scholarly journals Biomarkers of Environmental Toxicants: Exposure and Biological Effects

Toxics ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 37
Author(s):  
Robert J. Turesky ◽  
Kun Lu
Keyword(s):  
Disease Risk ◽  
Biological Effects ◽  
Environmental Toxicants

Biomarkers of environmental toxicants are measures of exposures and effects, some of which can serve to assess disease risk and interindividual susceptibilities [...]

The current state of mycotoxin biomarker development in humans and animals and the potential for application to plant systems

2011 ◽  
Vol 4 (3) ◽  
pp. 257-270 ◽  
Author(s):  
T. Baldwin ◽  
R. Riley ◽  
N. Zitomer ◽  
K. Voss ◽  
R. Coulombe Jr. ◽  
...  
Keyword(s):  
Disease Risk ◽  
Biological Effects ◽  
Fusarium Verticillioides ◽  
Laboratory Animals ◽  
Plant Tissues ◽  
Living Plant ◽  
Disease Symptoms ◽  
Mechanisms Of Toxicity ◽  
Livestock Feeds ◽  
Commercially Important

Filamentous fungi that contaminate livestock feeds and human food supply often produce toxigenic secondary metabolites known as mycotoxins. Among the hundreds of known mycotoxins, aflatoxins, deoxynivalenol, fumonisins, ochratoxin A and zearalenone are considered the most commercially important. Intense research on these mycotoxins, especially aflatoxin, has resulted in the development of 'biomarkers' used to link exposure to disease risk. In the case of aflatoxin this effort has led to the discovery of both exposure and mechanism-based biomarkers, which have proven essential for understanding aflatoxin's potential for causing disease in humans, including subtle effects on growth and immune response. Fumonisin biomarkers have also been used extensively in farm and laboratory animals to study the fumonisin-induced disruption of cellular and systemic physiology which leads to disease. This review summarises the status of mycotoxin biomarker development in humans and animals for the commercially important mycotoxins. Since the fungi responsible for the production of these mycotoxins are often endophytes that infect and colonise living plant tissues, accumulation of mycotoxins in the plant tissues may at times be associated with development of plant disease symptoms. The presence of mycotoxins, even in the absence of disease symptoms, may still have subtle biological effects on the physiology of plants. This review examines the question of whether or not the knowledge gained from mechanistic studies and development of biomarkers in animal and human systems is transferable to the study of mycotoxin effects on plant systems. Thus far, fumonisin has proven amenable to development of mechanism-based biomarkers to study maize seedling disease caused by the fumonisin producer, Fusarium verticillioides. Expanding our knowledge of mechanisms of toxicity and the overt and subtle effects on animal, human, and plant systems through the identification and validation of biomarkers will further our ability to monitor and limit the damage and economic impact of mycotoxins.

scholarly journals The role of nutrition in influencing mechanisms involved in environmentally mediated diseases

2018 ◽  
Vol 33 (1) ◽  
pp. 87-97 ◽  
Author(s):  
Bernhard Hennig ◽  
Michael C. Petriello ◽  
Mary V. Gamble ◽  
Young-Joon Surh ◽  
Laura A. Kresty ◽  
...  
Keyword(s):  
Flame Retardants ◽  
Disease Risk ◽  
Cumulative Risk ◽  
Southeast Asian ◽  
Environmental Toxicology ◽  
Environmental Toxicants ◽  
Omega 3 ◽  
Lifestyle Modifications ◽  
The World ◽  
The Impact

AbstractHuman exposure to environmental contaminants such as persistent chlorinated organics, heavy metals, pesticides, phthalates, flame retardants, electronic waste and airborne pollutants around the world, and especially in Southeast Asian regions, are significant and require urgent attention. Given this widespread contamination and abundance of such toxins as persistent organic pollutants (POPs) in the ecosystem, it is unlikely that remediation alone will be sufficient to address the health impacts associated with this exposure. Furthermore, we must assume that the impact on health of some of these contaminants results in populations with extraordinary vulnerabilities to disease risks. Further exacerbating risk; infectious diseases, poverty and malnutrition are common in the Southeast Asian regions of the world. Thus, exploring preventive measures of environmental exposure and disease risk through new paradigms of environmental toxicology, optimal and/or healthful nutrition and health is essential. For example, folic acid supplementation can lower blood arsenic levels, and plant-derived bioactive nutrients can lower cardiovascular and cancer risks linked to pollutant exposure. Data also indicate that diets enriched with bioactive food components such as polyphenols and omega-3 polyunsaturated fatty acids can prevent or decrease toxicant-induced inflammation. Thus, consuming healthy diets that exhibit high levels of antioxidant and anti-inflammatory properties, is a meaningful way to reduce the vulnerability to non-communicable diseases linked to environmental toxic insults. This nutritional paradigm in environmental toxicology requires further study in order to improve our understanding of the relationship between nutrition or other lifestyle modifications and toxicant-induced diseases. Understanding mechanistic relationships between nutritional modulation of environmental toxicants and susceptibility to disease development are important for both cumulative risk assessment and the design and implementation of future public health programs and behavioral interventions.

Neonatal exposure to BPA, BDE-99, and PCB produces persistent changes in hepatic transcriptome associated with gut dysbiosis in adult mouse livers

2021 ◽  
Author(s):  
Joe Jongpyo Lim ◽  
Moumita Dutta ◽  
Joseph L Dempsey ◽  
Hans-Joachim Lehmler ◽  
James MacDonald ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Gut Microbiome ◽  
Polybrominated Diphenyl Ethers ◽  
Early Life ◽  
Disease Risk ◽  
Neonatal Exposure ◽  
Environmental Toxicants ◽  
Early Life Exposure ◽  
Microbial Biomarkers ◽  
Hepatic Transcriptome

Abstract Recent evidence suggests that complex diseases can result from early life exposure to environmental toxicants. Polybrominated diphenyl ethers (PBDEs), and polychlorinated biphenyls (PCBs) are persistent organic pollutants (POPs) and remain a continuing risk to human health despite being banned from production. Developmental BPA exposure mediated-adult onset of liver cancer via epigenetic reprogramming mechanisms has been identified. Here, we investigated whether the gut microbiome and liver can be persistently reprogrammed following neonatal exposure to POPs, and the associations between microbial biomarkers and disease-prone changes in the hepatic transcriptome in adulthood, compared to BPA. C57BL/6 male and female mouse pups were orally administered vehicle, BPA, BDE-99 (a breast milk-enriched PBDE congener), or the Fox River PCB mixture (PCBs), once daily for three consecutive days (postnatal days [PND] 2 to 4). Tissues were collected at PND5 and PND60. Among the three chemicals investigated, early life exposure to BDE-99 produced the most prominent developmental reprogramming of the gut-liver axis, including hepatic inflammatory and cancer-prone signatures. In adulthood, neonatal BDE-99 exposure resulted in a persistent increase in Akkermansia muciniphila throughout the intestine, accompanied by increased hepatic levels of acetate and succinate, the known products of A. muciniphila. In males, this was positively associated with permissive epigenetic marks H3K4me1 and H3K27, which were enriched in loci near liver cancer-related genes that were dysregulated following neonatal exposure to BDE-99. Our findings provide novel insights that early life exposure to POPs can have a life-long impact on disease risk, which may partly be regulated by the gut microbiome.

scholarly journals Biological Impact of Unilateral Oophorectomy: Does the Number of Ovaries Really Matter?

2020 ◽  
Author(s):  
Maria Luisa Gasparri ◽  
Ilary Ruscito ◽  
Elena Ioana Braicu ◽  
Jalid Sehouli ◽  
Luca Tramontano ◽  
...  
Keyword(s):  
Neurological Disease ◽  
Disease Risk ◽  
Biological Effects ◽  
Age At Onset ◽  
Reproductive Age ◽  
Bilateral Oophorectomy ◽  
Compensatory Mechanisms ◽  
Manual Search ◽  
Risk Of Mortality ◽  
Increased Risk

AbstractAlthough unilateral oophorectomies are performed more often than bilateral ones in women of reproductive age, their clinical consequences have been less intensively investigated. Experimental models in animals have shown that compensatory mechanisms occur after a unilateral oophorectomy (UO). This review aims to summarize the available evidence on the biological effects of unilateral oophorectomy on women. Evaluated outcomes include age at onset of menopause, risk of cardiovascular and neurological disease, risk of mortality and fertility outcome after spontaneous conception or in vitro fertilization (IVF). Results were compared with findings reported after bilateral oophorectomy and/or ovarian excision and/or women with intact ovaries. An electronic database search was performed using PubMed and Scopus, followed by a manual search to identify controlled studies that compared women after UO with women with two intact ovaries. In particular, a systematic review of fertility outcomes after IVF was performed, and the data were summarized in a table. Women who underwent UO had a similar age at menopause and similar clinical pregnancy rate compared to women with two ovaries. However, decreased ovarian reserve affecting the quantity but not the quality of the ovarian pool after IVF was observed in the UO group. Furthermore, an increased risk of neurological disease and even an increased risk of mortality was observed in women with single ovary. These data need to be confirmed by further studies, and a plausible mechanism of action must be identified. At present, patients who undergo UO can be reassured with regard to their reproductive potential and their age at onset of menopause.

scholarly journals Maternal environmental exposure to bisphenols and epigenome-wide DNA methylation in infant cord blood

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Carolyn F McCabe ◽  
Vasantha Padmanabhan ◽  
Dana C Dolinoy ◽  
Steven E Domino ◽  
Tamara R Jones ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cord Blood ◽  
Disease Risk ◽  
Estimation Algorithm ◽  
First Trimester ◽  
Type I ◽  
Environmental Toxicants ◽  
Cell Type ◽  
Bisphenol S ◽  
Blood Leukocytes

Abstract Maternal prenatal exposures, including bisphenol A (BPA), are associated with offspring’s risk of disease later in life. Alterations in DNA methylation may be a mechanism through which altered prenatal conditions (e.g. maternal exposure to environmental toxicants) elicit this disease risk. In the Michigan Mother and Infant Pairs Cohort, maternal first-trimester urinary BPA, bisphenol F, and bisphenol S concentrations were tested for association with DNA methylation patterns in infant umbilical cord blood leukocytes (N = 69). We used the Illumina Infinium MethylationEPIC BeadChip to quantitatively evaluate DNA methylation across the epigenome; 822 020 probes passed pre-processing and quality checks. Single-site DNA methylation and bisphenol models were adjusted for infant sex, estimated cell-type proportions (determined using cell-type estimation algorithm), and batch as covariates. Thirty-eight CpG sites [false discovery rate (FDR) <0.05] were significantly associated with maternal BPA exposure. Increasing BPA concentrations were associated with lower DNA methylation at 87% of significant sites. BPA exposure associated DNA methylation sites were enriched for 38 pathways significant at FDR <0.05. The pathway or gene-set with the greatest odds of enrichment for differential methylation (FDR <0.05) was type I interferon receptor binding. This study provides a novel understanding of fetal response to maternal bisphenol exposure through epigenetic change.

Epigenetics

2019 ◽  
pp. 239-268
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Air Pollution ◽  
Disease Risk ◽  
Environmental Pollutants ◽  
State Regulation ◽  
Metal Exposure ◽  
Environmental Toxicants ◽  
Water Chlorination ◽  
Epigenetic Patterns

This chapter focuses on epigenetics: the study of stable, often heritable changes that influence gene expression but are not mediated by DNA sequence. These changes play crucial roles in chromatin state regulation which influences processes such as gene expression, DNA repair, and recombination. Evidence demonstrates that epigenetic patterns are altered by environmental factors which are associated with disease risk including diet, smoking, alcohol intake, environmental toxicants, and stress. Studiers have linked environmental pollutants with epigenetic variations particularly changes in DNA methylation, histone modifications, and microRNAs. Growing data have linked epigenetic alterations with heavy metal exposure, organic toxicants, and water chlorination by-products. Studies focusing on the effects of air pollution in humans demonstrate an association between exposure to air pollution and DNA methylation. Several classes of pesticides can modify epigenetic marks, including endocrine disruptors, persistent organic pollutants, arsenic, several herbicides, and insecticides. This chapter explores epigenetics.

scholarly journals High antioxidant - and anthocyanin contents of sour cherry cultivars may benefit the human health: international and Hungarian achievements on phytochemicals

2006 ◽  
Vol 12 (3) ◽  
Author(s):  
Zs. Veres ◽  
I. J. Holb ◽  
I. J. Nyéki ◽  
Z. Szabó ◽  
J. Remenyik ◽  
...  
Keyword(s):  
Human Health ◽  
Fruits And Vegetables ◽  
Disease Risk ◽  
Vegetable Consumption ◽  
Biological Effects ◽  
Sour Cherry ◽  
Specific Pattern ◽  
Published Data ◽  
Total Antioxidant ◽  
Endogenous Antioxidant

Evidence suggests that a diet with high fruit and vegetable consumption may decrease the risk of chronic diseases, such as cardiovascular diseases and cancer, and phytochemicals including phenolics, flavonoids and carotenoids from fruits and vegetables may play a key role in reducing chronic disease risk. Recent research has proved that sour cherry (Prunus cerasus L.) is a valuable natural source of some bioactive compounds important in human health preservation. According to the published data, the most important biological effects of sour cherry are connected — directly or indirectly — to their endogenous antioxidant behaviour as well as to their specific pattern of anthocyanin components. In the present work, we measured the total antioxidant capacity of some Hungarian sour cherry varieties in combination with their anthocyanin-, and vitamin-C content. In 2003, twelve clones were selected and grafted from a local sour cherry population called "Bosnyák" sour cherry grown in small home gardens and farms of the village Csengod (Great-Plain Region, South Hungary). Other Hungarian sour cherry varieties, i.e. cv. Újfehértói fürtos, cv. Érdi bőterrnő, cv. Debreceni bőterrnő, cv. Csengődi and cv. Kántorjánosi served as a control.

scholarly journals Exposing the Exposome with Global Metabolomics and Cognitive Computing

2017 ◽  
Author(s):  
Benedikt Warth ◽  
Scott Spangler ◽  
Mingliang Fang ◽  
Caroline H Johnson ◽  
Erica M Forsberg ◽  
...  
Keyword(s):  
Biological Effects ◽  
Toxic Effects ◽  
Environmental Toxicants ◽  
Cognitive Computing ◽  
Food Contaminants ◽  
New Paradigm ◽  
Chemical Structures ◽  
Health And Disease ◽  
User Friendly ◽  
The Impact

AbstractConcurrent exposure to a wide variety of xenobiotics and their combined toxic effects can play a pivotal role in health and disease, yet are largely unexplored. Investigating the totality of these exposures, i.e. the exposome, and their specific biological effects constitutes a new paradigm for environmental health but still lacks high-throughput, user-friendly technology. We demonstrate the utility of mass spectrometry-based global exposure metabolomics combined with tailored database queries and cognitive computing for comprehensive exposure assessment and the straightforward elucidation of biological effects. The METLIN Exposome database has been redesigned to help identify environmental toxicants, food contaminants and supplements, drugs, and antibiotics as well as their biotransformation products, through its expansion with over 700,000 chemical structures to now include more than 950,000 unique small molecules. More importantly, we demonstrate how the XCMS/METLIN platform now allows for the readout of the biological effect of a toxicant through metabolomic-derived pathway analysis and further, cognitive computing provides a means of assessing the role of a potential toxicant. The presented workflow addresses many of the outstanding methodological challenges current exposome research is facing and will serve to gain a deeper understanding of the impact of environmental exposures and combinatory toxic effects on human health.

scholarly journals Nutritional impact on Immunological maturation during Childhood in relation to the Environment (NICE): a prospective birth cohort in northern Sweden

BMJ Open ◽  
2018 ◽  
Vol 8 (10) ◽  
pp. e022013 ◽  
Author(s):  
Malin Barman ◽  
Fiona Murray ◽  
Angelina I Bernardi ◽  
Karin Broberg ◽  
Sven Bölte ◽  
...  
Keyword(s):  
Oral Health ◽  
Birth Cohort ◽  
Biological Samples ◽  
Disease Risk ◽  
Skin Prick Testing ◽  
Ethical Review ◽  
Environmental Toxicants ◽  
Birth Cohorts ◽  
The North ◽  
Prospective Birth Cohort

IntroductionPrenatal and neonatal environmental factors, such as nutrition, microbes and toxicants, may affect health throughout life. Many diseases, such as allergy and impaired child development, may be programmed already in utero or during early infancy. Birth cohorts are important tools to study associations between early life exposure and disease risk. Here, we describe the study protocol of the prospective birth cohort, ‘Nutritional impact on Immunological maturation during Childhood in relation to the Environment’ (NICE). The primary aim of the NICE cohort is to clarify the effect of key environmental exposures—diet, microbes and environmental toxicants—during pregnancy and early childhood, on the maturation of the infant’s immune system, including initiation of sensitisation and allergy as well as some secondary outcomes: infant growth, obesity, neurological development and oral health.Methods and analysisThe NICE cohort will recruit about 650 families during mid-pregnancy. The principal inclusion criterion will be planned birth at the Sunderby Hospital in the north of Sweden, during 2015–2018. Questionnaires data and biological samples will be collected at 10 time-points, from pregnancy until the children reach 4 years of age. Samples will be collected primarily from mothers and children, and from fathers. Biological samples include blood, urine, placenta, breast milk, meconium, faeces, saliva and hair. Information regarding allergic heredity, diet, socioeconomic status, lifestyle including smoking, siblings, pet ownership, etc will be collected using questionnaires. Sensitisation to common allergens will be assessed by skin prick testing and allergic disease will be diagnosed by a paediatrician at 1 and 4 years of age. At 4 years of age, the children will also be examined regarding growth, neurobehavioural and neurophysiological status and oral health.Ethics and disseminationThe NICE cohort has been approved by the Regional Ethical Review Board in Umeå, Sweden (2013/18-31M). Results will be disseminated through peer-reviewed journals and communicated on scientific conferences.

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