exposed offspring with the ROCK inhibitor Y-27632 for 8 weeks significantly improved smooth muscle cell condition, erectile function, and reduced fibrosis. Thus, prenatal DBP exposure induces ED in offspring through RhoA/ROCK pathway activation, and the ROCK inhibitor Y-27632 shows potential as an effective treatment for DBP-induced ED.

Perinatal exposure to Aroclor 1254 disrupts thyrotropin-releasing hormone mRNA expression in the paraventricular nucleus of male and female rats.

Polychlorinated biphenyls (PCBs) are industrial pollutants that act as endocrine disruptors and alter thyroid function. However, it is still unclear whether PCBs can affect hypothalamic thyrotropin releasing hormone (Trh) mRNA expression through TH signaling disruption. As salt-loading dehydration induces tertiary hypothyroidism in the hypothalamic parvocellular paraventricular nuclei (paPVN), and perinatal exposure to Aroclor 1254 (A1254) disrupts the hydric balance in rats, we hypothesized that TRH synthesis could be altered during dehydration in TRH neurons that control the hypothalamic-pituitary-thyroid (HPT) axis activity in rats perinatally exposed to A1254. We examined Trh mRNA expression in the paPVN and the response to salt-loading dehydration (hyperosmotic (hyper) stress) in the progeny of Wistar pregnant rats receiving 0 mg/kg BW (control) or 30 mg/kg BW A1254 daily from gestational days 10-19. Three-month-old offspring were subjected to normosmotic or hyper conditions and Trh mRNA, glucocorticoid receptor (GR) mRNA expression were measured in the PVN by RT-PCR. TRH mRNA and TRH+ neurons were measured in the paPVN by fluorescent in situ hybridization (FISH). As expected, Trh mRNA levels were decreased in the paPVN of male and female rats in the hyper group. Basal Trh mRNA expression and serum TSH were decreased in male rats in the A1254 group. Notably, Trh mRNA levels were further decreased in the paPVN of male and female A1254 + hyper rats, in which the GR mRNA expression was significantly decreased. These results support the hypothesis that perinatal exposure to A1254 results in inadequate adaptive response of the HPT axis in adulthood and contributes to dysregulation of the HPT axis response to salt-loading dehydration.

Bisphenol AF Caused Reproductive Toxicity in Rats and Cineole Co-Treatment Exhibited Protective Effect.

Bisphenol AF (BPAF) is increasingly used and now found in products intended for human consumption. The protective effect of 1,8-cineole (CIN) against BPAF-induced reproductive toxicity was investigated. Four groups were created, with each group consisting of eight rats: control, BPAF (200 mg/kg), CIN (200 mg/kg), and BPAF + CIN groups. The results demonstrated that the BPAF group exhibited a decline in testosterone levels and a decrease in sperm parameters compared with the control. Additionally, higher levels of MDA were observed, along with lower levels of GSH and GPx activity. CAT activity also decreased slightly. Tnf-α, Nf-κB levels were significantly higher, and caspase-3 expression was elevated, while PCNA expression decreased. BPAF significantly increased tissue degeneration compared with the control. However, the BPAF + CIN group showed statistically significant improvements in sperm parameters, except for concentration. They also exhibited an increase in testosterone levels and an improvement in MDA and GSH levels compared with the BPAF group. However, GPx activity partially enhanced. Tnf-α and Nf-κB levels were significantly reduced, and caspase-3 levels declined while PCNA and Bcl-2 levels increased. The Johnsen Testicular Biopsy score showed a substantial increase. Overall, these results suggest that CIN co-treatment in rats enhanced reproductive health and exhibited antioxidant, antiapoptotic, and anti-inflammatory properties against BPAF-induced testicular damage.

Evaluation of Bisphenol S (BPS) toxicity on the reproductive system of Channa striatus: Insights for environmental risk assessment.

Aquatic ecosystems face significant exposure to endocrine-disrupting chemicals (EDCs), which can mimic, block, or alter the synthesis of endogenous hormones. Bisphenol A (BPA), a widely known EDC, has been phased out from consumer products due to concerns about its potential impacts on human health. In its place, bisphenol S (BPS), an organic compound, has been increasingly used in the production of polycarbonate plastics, epoxy resins, thermal receipt papers, and currency. Vitellogenin (Vtg), a yolk precursor protein synthesized in the liver and present in oviparous fish, particularly males, serves as a pertinent biomarker for studying the effects of estrogenic EDCs on fish. This study aimed to assess the impact of BPS on reproductive parameters and hepatic vitellogenin expression in Channa striatus. The LC50 of BPS was determined to be 128.8 mg/L. Experimental groups included control and BPS-exposed fish, with sub-lethal concentrations of BPS (1 mg/L, 4 mg/L, and 12 mg/L) administered and effects monitored at seven- and twenty-one-day intervals. Significant decreases in gonadosomatic index (GSI), ova diameter, and fecundity were observed in BPS-exposed Channa striatus. Hepatic Vtg mRNA expression was downregulated in female and upregulated in male following BPS exposure. Serum hormone analysis confirmed the estrogenic activity of BPS. These findings underscore BPS's ability as an endocrine disruptor to interfere with hormone synthesis and disrupt spermatogenesis and oogenesis processes in Channa striatus. This research contributes to understanding the endocrine-disrupting effects of BPS on aquatic organisms, highlighting potential ecological implications and the need for continued monitoring and regulatory considerations.

Environmental endocrine disruptor-induced mitochondrial dysfunction: a potential mechanism underlying diabetes and its complications.

Diabetes and its complications significantly affect individuals' quality of life. The etiology of diabetes mellitus and its associated complications is complex and not yet fully understood. There is an increasing emphasis on investigating the effects of endocrine disruptors on diabetes, as these substances can impact cellular processes, energy production, and utilization, ultimately leading to disturbances in energy homeostasis. Mitochondria play a crucial role in cellular energy generation, and any impairment in these organelles can increase susceptibility to diabetes. This review examines the most recent epidemiological and pathogenic evidence concerning the link between endocrine disruptors and diabetes, including its complications. The analysis suggests that endocrine disruptor-induced mitochondrial dysfunction-characterized by disruptions in the mitochondrial electron transport chain, dysregulation of calcium ions (Ca2+), overproduction of reactive oxygen species (ROS), and initiation of signaling pathways related to mitochondrial apoptosis-may be key mechanisms connecting endocrine disruptors to the development of diabetes and its complications.

Vitamin E alleviates glyphosate-based herbicide-induced progesterone secretion inhibition and oxidative stress increase in chicken primary granulosa cells.

Glyphosate-based herbicides (GBH) are the most extensively used herbicides worldwide. Despite a presumed nondangerousness for animals, several studies reported negative effects after a GBH exposure in several animal models including birds, notably on reproductive functions. Several studies concerning the advantages of Vitamin E (VE) for antioxidant activity but also growth and reproduction have been reported in birds. However, it remains unclear whether VE could alleviate the negative effect of GBHs on chicken ovarian cells. Here we exposed chicken primary granulosa cells (GCs) from F1 and F3/4 follicles to growing doses of GBH (0.036, 0.36, 3.6, and 36 gly eq/L), with or without VE supplementation (1 mg/L) and investigated cell viability, proliferation, oxidative stress and steroidogenesis. GBH exposure did not affect F1 and F3 GCs viability but it increased cell proliferation only in F1 GCs and this effect was not altered by VE. In both F1 and F3/4 GCs, GBH exposure increased total oxidant status (TOS), reduced total antioxidant status (TAS) and consequently increased index of oxidative stress (OSI) in dose dependent manner. This latter effect for GBH 36 mg eq gly/L was totally abolished in response to VE. In both F1 and F3/4 GCs, GBH exposure reduced progesterone secretion in a dose dependent manner and this effect with GBH 0.36 and 1.8 mg eq glyphosate/L was alleviated by VE. However, we did not observe any effect of GBH and VE on the gene expression of several components of the steroidogenesis process. Taken together, these results show that GBH may have endocrine disruptor effects, and that these effects might be alleviated by antioxidant VE supplementation.

Bacterial bioremediation as a sustainable strategy for the mitigation of Bisphenol-A.

In the era dominated by plastic, the widespread use of plastic in our daily lives has led to a growing accumulation of its degraded byproducts, such as microplastics and plastic additives like Bisphenol A (BPA). BPA is recognized as one of the earliest man-made substances that exhibit endocrine-disrupting properties. It is frequently employed in the manufacturing of epoxy resins, polycarbonates, dental fillings, food storage containers, infant bottles, and water containers. BPA is linked to a range of health issues including obesity, diabetes, chronic respiratory illnesses, cardiovascular diseases, and reproductive abnormalities. This study examines the bacterial bioremediation of the BPA, which is found in many sources and is known for its hazardous effects on the environment. The metabolic pathways for the breakdown of BPA in important bacterial strains were hypothesized based on the observed altered intermediate metabolites during the degradation of BPA. This review discusses the enzymes and genes involved in the bacterial degradation of BPA. The utilization of naturally occurring microorganisms is the most efficient and cost-effective method due to their selectivity of strains, ensuring sustainability.