Environmental pollutants exposure and male reproductive toxicity: The role of epigenetic modifications

Toxicology ◽  
2021 ◽  
Vol 456 ◽  
pp. 152780
Author(s):  
Xuejingping Han ◽  
Qingyu Huang
Keyword(s):  
Reproductive Toxicity ◽  
Environmental Pollutants ◽  
Epigenetic Modifications

scholarly journals Role of Chronic Alcoholism Causing Cancer in Omnivores and Vegetarians through Epigenetic Modifications

2020 ◽  
Vol 07 (03) ◽  
pp. 080-086
Author(s):  
Syed Aaquil Hasan Syed Javid Hasan ◽  
Raisa Arifanie O'Zelian Pawirotaroeno ◽  
Syed Abrar Hasan Syed Javid Hasan ◽  
Elene Abzianidze
Keyword(s):  
Folate Deficiency ◽  
Chronic Alcoholism ◽  
Epigenetic Modifications ◽  
Alcohol Metabolism ◽  
Dna Hypomethylation ◽  
Contributing Factors ◽  
Vitamin Deficiencies ◽  
Adenosyl Methionine ◽  
And Oxidative Stress

AbstractOne of the significant consequences of alcohol consumption is cancer formation via several contributing factors such as action of alcohol metabolites, vitamin deficiencies, and oxidative stress. All these factors have been shown to cause epigenetic modifications via DNA hypomethylation, thus forming a basis for cancer development. Several published reviews and studies were systematically reviewed. Omnivores and vegetarians differ in terms of nutritional intake and deficiencies. As folate deficiency was found to be common among the omnivores, chronic alcoholism could possibly cause damage and eventually cancer in an omnivorous individual via DNA hypomethylation due to folate deficiency. Furthermore, as niacin was found to be deficient among vegetarians, damage in vegetarian chronic alcoholics could be due to increased NADH/NAD+ ratio, thus slowing alcohol metabolism in liver leading to increased alcohol and acetaldehyde which inhibit methyltransferase enzymes, eventually leading to DNA hypomethylation. Hence correcting the concerned deficiency and supplementation with S-adenosyl methionine could prove to be protective in chronic alcohol use.

Prenatal exposure to persistent organic pollutants as a risk factor of offspring metabolic syndrome development during childhood

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Marlene Cervantes González
Keyword(s):  
Metabolic Syndrome ◽  
Organic Pollutants ◽  
Prenatal Exposure ◽  
Persistent Organic Pollutants ◽  
Animal Studies ◽  
Polychlorinated Biphenyl ◽  
Environmental Pollutants ◽  
Epidemiological Studies ◽  
Experimental Findings

Abstract Persistent Organic Pollutants (POPs) are exogenous, artificially made chemicals that can disrupt the biological system of individuals and animals. POPs encompass a variety of chemicals including, dioxins, organochlorines (OCs), polychlorinated biphenyl (PCBs), and perfluoroalkyl substances (PFASs) that contain a long half-life and highly resistant to biodegradation. These environmental pollutants accumulate over time in adipose tissues of living organisms and alter various insulin function-related genes. Childhood Metabolic Syndrome (MetS) consists of multiple cardiovascular risk factors, insulin function being one of them. Over the years, the incidence of the syndrome has increased dramatically. It is imperative to explore the role of persistent organic pollutants in the development of Childhood Metabolic Syndrome. Some epidemiological studies have reported an association between prenatal exposure to POPs and offspring MetS development throughout childhood. These findings have been replicated in animal studies in which these pollutants exercise negative health outcomes such as obesity and increased waist circumference. This review discusses the role of prenatal exposure to POPs among offspring who develop MetS in childhood, the latest research on the MetS concept, epidemiological and experimental findings on MetS, and the POPs modes of action. This literature review identified consistent research results on this topic. Even though the studies in this review had many strengths, one major weakness was the usage of different combinations of MetS criteria to measure the outcomes. These findings elucidate the urgent need to solidify the pediatric MetS definition. An accurate definition will permit scientists to measure the MetS as a health outcome properly and allow clinicians to diagnose pediatric MetS and provide individualized treatment appropriately.

Centering microbes in the emerging role of integrative biology in understanding environmental change

2021 ◽  
Author(s):  
Ebony I Weems ◽  
Noé U de la Sancha ◽  
Laurel J Anderson ◽  
Carlos Zambrana-Torrelio ◽  
Ronaldo P Ferraris
Keyword(s):  
Infectious Disease ◽  
Gut Microbiome ◽  
Environmental Changes ◽  
Scale Effects ◽  
Environmental Pollutants ◽  
Data Sets ◽  
Integrative Biology ◽  
Concerted Effort ◽  
Ecosystem Disturbance

Synopsis We argue that the current environmental changes stressing the Earth’s biological systems urgently require study from an integrated perspective to reveal unexpected, cross-scale interactions, particularly between microbes and macroscale phenomena. Such interactions are the basis of a mechanistic understanding of the important connections between deforestation and emerging infectious disease, feedback between ecosystem disturbance and the gut microbiome, and the cross-scale effects of environmental pollutants. These kinds of questions can be answered with existing techniques and data, but a concerted effort is necessary to better coordinate studies and data sets from different disciplines to fully leverage their potential.

scholarly journals Cadmium toxicity in plants

2005 ◽  
Vol 17 (1) ◽  
pp. 21-34 ◽  
Author(s):  
María P. Benavides ◽  
Susana M. Gallego ◽  
María L. Tomaro
Keyword(s):  
Metal Ions ◽  
Cadmium Toxicity ◽  
Environmental Pollutants ◽  
Environmental Pollutant ◽  
Present Knowledge ◽  
Plant Responses ◽  
Cellular Mechanisms ◽  
Higher Plant ◽  
Potential Damage

Heavy metals are important environmental pollutants and their toxicity is a problem of increasing significance for ecological, evolutionary, nutritional, and environmental reasons. Plants posses homeostatic cellular mechanisms to regulate the concentration of metal ions inside the cell to minimize the potential damage that could result from the exposure to nonessential metal ions. This paper summarizes present knowledge in the field of higher plant responses to cadmium, an important environmental pollutant. Knowledge concerning metal toxicity, including mechanisms of cadmium homeostasis, uptake, transport and accumulation are evaluated. The role of the cell wall, the plasma membrane and the mycorrhizas, as the main barriers against cadmium entrance to the cell, as well as some aspects related to phytochelatin-based sequestration and compartmentalization processes are also reviewed. Cadmium-induced oxidative stress was also considered as one of the most studied topics of cadmium toxicity.

scholarly journals Epigenetic mechanisms in sexual differentiation of the brain and behaviour

2016 ◽  
Vol 371 (1688) ◽  
pp. 20150114 ◽  
Author(s):  
Nancy G. Forger
Keyword(s):  
Gene Expression ◽  
Sex Differences ◽  
Sexual Differentiation ◽  
Wide Distribution ◽  
Epigenetic Modifications ◽  
Epigenetic Mechanism ◽  
Epigenetic Mechanisms ◽  
Genome Wide ◽  
The Brain

Circumstantial evidence alone argues that the establishment and maintenance of sex differences in the brain depend on epigenetic modifications of chromatin structure. More direct evidence has recently been obtained from two types of studies: those manipulating a particular epigenetic mechanism, and those examining the genome-wide distribution of specific epigenetic marks. The manipulation of histone acetylation or DNA methylation disrupts the development of several neural sex differences in rodents. Taken together, however, the evidence suggests there is unlikely to be a simple formula for masculine or feminine development of the brain and behaviour; instead, underlying epigenetic mechanisms may vary by brain region or even by dependent variable within a region. Whole-genome studies related to sex differences in the brain have only very recently been reported, but suggest that males and females may use different combinations of epigenetic modifications to control gene expression, even in cases where gene expression does not differ between the sexes. Finally, recent findings are discussed that are likely to direct future studies on the role of epigenetic mechanisms in sexual differentiation of the brain and behaviour.

Altered Protein Expressions in Chronic PCB-153–Induced Human Liver (HepG2) Cells

2007 ◽  
Vol 26 (3) ◽  
pp. 203-212 ◽  
Author(s):  
Somiranjan Ghosh ◽  
Supriyo De ◽  
Sisir K. Dutta
Keyword(s):  
Tumor Suppressor ◽  
Hepg2 Cells ◽  
Chronic Exposure ◽  
Human Liver ◽  
Environmental Pollutants ◽  
Regulator Protein ◽  
Blue Growth ◽  
Growth Assay ◽  
Related Proteins

Polychlorinated biphenyls (PCBs) are a group of persistent and widely distributed environmental pollutants that have various deleterious effects, e.g., neurotoxic, endocrine disruption and reproductive abnormalities, including cancers. Chronic exposure to environmentally hazardous chemicals like PCBs is of great concern to human health. It has been reported earlier that apoptotic proteins change in rats under chronic PCB treatment. It is of importance to determine if chronically exposed human cells develop a different protein expression. In the present study, the authors chronically exposed metabolically competent human liver (HepG2) cells at 50 to 100 μM to examine the role of the well-known environmentally hazardous pollutant non-coplanar 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB-153) to study cell death. After 12 weeks of exposure these cells showed significant changes in apoptotic death in subsequent trypan blue growth assay, fluorescence microscopy, DNA fragmentation, and immunoblotting studies. Interestingly, chronically exposed cells showed marked differences in apoptotic and/or death-related proteins (e.g., Bcl2, Bak, and the pro and active forms of caspase-9, which were up-regulated), in contrast to acutely exposed (i.e., 48-h PCB-153 exposed) cells, which maintained linear growth despite repeated exposures. Similarly, tumor suppressor protein p53, proto-oncogene c- myc, and cell cycle regulator protein p21 were also up-regulated compared to nonchronically exposed HepG2 Cells. The results indicated that PCB-153–induced chronic exposure significantly altered different apoptotic (e.g., Bcl2, Bak, caspase-3) and tumor suppressor (e.g., p21, p53, and c-myc) proteins in the cellular model. These results suggest that chronic exposure to PCB-153 can induce cell survival by altering several apoptotic and tumor suppressor proteins.

scholarly journals STAT3, a Hub Protein of Cellular Signaling Pathways, Is Triggered by β-Hexaclorocyclohexane

2018 ◽  
Vol 19 (7) ◽  
pp. 2108 ◽  
Author(s):  
Elisabetta Rubini ◽  
Fabio Altieri ◽  
Silvia Chichiarelli ◽  
Flavia Giamogante ◽  
Stefania Carissimi ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Cellular Signaling ◽  
Environmental Pollutants ◽  
Altered Expression ◽  
Exposed Population ◽  
Wide Range ◽  
Hepg2 Cell Lines

Background: Organochlorine pesticides (OCPs) are widely distributed in the environment and their toxicity is mostly associated with the molecular mechanisms of endocrine disruption. Among OCPs, particular attention was focused on the effects of β-hexaclorocyclohexane (β-HCH), a widely common pollutant. A detailed epidemiological study carried out on exposed population in the “Valle del Sacco” found correlations between the incidence of a wide range of diseases and the occurrence of β-HCH contamination. Taking into account the pleiotropic role of the protein signal transducer and activator of transcription 3 (STAT3), its function as a hub protein in cellular signaling pathways triggered by β-HCH was investigated in different cell lines corresponding to tissues that are especially vulnerable to damage by environmental pollutants. Materials and Methods: Human prostate cancer (LNCaP), human breast cancer (MCF-7 and MDA-MB 468), and human hepatoma (HepG2) cell lines were treated with 10 μM β-HCH in the presence or absence of specific inhibitors for different receptors. All samples were subjected to analysis by immunoblotting and RT-qPCR. Results and Conclusions: The preliminary results allow us to hypothesize the involvement of STAT3, through both its canonical and non-canonical pathways, in response to β-HCH. Moreover, we ascertained the role of STAT3 as a master regulator of energy metabolism via the altered expression and localization of HIF-1α and PKM2, respectively, resulting in a Warburg-like effect.

The role of boron nitride nanotube as a new chemical sensor and potential reservoir for hydrogen halides environmental pollutants

2016 ◽  
Vol 98 ◽  
pp. 325-331 ◽  
Author(s):  
Mehdi Yoosefian ◽  
Nazanin Etminan ◽  
Maryam Zeraati Moghani ◽  
Samaneh Mirzaei ◽  
Shima Abbasi
Keyword(s):  
Boron Nitride ◽  
Chemical Sensor ◽  
Environmental Pollutants ◽  
Boron Nitride Nanotube ◽  
Hydrogen Halides ◽  
Potential Reservoir
Sign in / Sign up

Export Citation Format

Share Document