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Hope and Trauma in a Poisoned Land was a community engaged regional art exhibition that began as a mixed-method research project. The original purpose was to give voice to the stories of indigenous people living in uranium-contaminated regions of the Navajo Nation. It quickly expanded into a social practice art project, allowing for collaboration between individuals, artists, community members, and several different institutions. Participating artists attended a 4-day informational and interactive workshop about the uranium mining legacy, so that they fully understood contamination issues; the goal was for them to create art from an informed place. The investigators examined the psychological impact of the workshop and the exhibition on the artists as well as the community at large. We found that the greater the emotional impact on the artist, the greater their absorption while making the art and the greater their artwork creativity, as rated by objective evaluators. Community attendees reported increased knowledge about the issue, as well as feeling inspired to take action. Through engaging a community advisory council and artists and patrons on an intellectual, aesthetic, emotional, and compassionate level, we documented how this social practice art exhibition had an impact on our community. [ABSTRACT FROM AUTHOR]

Human brain development is a complex process, and animal models often have significant limitations. To address this, researchers have developed pluripotent stem cell-derived three-dimensional structures, known as brain-like organoids, to more accurately model early human brain development and disease. To enable more consistent and intuitive reproduction of early brain development, in this study, we incorporated forebrain organoid culture technology into the traditional unguided method of brain organoid culture. This involved embedding organoids in matrigel for only 7 days during the rapid expansion phase of the neural epithelium and then removing them from the matrigel for further cultivation, resulting in a new type of human brain organoid system. This cerebral organoid system replicated the temporospatial characteristics of early human brain development, including neuroepithelium derivation, neural progenitor cell production and maintenance, neuron differentiation and migration, and cortical layer patterning and formation, providing more consistent and reproducible organoids for developmental modeling and toxicology testing. As a proof of concept, we applied the heavy metal cadmium to this newly improved organoid system to test whether it could be used to evaluate the neurotoxicity of environmental toxins. Brain organoids exposed to cadmium for 7 or 14 days manifested severe damage and abnormalities in their neurodevelopmental patterns, including bursts of cortical cell death and premature differentiation. Cadmium exposure caused progressive depletion of neural progenitor cells and loss of organoid integrity, accompanied by compensatory cell proliferation at ectopic locations. The convenience, flexibility, and controllability of this newly developed organoid platform make it a powerful and affordable alternative to animal models for use in neurodevelopmental, neurological, and neurotoxicological studies.

Background: Exposure to environmental toxins is a growing concern globally, particularly due to its potential impact on the developmental milestones of infants. This cross-sectional study aims to elucidate the relationship between environmental toxin exposure and the attainment of developmental milestones in infants. Methods: The study was conducted with a sample size of 120 infants aged between 6 to 18 months. We used a structured questionnaire to collect data on exposure levels, coupled with developmental screenings conducted by pediatric experts. Environmental toxins were quantified through household surveys and proximity to known pollution sources. Results: Preliminary analyses indicate a correlation between high levels of toxin exposure and delayed achievement of certain developmental milestones. Specific toxins, such as lead and certain air pollutants, were notably associated with these delays. Conclusion: The findings suggest a significant association between environmental toxin exposure and developmental delays in infants. These results underscore the need for stricter environmental regulations and targeted public health interventions to mitigate exposure in vulnerable populations. [ABSTRACT FROM AUTHOR]

The aim of the research was to investigate the resistance and efficacy of the fungi Aspergillus awamori in removing heavy metals. We conducted an analysis of the fungus's tolerance to several heavy metals by measuring the dry weight and using a plate method. The fungus exhibited growth in concentrations and lowest growth was observed in a concentration of 400 ppm of Cd. The heavy metals were successfully removed with the following orders: Zn> Co, > Ag, > Hg and Cu. The optimal parameters for the elimination of 100 mg/L of heavy metals were a temperature of 28°C, a pH range of 4.0 to 5.5, a heavy metal concentration of 100 ppm, and a biomass of fungi of 1 g. [ABSTRACT FROM AUTHOR]

Environmental toxins pose significant threats to ecosystems and human health. Monitoring and assessing these toxins are crucial for effective environmental management and public health protection. Recently, plant species have garnered increasing attention as potential bioindicators for identifying and evaluating ecological toxins. Since plants often come into touch with harmful compounds in soil, water, and the atmosphere, they are particularly valuable for analyzing how human activities influence the terrestrial ecosystem, the aquatic system, and the atmosphere. This review paper emphasizes using plant species as a resource for tracking environmental pollution and analyzing contaminants. We focused on plants because they are significant indicators of soil, water, and air quality changes. Many plants have been used as bio-indicators to assess and predict pollution, toxicity, and environmental changes. These include Allium cepa, Vicia faba, Pisum sativum, Zea mays, Nicotiana tabacum, lichens, and mosses. The idea of bioindicators is discussed in the current paper, with a focus on plants as possible candidates for bioindicators for toxin assessment and related outcomes. [ABSTRACT FROM AUTHOR]

Recent evidence indicates that exposure to environmental toxins, both short-term and long-term, can increase the risk of developing neurological disorders, including neurodegenerative diseases (i.e., Alzheimer's disease and other dementias) and acute brain injury (i.e., stroke). For stroke, the latest systematic analysis revealed that exposure to ambient particulate matter is the second most frequent stroke risk after high blood pressure. However, preclinical and clinical stroke investigations on the deleterious consequences of environmental pollutants are scarce. This review examines recent evidence of how environmental toxins, absorbed along the digestive tract or inhaled through the lungs, affect the host cellular response. We particularly address the consequences of environmental toxins on the immune response and the microbiome at the gut and lung barrier sites. Additionally, this review highlights findings showing the potential contribution of environmental toxins to an increased risk of stroke. A better understanding of the biological mechanisms underlying exposure to environmental toxins has the potential to mitigate stroke risk and other neurological disorders. [ABSTRACT FROM AUTHOR]

The goal of Working Group 1 in the Breastmilk Ecology: Genesis of Infant Nutrition (BEGIN) Project was to outline factors influencing biological processes governing human milk secretion and to evaluate our current knowledge of these processes. Many factors regulate mammary gland development in utero, during puberty, in pregnancy, through secretory activation, and at weaning. These factors include breast anatomy, breast vasculature, diet, and the lactating parent's hormonal milieu including estrogen, progesterone, placental lactogen, cortisol, prolactin, and growth hormone. We examine the effects of time of day and postpartum interval on milk secretion, along with the role and mechanisms of lactating parent-infant interactions on milk secretion and bonding, with particular attention to the actions of oxytocin on the mammary gland and the pleasure systems in the brain. We then consider the potential effects of clinical conditions including infection, pre-eclampsia, preterm birth, cardiovascular health, inflammatory states, mastitis, and particularly, gestational diabetes and obesity. Although we know a great deal about the transporter systems by which zinc and calcium pass from the blood stream into milk, the interactions and cellular localization of transporters that carry substrates such as glucose, amino acids, copper, and the many other trace metals present in human milk across plasma and intracellular membranes require more research. We pose the question of how cultured mammary alveolar cells and animal models can help answer lingering questions about the mechanisms and regulation of human milk secretion. We raise questions about the role of the lactating parent and the infant microbiome and the immune system during breast development, secretion of immune molecules into milk, and protection of the breast from pathogens. Finally, we consider the effect of medications, recreational and illicit drugs, pesticides, and endocrine-disrupting chemicals on milk secretion and composition, emphasizing that this area needs much more research attention.

Environmental toxins pose significant threats to ecosystems and human health. Monitoring and assessing these toxins are crucial for effective environmental management and public health protection. Recently, plant species have garnered increasing attention as potential bioindicators for identifying and evaluating ecological toxins. Since plants often come into touch with harmful compounds in soil, water, and the atmosphere, they are particularly valuable for analyzing how human activities influence the terrestrial ecosystem, the aquatic system, and the atmosphere. This review paper emphasizes using plant species as a resource for tracking environmental pollution and analyzing contaminants. We focused on plants because they are significant indicators of soil, water, and air quality changes. Many plants have been used as bio-indicators to assess and predict pollution, toxicity, and environmental changes. These include Allium cepa, Vicia faba, Pisum sativum, Zea mays, Nicotiana tabacum, lichens, and mosses. The idea of bioindicators is discussed in the current paper, with a focus on plants as possible candidates for bioindicators for toxin assessment and related outcomes.

Abstract Background Chronic Kidney Disease of unknown cause (CKDu) a disease of exclusion, and remains unexplained in various parts of the world, including India. Previous studies have reported mixed findings about the role of heavy metals or agrochemicals in CKDu. These studies compared CKDu with healthy controls but lacked subjects with CKD as controls. The purpose of this study was to test the hypothesis whether heavy metals, i.e. Arsenic (As), Cadmium (Cd), Lead (Pb), and Chromium (Cr) are associated with CKDu, in central India. Methods The study was conducted in a case-control manner at a tertiary care hospital. CKDu cases (n = 60) were compared with CKD (n = 62) and healthy subjects (n = 54). Blood and urine levels of As, Cd, Pb, and Cr were measured by Inductively Coupled Plasma- Optical Emission Spectrometry. Pesticide use, painkillers, smoking, and alcohol addiction were also evaluated. The median blood and urine metal levels were compared among the groups by the Kruskal-Wallis rank sum test. Results CKDu had significantly higher pesticide and surface water usage as a source of drinking water. Blood As levels (median, IQR) were significantly higher in CKDu 91.97 (1.3–132.7) µg/L compared to CKD 4.5 (0.0–58.8) µg/L and healthy subjects 39.01 (4.8–67.4) µg/L (p .05). Urinary Cd, Pb and Cr were undetectable in healthy subjects and were significantly higher in CKDu and CKD compared to healthy subjects (P =

Background: Chronic Kidney Disease of unknown cause (CKDu) a disease of exclusion, and remains unexplained in various parts of the world, including India. Previous studies have reported mixed findings about the role of heavy metals or agrochemicals in CKDu. These studies compared CKDu with healthy controls but lacked subjects with CKD as controls. The purpose of this study was to test the hypothesis whether heavy metals, i.e. Arsenic (As), Cadmium (Cd), Lead (Pb), and Chromium (Cr) are associated with CKDu, in central India. Methods: The study was conducted in a case-control manner at a tertiary care hospital. CKDu cases (n = 60) were compared with CKD (n = 62) and healthy subjects (n = 54). Blood and urine levels of As, Cd, Pb, and Cr were measured by Inductively Coupled Plasma- Optical Emission Spectrometry. Pesticide use, painkillers, smoking, and alcohol addiction were also evaluated. The median blood and urine metal levels were compared among the groups by the Kruskal-Wallis rank sum test. Results: CKDu had significantly higher pesticide and surface water usage as a source of drinking water. Blood As levels (median, IQR) were significantly higher in CKDu 91.97 (1.3–132.7) µg/L compared to CKD 4.5 (0.0–58.8) µg/L and healthy subjects 39.01 (4.8–67.4) µg/L (p < 0.001) On multinominal regression age and sex adjusted blood As was independently associated with CKDu[ OR 1.013 (95%CI 1.003–1.024) P <.05].Blood and urinary Cd, Pb, and Cr were higher in CKD compared to CKDu (p >.05). Urinary Cd, Pb and Cr were undetectable in healthy subjects and were significantly higher in CKDu and CKD compared to healthy subjects (P = < 0.001). There was a significant correlation of Cd, Pb and Cr in blood and urine with each other in CKDu and CKD subjects as compared to healthy subjects. Surface water use also associated with CKDu [OR 3.178 (95%CI 1.029–9.818) p <.05). Conclusion: The study showed an independent association of age and sex adjusted blood As with CKDu in this Indian cohort. Subjects with renal dysfunction (CKDu and CKD) were found to have significantly higher metal burden of Pb, Cd, As, and Cr as compared to healthy controls. CKDu subjects had significantly higher pesticide and surface water usage, which may be the source of differential As exposure in these subjects. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular system is saddled with responsibility of pumping blood into circulation, thereby providing nourishment to tissues and removal of metabolic wastes. However, several environmental factors limit this simple but crucial function. It is still difficult to establish a link between environmental toxins and cardiovascular disease. Examining the research connecting alterations in the cardiovascular system to some of the most frequent environmental exposures is the goal of this review. Methods: Literature review was conducted by searching the keyword environmental contaminants and cardiovascular disease in major search engines such as Google Scholar, PubMed, Scopus, ScienceDirect, and ResearchGate. Results: Studies repeatedly show a decrease in the cardiovascular system's functionality that cannot be fully explained by obesity, recognized genetic factors, or dietary and lifestyle modifications alone. Over the same period of time as this declines in heart and vascular function, human exposures have undergone a significant change. Nearly 2,000 new compounds are launched each year, and more over 80,000 substances have been registered with the US National Toxicology Program. Many of them are recognized poisons, including heavy metals, phthalates, polycyclic aromatic hydrocarbons, polyfluoroalkyl compounds, microplastics/nanoplastics, and organophosphate esters, which have been outlawed or severely regulated in other nations due to their known systemic harmful effects. Many of these chemicals still have legal exposure limits in the majority of developing nations, despite being recognized to impair the cardiovascular system. Conclusion: Various pathological mechanisms were highlighted in this review. However, exposure avoidance and risk reduction are crucial for the health of cardiovascular system. [ABSTRACT FROM AUTHOR]

IntroductionMilitary personnel and local civilians at various deployment locations are plagued with serious health conditions. Evidence points to burn pit emissions as the cause of these pathologies; however, similar diseases are also caused by environmental exposures, smoking, genetic predispositions, or other comorbidities. Burn pits, which are large smoldering piles of refuse ignited with jet or diesel fuel, contain human and medical waste as well as paint, plastics, ammunition, and other materials—each of which can be attributed to health concerns in other industrial settings. Here we compare various pathologies attributable to toxic aerosol exposures and discuss distinct pathologies that may be linked to burn pit exposures.ObjectivesWe performed a literature review where we provide information on toxic exposures that may pose relevance to burn pit exposure and furthermore, highlight what is already known about burn pit exposures and what steps need to be taken to diagnose and correlate certain respiratory pathologies to chronic exposure from overseas burn pits.Data sourcesWe conducted searches through PubMed and Google Scholar to determine where gaps in our knowledge of burn pit exposure lie. Thorough review on jet-fuel properties and particulate matter were performed as supporting evidence of potential toxins from burn pit emissions.ResultsTo date, studies on burn pit emissions consist mainly of systematic reviews and discussions to address the problem, with very few acute-exposure studies and little to no chronic-exposure studies. We found that symptoms range from respiratory pathologies to neurological deficits, but treatment has been limited as medical facilities, such as the Veterans Administration (VA), require proof that a condition is service-connected.ConclusionsTo determine the effects of burn pit exposure on humans, chronic exposure to mimicked burn pit emissions is necessary to draw definitive conclusions between phenotypic differences in pathologies linked to exposure. By determining phenotypic differences, conclusions can be made about the pathologic origins, potentially leading to future diagnoses and treatments for veterans and affected civilians.

The zebrafish (Danio rerio), a small fish belonging to the Cyprinidae family, is one of the most popular animal models used in laboratory studies, including toxicology. It has many beneficial features, such as transparent body structure, easy and economical breeding, a large number of offspring and a short life cycle. In addition, the genome of the zebrafish shows a high homology to the human genome, which makes this fish an attractive research model. The article points to the contemporary challenges of toxicology in terms of neurotoxicity, teratotoxicity and genotoxicity, which can be analysed based on the results of studies carried out on the zebrafish model. The dynamic implementation of new factors, such as nanoparticles, e-cigarettes, new generations of cosmetics or a wide range of chemical enhancers into human living and working environments, can have serious consequences for the health of the general population and the ecosystem as a whole. The work presents the latest research results regarding, among others, neurotoxic effects of ethanol, teratotoxic and neurotoxic effects of e-cigarettes, teratotoxic, neurotoxic and genotoxic effects of selected nanoparticles and microplastics assessed in experiments using the zebrafish model. The characteristics of the micronucleus test and the comet test are also presented as the most frequently chosen methods for assessing the genotoxic effect of xenobiotics in studies on the Danio rerio model.The results of the studies underline the need for further analysis and monitoring of the effects of these substances, in particular harmful effects on living organisms, and for remedial measures to protect the environment. As we have tried to demonstrate in this article, one of the very convenient possibilities in this respect is the use of the striped zebrafish model. A particularly valuable premise in assessing the genotoxic effects of xenobiotics in this case is the above-mentioned high homology of the Danio rerio and human genomes.

Among the premenopausal women, Polycystic Ovary Syndrome (PCOS) is the most prevalent endocrinopathy affecting the reproductive system and metabolic rhythms leading to disrupted menstrual cycle. Being heterogeneous in nature it is characterized by complex symptomology of oligomennorhoea, excess of androgens triggering masculine phenotypic appearance and/or multiple follicular ovaries. The etiology of this complex disorder remains somewhat doubtful and the researchers hypothesize multisystem links in the pathogenesis of this disease. In this review, we attempt to present several hypotheses that tend to contribute to the etiology of PCOS. Metabolic inflexibility, aberrant pattern of gonadotropin signaling along with the evolutionary, genetic and environmental factors have been discussed. Considered a lifelong endocrinological implication, no universal treatment is available for PCOS so far however; multiple drug therapy is often advised along with simple life style intervention is mainly advised to manage its cardinal symptoms. Here we aimed to present a summarized view of pathophysiological links of PCOS with potential therapeutic strategies. [ABSTRACT FROM AUTHOR]

The relationship between the congenital defect of gastroschisis and environmental toxins is poorly understood. We examined gastroschisis incidence, risk factors, and spatial association in a geographic region with known environmental pollution and hazardous waste sites. An observational study of fetal and neonatal gastroschisis diagnosed from 1/1/2006 to 12/31/2020 was conducted in a southern West Virginia (WV) tertiary care hospital. Emerging hot spot analysis and Ripley's K-Function examined the spatial relationship between gastroschisis cases and Environmental Protection Agency (EPA) Federal Registry Sites (FRS). A total of 63 gastroschisis cases provided a prevalence rate of 14.6 per 10000 live births. Gastroschisis was associated with younger maternal age, decreased pre-pregnancy BMI, and increased maternal tobacco use. Relative to FRS sites, spatial clusters were identified with emerging hot spot analysis. Observed Ripley K was higher at all measured bands. Results suggest a potential geographic association between gastroschisis cases and EPA-designated hazardous waste sites. [ABSTRACT FROM AUTHOR]

The experience of poverty embodies complex, multidimensional stressors that may adversely affect physiological and psychological domains of functioning. Compounded by racial/ethnic discrimination, the financial aspect of family poverty typically coincides with additional social and physical environmental risks such as pollution exposure, housing burden, elevated neighborhood unemployment, and lower neighborhood education levels. In this study, we investigated the associations of multidimensional social disadvantage throughout adolescence with autonomic nervous system (ANS) functioning at 17 years. Two hundred and twenty nine low-income Mexican-American adolescents (48.6% female) and their parents were assessed annually between the ages of 10 and 16. Participants' census tracts were matched with corresponding annual administrative data of neighborhood housing burden, education, unemployment, drinking water quality, and fine particulate matter. We combined measures of adolescents' electrodermal response and respiratory sinuses arrhythmia at rest and during a social exclusion challenge (Cyberball) to use as ANS indices of sympathetic and parasympathetic activity, respectively. Controlling for family income-to-needs, youth exposed to greater cumulative water and air pollution from ages 10-16 displayed altered patterns of autonomic functioning at rest and during the social challenge. Conversely, youth living in areas with higher housing burden displayed healthy patterns of autonomic functioning. Altogether, results suggest that toxin exposure in youths' physical environments disrupts the ANS, representing a plausible mechanism by which pollutants and social disadvantage influence later physical and mental health.

The field of evolutionary health is relatively new, and over the last several decades, has come to signify the interest in the extent of mismatch between factors common in our modern world, and our evolutionary milieu, which is a combination of genetic and environmental interactions that have influenced our development over the course of many thousands, if not hundreds of thousands of years.We have covered a wide variety of topics during our conferences; this includes, brain function, sleep and light, various components of the diet, aging, cardiovascular disease, human brain development, exercise, bone health, obesity, vitamin levels, hormonal regulation, inflammation and cancer, with the emphasis on the degree of mismatch between our hominid ancestors and modern humans today. With this most recent conference, we have added topics such as psychological and physical stress, the gut microbiome and the potential role of biomimetics in environmental stressors.We’d like to thank the Journal of Evolutionary Health for allowing us to publish some of the abstracts from our most recent conference.

Recent evidence indicates that exposure to environmental toxins, both short-term and long-term, can increase the risk of developing neurological disorders, including neurodegenerative diseases (i.e., Alzheimer’s disease and other dementias) and acute brain injury (i.e., stroke). For stroke, the latest systematic analysis revealed that exposure to ambient particulate matter is the second most frequent stroke risk after high blood pressure. However, preclinical and clinical stroke investigations on the deleterious consequences of environmental pollutants are scarce. This review examines recent evidence of how environmental toxins, absorbed along the digestive tract or inhaled through the lungs, affect the host cellular response. We particularly address the consequences of environmental toxins on the immune response and the microbiome at the gut and lung barrier sites. Additionally, this review highlights findings showing the potential contribution of environmental toxins to an increased risk of stroke. A better understanding of the biological mechanisms underlying exposure to environmental toxins has the potential to mitigate stroke risk and other neurological disorders.

Environmental toxins have the potential to disrupt the animal gut microbiome (AGM), which can lead to various gut-associated diseases such as inflammatory bowel disease (IBD) and colorectal cancer. In this review, we provide an overview of environmental toxins, their sources, and exposure routes. We also discuss the importance of AGM in maintaining human health and the effects of environmental toxins on AGM, including dysbiosis, alterations in diversity, and microbial metabolism. We present evidence linking environmental toxins exposure to gut-associated diseases and mechanisms by which environmental toxins affect AGM. We also highlight factors that influence the effects of environmental toxins on AGM, such as dose, duration, and individual susceptibility. Finally, we discuss strategies to mitigate the effects of environmental toxins on AGM, including prebiotics, probiotics, and dietary interventions, as well as regulatory aspects of environmental toxins, including safety thresholds, exposure limits, and risk assessment. We conclude by discussing future research directions and the potential for personalized approaches, targeted detoxification, and ecological restoration of AGM to prevent and treat gut-associated diseases.

Background: Risk factors for pancreatic ductal adenocarcinoma (PDAC) include tobacco/alcohol abuse, genetic predisposition, insulin resistance, and pancreatic cysts. Despite these well-established risk factors and the screening of high-risk individuals, some people still develop PDAC. This study aims to explore a potential risk factor for PDAC by investigating the association between fungal toxins (FT) and environmental toxins (ET) and the disease. We predicted that individuals with PDAC would have higher levels of these toxins compared to healthy controls. The rationale behind this hypothesis is that exposure to FT and ET might contribute to the development of PDAC by elevating cancer risk. Methods: A pilot retrospective cohort study was conducted at Moffitt Cancer Center from 2022 to 2023. This study compared FT and ET levels, demographic data, and PDAC features between subjects with PDAC and healthy controls. Results: Forty subjects were enrolled in the study, comprising 20 with pancreatic ductal adenocarcinoma (PDAC) and 20 healthy controls. Baseline demographics were similar between the two groups. Among the PDAC subjects, the most common tumor location was the head of the pancreas (55%); 30% had locally advanced disease, 45% were borderline resectable, and 10% had metastatic disease. Compared to the controls, subjects with PDAC had significantly higher levels of fungal toxins (FTs) including ochratoxin, gliotoxin, and citrinin (p < 0.05). Additionally, PDAC patients had significantly elevated levels of environmental toxins (ETs) such as methyl tert-butyl ether (MTBE), xylene, styrene, acrylonitrile, perchlorate, diphenyl phosphate, bromopropane, organophosphates, acrolein, tiglylglycine, and diethylphosphate (p < 0.05). Conclusion: Our study demonstrates that subjects with PDAC, without other risk factors, have higher FT and ET levels than controls. Further studies are needed to evaluate whether ET and FT exposure can be clinically utilized as a risk factor for PDAC development. [ABSTRACT FROM AUTHOR]

The developing nervous system is remarkably sensitive to environmental signals, including disruptive toxins, such as polybrominated diphenyl ethers (PBDEs). PBDEs are an environmentally pervasive class of brominated flame retardants whose neurodevelopmental toxicity mechanisms remain largely unclear. Using dissociated cortical neurons from embryonic Rattus norvegicus, we found here that chronic exposure to 6-OH-BDE-47, one of the most prevalent hydroxylated PBDE metabolites, suppresses both spontaneous and evoked neuronal electrical activity. On the basis of our previous work on mitogen-activated protein kinase (MAPK)/extracellular signal-related kinase (ERK) (MEK) biology and our observation that 6-OH-BDE-47 is structurally similar to kinase inhibitors, we hypothesized that certain hydroxylated PBDEs mediate neurotoxicity, at least in part, by impairing the MEK-ERK axis of MAPK signal transduction. We tested this hypothesis on three experimental platforms: 1) in silico, where modeling ligand-protein docking suggested that 6-OH-BDE-47 is a promiscuous ATP-competitive kinase inhibitor; 2) in vitro in dissociated neurons, where 6-OH-BDE-47 and another specific hydroxylated BDE metabolite similarly impaired phosphorylation of MEK/ERK1/2 and activity-induced transcription of a neuronal immediate early gene; and 3) in vivo in Drosophila melanogaster, where developmental exposures to 6-OH-BDE-47 and a MAPK inhibitor resulted in offspring displaying similarly increased frequency of mushroom-body β-lobe midline crossing, a metric of axonal guidance. Taken together, our results support that certain ortho-hydroxylated PBDE metabolites are promiscuous kinase inhibitors and can cause disruptions of critical neurodevelopmental processes, including neuronal electrical activity, pre-synaptic functions, MEK-ERK signaling, and axonal guidance.

Disruption of epigenetic regulation by environmental toxins is an emerging area of focus for understanding the latter's impact on human health. Polybrominated diphenyl ethers (PBDEs), one such group of toxins, are an environmentally pervasive class of brominated flame retardants that have been extensively used as coatings on a wide range of consumer products. Their environmental stability, propensity for bioaccumulation, and known links to adverse health effects have evoked extensive research to characterize underlying biological mechanisms of toxicity. Of particular concern is the growing body of evidence correlating human exposure levels to behavioral deficits related to neurodevelopmental disorders. The developing nervous system is particularly sensitive to influence by environmental signals, including dysregulation by toxins. Several major modes of actions have been identified, but a clear understanding of how observed effects relate to negative impacts on human health has not been established. Here, we review the current body of evidence for PBDE-induced epigenetic disruptions, including DNA methylation, chromatin dynamics, and non-coding RNA expression while discussing the potential relationship between PBDEs and neurodevelopmental disorders.

Parkinson’s disease (PD) is a neurodegenerative disorder causing severe social and economic burdens. The origin of PD has been usually attributed to mitochondrial dysfunction. To this end, mitochondrial transcription regulators become attractive subjects for understanding PD pathogenesis. Previously, we found that the expression of mitochondrial transcription termination factor 3 (MTERF3) was reduced in MPP+-induced mice model of PD. In the present study, we probe the function of MTERF3 and its role in MPP+-induced cellular model of PD. Initially, we observe that MTERF3 expression is also reduced in MPP+-induced cellular model of PD, which can be mainly attributed to the increase of MTERF3 degradation. Next, we examine the effect of MTERF3 knockdown and overexpression on the replication, transcription, and translation of mitochondrial DNA (mtDNA). We show that knockdown and overexpression of MTERF3 have opposite effects on mtDNA transcript level but similar effects on mtDNA expression level, in line with MTERF3’s dual roles in mtDNA transcription and translation. In addition, we examine the effect of MTERF3 knockdown and overexpression on mitochondrial function with and without MPP+ treatment, and find that MTERF3 seems to play a generally protective role in MPP+-induced mitochondrial dysfunction. Together, this work suggests a regulatory role of MTERF3 in MPP+-induced cellular model of PD and may provide clues in designing novel therapeutics against PD.

Exogenous heavy metals or non-metallic waste products, for example lanthanide or iodinated contrast media for radiological procedures, may interfere with the biochemical pools in patients and in common food sources, creating an excess buildup of exogenous compounds which may reach toxic levels. Although the mechanisms are unknown, our experiments were designed to test if this toxicity can be attributed to “transmetallation” or “chelation” reactions freeing up lanthanides or chelated transition metals in acidic fruits used as phantoms representing the biologically active and mineral-rich carbohydrate matrix. The rapid breakdown of stable contrast agents have been reported at a lower pH. The interaction of such agents with native metals was examined by direct imaging of contrast infused fresh apples and sweet potatoes using low energy X-rays (40–44 kVp) and by magnetic resonance imaging at 1.5 and 3T. The stability of the exogenous agents seemed to depend on endogenous counterions and biometals in these fruits. Proton spin echo MR intensity is sensitive to paramagnetic minerals and low energy X-ray photons are sensitively absorbed by photoelectric effects in all abundant minerals and were compared before and after the infusion of radiologic contrasts. Endogenous iron and manganese are believed to accumulate due to interactions with exogenous iodine and gadolinium in and around the infusion spots. X-ray imaging had lower sensitivity (detection limit approximately 1 part in 104), while MRI sensitivity was two orders of magnitude higher (approximately 1 part in 106), but only for paramagnetic minerals like Mn and Fe in our samples. MRI evidence of such a release of metal ions from the native pool implicates transmetallation and chelation reactions that were triggered by infused contrast agents. Since Fe and Mn play significant roles in the function of metalloenzymes, our results suggest that transmetallation and chelation could be a plausible mechanism for contrast induced toxicity in vivo.

Background & Aims: The prevalence and aetiology of liver fibrosis vary over time and impact racial/ethnic groups unevenly. This study measured time trends and identified factors associated with advanced liver fibrosis in the United States. Methods: Standardised methods were used to analyse data on 47,422 participants (≥20 years old) in the National Health and Nutrition Examination Survey (1999–2018). Advanced liver fibrosis was defined as Fibrosis-4 ≥2.67 and/or Forns index ≥6.9 and elevated alanine aminotransferase. Results: The estimated number of people with advanced liver fibrosis increased from 1.3 million (95% CI 0.8–1.9) to 3.5 million (95% CI 2.8–4.2), a nearly threefold increase. Prevalence was higher in non-Hispanic Black and Mexican American persons than in non-Hispanic White persons. In multivariable logistic regression analysis, cadmium was an independent risk factor in all racial/ethnic groups. Smoking and current excessive alcohol use were risk factors in most. Importantly, compared with non-Hispanic White persons, non-Hispanic Black persons had a distinctive set of risk factors that included poverty (odds ratio [OR] 2.09; 95% CI 1.44–3.03) and susceptibility to lead exposure (OR 3.25; 95% CI 1.95–5.43) but did not include diabetes (OR 0.88; 95% CI 0.61–1.27; p =0.52). Non-Hispanic Black persons were more likely to have high exposure to lead, cadmium, polychlorinated biphenyls, and poverty than non-Hispanic White persons. Conclusions: The number of people with advanced liver fibrosis has increased, creating a need to expand the liver care workforce. The risk factors for advanced fibrosis vary by race/ethnicity. These differences provide useful information for designing screening programmes. Poverty and toxic exposures were associated with the high prevalence of advanced liver fibrosis in non-Hispanic Black persons and need to be addressed. Impact and Implications: Because liver disease often produces few warning signs, simple and inexpensive screening tests that can be performed by non-specialists are needed to allow timely diagnosis and linkage to care. This study shows that non-Hispanic Black persons have a distinctive set of risk factors that need to be taken into account when designing liver disease screening programs. Exposure to exogenous toxins may be especially important risk factors for advanced liver fibrosis in non-Hispanic Black persons.

Introduction Post-partum depression (PPD) affects up to 19.1% of pregnancies and is associated with increased levels of proinflammatory cytokines, inflammation, and reductions in brain-derived neurotrophic factor (BDNF). Previous work by our team suggests that environmental toxins such as polybrominated diphenyl ethers (PBDEs) enhance placental inflammation and reduce BDNF production. Nearly, 100% of studied women in California have some level of exposure to these compounds due to extensive use of the flame retardants. High levels of exposure to PBDEs has been linked to increased risk of adverse pregnancy complications associated with placental inflammation such as preterm birth and gestational diabetes but their effects on risk of PPD is unclear. Objective To determine if PPD is associated with higher levels of PBDE-47, the most common PBDE congener in maternal plasma. Methods PBDE-47 was quantified in first trimester plasma samples collected from a cohort of 367 asymptomatic pregnant women that were routinely screened for depressive symptoms for 1 year post-partum. Data were analyzed using general linear models and multivariable logistic regression to determine if higher levels of PBDE-47 in the first trimester are associated with development of PPD. Results Women who developed PPD (n = 22) had significantly higher PBDE-47 levels in their plasma (p=.031) relative to those in which PPD was not diagnosed. Logistic regression analysis suggested that each two-fold increase in PBDE-47 concentrations increased the risk of PPD by 22% (OR = 1.22, 95% CI: 1.03, 1.47). Groups were similar regarding PTB rate, race-ethnicity, parity, child’s sex, maternal pre-pregnancy obesity status, maternal age, family income, and study center. Results remained significant after adjustment for these possible confounding factors. Conclusions These results suggest that PBDE-47 exposure in the first trimester is associated with increased risk of PPD. [ABSTRACT FROM AUTHOR]

Release of toxic substances in water bodies from various sources is a major threat to ecologically most vulnerable aquatic food-chain. Again, planktons which hold the whole aquatic ecosystem by serving as the basic food sources, appear to be the most sensitive aquatic organisms to environmental toxins. Consequently all the fish species from prey to predator find it hard to survive in the toxic environment, severely affecting the fishing yields. The unpleasant truth is that toxicants in the environment are continuously increasing due to different natural and human activities. Thus, it is worthy to study a fishery model in the presence of environmental toxins. In this paper, we design a toxicated intraguild fishery model where the shared biotic resource fixes the logistic carrying capacities for both prey and predator fish species. We also introduce the concept of time delay to consider the gestation time for prey and predator species. We locate all the possible equilibria and then investigate the local asymptotic stable behaviour of the coexistence equilibrium point. For the delayed model, we analysis the occurrence of Hopf bifurcation by taking time delay as a bifurcation parameter. It establishes that the delayed model goes under Hopf bifurcation when the delay passes through a certain threshold value. Then, we construct a quadratic cost function to find a sustainable harvesting policy for the process of maximizing monetary profit from harvesting yields. The proposed work is finally validated by numerical simulations. Some future directions are also included after the concluding remarks. [ABSTRACT FROM AUTHOR]

Chronic exposure to some environmental polluting chemicals (EPCs) is strongly associated with metabolic syndrome, and insulin resistance is a major biochemical abnormality in the skeletal muscle in patients with metabolic syndrome. However, the causal relationship is inconsistent and little is known about how EPCs affect the insulin signaling cascade in skeletal muscle. Here, we investigated whether exposure to 100 pM of 2,3,7,8-tetrachlorodibenzodioxin (TCDD) as a low dose of dioxin induces insulin resistance in C2C12 myocytes. The treatment with TCDD inhibited the insulin-stimulated glucose uptake and translocation of glucose transporter 4 (GLUT4). The low-dose TCDD reduced the expression of insulin receptor β (IRβ) and insulin receptor substrate (IRS)-1 without affecting the phosphorylation of Akt. The TCDD impaired mitochondrial activities, leading to reactive oxygen species (ROS) production and the blockage of insulin-induced Ca2+ release. All TCDD-mediated effects related to insulin resistance were still observed in aryl hydrocarbon receptor (AhR)-deficient myocytes and prevented by MitoTEMPO, a mitochondria-targeting ROS scavenger. These results suggest that low-dose TCDD stress may induce muscle insulin resistance AhR-independently and that mitochondrial oxidative stress is a novel therapeutic target for dioxin-induced insulin resistance. [ABSTRACT FROM AUTHOR]

Biosynthesized nanocomposites, particularly those incorporating carbon-based materials, exhibit exceptional tunability and multifunctionality, surpassing the capabilities of conventional materials in these aspects. Developing practical solutions is critical to address environmental toxins from pharmaceuticals, heavy metals, pesticides, and dyes. Biomass waste is a readily available carbon source, which emerges as a promising material for producing biochar due to its inherent advantages: abundance, low cost, and environmentally friendly nature. This distribution mainly uses carbon-based materials (CBMs) and biomass waste in wastewater treatment. This review paper investigates several CBM types, including carbon aerogels, nanotubes, graphene, and activated carbon. The development of bio-derived carbon-based nanomaterials are discussed, along with the properties and composition of carbon materials derived from biomass waste and various cycles, such as photodegradation, adsorption, and high-level oxidation processes for natural remediation. In conclusion, this review examines the challenges associated with biochar utilization, including cost, recovery, and practical implementation. [Display omitted] • The primary characteristics, methodologies, and usage of biochar-based carbon for environmental remediation. • The use of carbon-based materials derived from biomass. • This review also focuses on various carbon-based materials and combination strategies. • Biomass derived carbon nanocomposites are cost effective, emerging and promising technique. • Composites made from biochar used to clean up contaminated areas in a sustainable way. [ABSTRACT FROM AUTHOR]

Man and environment have a strong connection with each other for their functioning. Environmental toxins which can be natural or manmade result in the loss of this balance by causing systemic inflammatory response within the human body, with the brain being the most affected target end-organ. These problems are more prominent in Third World countries, where environmental regulations laws are either relaxed or non-existent. These neurotoxins play a very important aetiological role in the manifestation of various neurodegenerative diseases, neurodevelopmental disorders and psychiatric disorders. Environmental neurotoxicity results from inhibition of mitochondrial activity, excess oxidative stress leading to neuroinflammation, and promoting apoptosis and neuronal cell death. Having the know-how of these neurotoxins will provide insight into the process of neurodegeneration and will result in further designing of studies to delve into processes and mechanisms of neuronal regeneration and axonal sprouting. This review highlights the various central nervous system disorders associated with exposure to environmental neurotoxins and discusses the way forward to prevent or halt the process of neurodegeneration.

Electromagnetic signals from everyday wireless technologies are an ever-present environmental stressor, affecting biological systems. In this article, we substantiate this statement based on the weight of evidence from papers collated within the ORSAA database (ODEB), focusing on the biological and health effects of electromagnetic fields and radiation. More specifically, the experiments investigating exposures from real-world devices and the epidemiology studies examining the effects of living near mobile phone base stations were extracted from ODEB and the number of papers showing effects was compared with the number showing no effects. The results showed that two-thirds of the experimental and epidemiological papers found significant biological effects. The breadth of biological and health categories where effects have been found was subsequently explored, revealing hundreds of papers showing fundamental biological processes that are impacted, such as protein damage, biochemical changes and oxidative stress. This understanding is targeted toward health professionals and policy makers who have not been exposed to this issue during training. To inform this readership, some of the major biological effect categories and plausible mechanisms of action from the reviewed literature are described. Also presented are a set of best practice guidelines for treating patients affected by electromagnetic exposures and for using technology safely in health care settings. In conclusion, there is an extensive evidence base revealing that significant stress to human biological systems is being imposed by exposure to everyday wireless communication devices and supporting infrastructure. This evidence is compelling enough to warrant an update in medical education and practice.

Man and environment have a strong connection with each other for their functioning. Environmental toxins which can be natural or manmade result in the loss of this balance by causing systemic inflammatory response within the human body, with the brain being the most affected target end-organ. These problems are more prominent in Third World countries, where environmental regulations laws are either relaxed or non-existent. These neurotoxins play a very important aetiological role in the manifestation of various neurodegenerative diseases, neurodevelopmental disorders and psychiatric disorders. Environmental neurotoxicity results from inhibition of mitochondrial activity, excess oxidative stress leading to neuroinflammation, and promoting apoptosis and neuronal cell death. Having the know-how of these neurotoxins will provide insight into the process of neurodegeneration and will result in further designing of studies to delve into processes and mechanisms of neuronal regeneration and axonal sprouting. This review highlights the various central nervous system disorders associated with exposure to environmental neurotoxins and discusses the way forward to prevent or halt the process of neurodegeneration. [ABSTRACT FROM AUTHOR]

Background: Risk factors for pancreatic ductal adenocarcinoma (PDAC) include tobacco/alcohol abuse, genetic predisposition, insulin resistance, and pancreatic cysts. Despite these well-established risk factors and the screening of high-risk individuals, some people still develop PDAC. This study aims to explore a potential risk factor for PDAC by investigating the association between fungal toxins (FT) and environmental toxins (ET) and the disease. We predicted that individuals with PDAC would have higher levels of these toxins compared to healthy controls. The rationale behind this hypothesis is that exposure to FT and ET might contribute to the development of PDAC by elevating cancer risk., Methods: A pilot retrospective cohort study was conducted at Moffitt Cancer Center from 2022 to 2023. This study compared FT and ET levels, demographic data, and PDAC features between subjects with PDAC and healthy controls., Results: Forty subjects were enrolled in the study, comprising 20 with pancreatic ductal adenocarcinoma (PDAC) and 20 healthy controls. Baseline demographics were similar between the two groups. Among the PDAC subjects, the most common tumor location was the head of the pancreas (55%); 30% had locally advanced disease, 45% were borderline resectable, and 10% had metastatic disease. Compared to the controls, subjects with PDAC had significantly higher levels of fungal toxins (FTs) including ochratoxin, gliotoxin, and citrinin (p < 0.05). Additionally, PDAC patients had significantly elevated levels of environmental toxins (ETs) such as methyl tert-butyl ether (MTBE), xylene, styrene, acrylonitrile, perchlorate, diphenyl phosphate, bromopropane, organophosphates, acrolein, tiglylglycine, and diethylphosphate (p < 0.05)., Conclusion: Our study demonstrates that subjects with PDAC, without other risk factors, have higher FT and ET levels than controls. Further studies are needed to evaluate whether ET and FT exposure can be clinically utilized as a risk factor for PDAC development., (© 2024. The Author(s).)

Environmental pollution is an inevitable ecological issue accompanying the process of socialization, with increasing attention to its impacts on individual organisms and ecological chains. The reproductive system, responsible for transmitting genetic material in animals, is one of the most sensitive systems to environmental toxins. Research reveals that Sertoli cells are the primary target cells for the action of environmental toxins. Different environmental toxins mostly affect the blood-testis barrier and lead to male reproductive disorders by disrupting Sertoli cells. Therefore, this article provides an in-depth exploration of the toxic mechanisms of various types of environmental toxins on the male testes. It reveals the dynamic processes of tight junctions in the blood-testis barrier affected by environmental toxins and their specific roles in the reconstruction process., (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

This article reviews the effects of chronic fluorosis on the brain and possible mechanisms. We used PubMed, Medline and Cochraine databases to collect data on fluorosis, brain injury, and pathogenesis. A large number of in vivo and in vitro studies and epidemiological investigations have found that chronic fluorosis can cause brain damage, resulting in abnormal brain structure and brain function.Chronic fluorosis not only causes a decline in concentration, learning, and memory, but also has mental symptoms such as anxiety, tension, and depression. Several possible mechanisms that have been proposed: the oxidative stress and inflammation theory, neural cell apoptosis theory, neurotransmitter imbalance theory, as well as the doctrine of the interaction of fluorine with other elements. However, the specific mechanism of chronic fluorosis on brain damage is still unclear. Thus, a better understanding of the mechanisms via which chronic fluorosis causes brain damage is of great significance to protect the physical and mental health of people in developing countries, especially those living in the endemic areas of fluorosis. In brief, further investigation concerning the influence of fluoride on the brain should be conducted as the neural damage induced by it may bring about a huge problem in public health, especially considering growing environmental pollution.

Exogenous heavy metals or non-metallic waste products, for example lanthanide or iodinated contrast media for radiological procedures, may interfere with the biochemical pools in patients and in common food sources, creating an excess buildup of exogenous compounds which may reach toxic levels. Although the mechanisms are unknown, our experiments were designed to test if this toxicity can be attributed to "transmetallation" or "chelation" reactions freeing up lanthanides or chelated transition metals in acidic fruits used as phantoms representing the biologically active and mineral-rich carbohydrate matrix. The rapid breakdown of stable contrast agents have been reported at a lower pH. The interaction of such agents with native metals was examined by direct imaging of contrast infused fresh apples and sweet potatoes using low energy X-rays (40–44 kVp) and by magnetic resonance imaging at 1.5 and 3T. The stability of the exogenous agents seemed to depend on endogenous counterions and biometals in these fruits. Proton spin echo MR intensity is sensitive to paramagnetic minerals and low energy X-ray photons are sensitively absorbed by photoelectric effects in all abundant minerals and were compared before and after the infusion of radiologic contrasts. Endogenous iron and manganese are believed to accumulate due to interactions with exogenous iodine and gadolinium in and around the infusion spots. X-ray imaging had lower sensitivity (detection limit approximately 1 part in 104), while MRI sensitivity was two orders of magnitude higher (approximately 1 part in 106), but only for paramagnetic minerals like Mn and Fe in our samples. MRI evidence of such a release of metal ions from the native pool implicates transmetallation and chelation reactions that were triggered by infused contrast agents. Since Fe and Mn play significant roles in the function of metalloenzymes, our results suggest that transmetallation and chelation could be a plausible mechanism for contrast induced toxicity in vivo. [ABSTRACT FROM AUTHOR]

This commentary reflects on research studies included in this special issue, Black Lives Matter! Systems of Oppression Affecting Black Youth. A key finding in these studies is significance of developmental and social behavioral sciences to center systemic racism and oppression in studies of Black youth to more fully understand and explain how contextual factors and processes impact their everyday life experiences. This collection of papers offers insights and recommendations of ways advance research studies by expanding research to include upstream policies and practices and explain their roles in perpetuating oppression and discrimination. Applying multi‐socio‐ecological theoretical frameworks may demonstrate effective pathways to reduce environmental toxins that hinder positive health and well‐being for adolescents, their families, and communities. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancer types with a limited overall survival rate due to the asymptomatic progression of symptoms in metastatic stages of the malignancy and the lack of an early reliable diagnostic biomarker. MicroRNAs (miRs/miRNAs) are small (~18–24 nucleotides), endogenous, non-coding RNAs, which are closely linked to the development of numerous malignancies comprising PDAC. Recent studies have described the role of environmental pollutants such as nickel (Ni) in PDAC, but the mechanisms of Ni-mediated toxicity in cancer are still not completely understood. Specifically, Ni has been found to alter the expression and function of miRs in several malignancies, leading to changes in target gene expression. In this study, we found that levels of Ni were significantly higher in cancerous tissue, thus implicating Ni in pancreatic carcinogenesis. Hence, in vitro studies followed by using both normal and pancreatic tumor cell lines and increasing Ni concentration increased lethality. Comparing LC50 values, Ni-acetate groups demonstrated lower values needed than in NiCl2 groups, suggesting greater Ni-acetate. Panc-10.05 cell line appeared the most sensitive to Ni compounds. Exposure to Ni-acetate resulted in an increased phospho-AKT, and decreased FOXO1 expression in Panc-10.05 cells, while NiCl2 also increased PTEN expression in Panc-10.05 cells. Specifically, following NiCl2 exposure to PDAC cells, the expression levels of miR-221 and miR-155 were significantly upregulated, while the expression levels of miR-126 were significantly decreased. Hence, our study has suggested pilot insights to indicate that the environmental pollutant Ni plays an important role in the progression of PDAC by promoting an association between miRs and Ni exposure during PDAC pathogenesis. [ABSTRACT FROM AUTHOR]

Lead acetate (PbAc) is one of the toxic metals in the environment which causes many effects on different organs of the body. And due to the importance of the olive tree, with its healthy and protective elements against many diseases, the leaf extract of this tree was chosen in our study. Therefore, the aim of this study was to investigate the role of olive leaf (Olea europea L.) extract (OLE) against PbAc-induced sperm toxicity, sex hormone changes, oxidative stress, and histopathological changes in rats. Twenty male Wistar rats were divided into four groups (group 1, as control; group 2, OLE; group 3, PbAc; group 4, PbAc+OLE). In the PbAc group, the body weight, testis and epididymis weights, sexual hormones, sperm characteristics, GR, GPx, GST, GSH, SOD, and CAT were significantly decreased, and the sperm abnormality and TBARS level were significant increase when compared with control and OLE groups. Also, numerous damages to testicular tissue were observed in the PbAc group when compared to the control group, while the treatment with OLE in the fourth group led to improvement of sex hormones, semen characteristics, oxidative stress, and testicular tissue damage caused by PbAc. It can be concluded that OLE has a protective and ameliorative effects against PbAc-induced oxidative stress, apoptosis and alterations in testicular tissue, and sperm quality in rats. [ABSTRACT FROM AUTHOR]

In the present study, we investigate the selective feeding of zooplankton on phytoplankton infected by free-viruses in the presence of environmental toxins in the marine ecosystem. The environmental toxins assume to decrease the growth rate of susceptible phytoplankton, and increase the death rate of infected phytoplankton and zooplankton. Global sensitivity analysis identifies important parameters of the system having crucial impact on the aquatic health. The coexistence equilibrium of the system stabilizes on increasing the parameters related to inhibition of phytoplankton growth due to environmental toxins and the force of infection, and destabilizes on increasing the carrying capacity of susceptible phytoplankton and preference of zooplankton on infected phytoplankton. The chance of extinction of free-viruses increases on increasing the preference of zooplankton on infected phytoplankton or decreasing the force of infection. Moreover, if the input rate of environmental toxins is high, then the system becomes zooplankton-free for higher values of force of infection. On increasing the values of preference of zooplankton on infected phytoplankton, the system exhibits transition from stable coexistence to oscillations around coexistence equilibrium to oscillations around disease-free equilibrium. We observe that the presence of free-viruses and environmental toxins in the system drive zooplankton population to very low equilibrium values but the ecological balance of the aquatic food web can be maintained by modulating the decay (depletion) rate of free-viruses (environmental toxins).

Deoxynivalenol (DON) is a prevalent Fusarium mycotoxin, occurs predominantly in the global environment, especially in cereals, animal feed and food commodities. The widespread contamination causes a serious risk to human and animal health. DON usually impairs weight gain, which is presumably from its capacity to reduce feed intake by interfering with intestinal motility. To clarify the role of smooth muscle cells (SMCs) contractility in intestinal motility and growth inhibition caused by DON, twelve weaned piglets were firstly divided into two groups to feed control or Fusarium mycotoxin-contaminated (MC) diet. Results showed that the final body weight, average daily gain and average daily feed intake were significantly reduced in piglets fed the MC diet. Exposure to the MC diet also significantly decreased the thickness of smooth muscle layer and SMCs contractile markers expression (myosin heavy chain 11, smooth muscle actin gamma 2, transgelin, calponin 1) in jejunum and ileum of piglets. Furthermore, oral DON supplementation (3 mg/kg body weight) to mice in six consecutive days could significantly inhibit the upper intestinal transit, impede normal defecation and downregulate SMCs contractile markers expression in small intestine. Finally, we generated a porcine enteric smooth muscle cell line (PISMC), and found that DON could depress its contractility by decreasing PISMC proliferation, migration and contractile markers expression. In conclusion, these findings in vivo and in vitro suggest that DON, as a common environmental toxin, can not only reduce proliferative and motile phenotype, but also decrease contractile apparatus components (contractile markers expression) in SMCs, which in turn influences SMCs contractility and then interferes with intestinal motility and growth performance.

Alteration in DNA methylation after aluminum exposure has been shown to contribute in pathogenesis of Alzheimer's disease (AD). This study is aimed to determine the effect of Al exposure (42 and 60 days) on learning and memory and the expression of proteins involved in DNA methylation (MBD1, MBD2, MBD3, MeCP2 (methyl CpG binding protein 2), DnMT1 and DnMT3a). Male BALB/c mice were treated with AlCl3 for either 42 days or 60 days. After treatment completion, learning and memory were compared to the control group using novel object recognition test, elevated plus maze test, open field test, and Morris water maze test. The treated animals and their respective controls were sacrificed after cognitive testing and samples from their whole cortex and hippocampus were harvested for gene expression analysis. Mice treated with AlCl3 showed significant cognitive deficit with impaired short-term memory, elevated anxiety, and deterioration in spatial and reference memory. The AlCl3 treatment showed significant reduction in the expression of MBDs in the whole cortex at 60 days of treatment as compared to control. AlCl3-treated animals showed decreased expression of MBDs and DnMT3a in the hippocampus for longer treated animals but strikingly, MBD2 showed significantly increased expression in AlCl3-treated animals at 60 days p ≤ 0.001. In conclusion, this study showed that AlCl3-treated animals showed significant memory and cognitive deficits and it is associated with significant changes in the expression of proteins involved in DNA methylation mechanism. Moreover, different Al exposure duration had slightly different effects. [ABSTRACT FROM AUTHOR]