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Arsenic is a very potent toxicant. One major susceptibility factor for arsenic-related toxicity is the efficiency of arsenic metabolism. The efficiency, in turn, is associated with non-coding single nucleotide polymorphisms (SNPs) in the arsenic methyltransferase AS3MT on chromosome 10q24. However, the mechanism of action for these SNPs is not yet clarified. Here, we assessed the influence of genetic variation in AS3MT on DNA methylation and gene expression within 10q24, in people exposed to arsenic in drinking water. DNA was extracted from peripheral blood from women in the Argentinean Andes (N = 103) and from cord blood from new-borns in Bangladesh (N = 127). AS3MT SNPs were analyzed with Sequenom or Taqman assays. Whole genome epigenetic analysis with Infinium HumanMethylation450 BeadChip was performed on bisulphite-treated DNA. Whole genome gene expression analysis was performed with Illumina DirectHyb HumanHT-12 v4.0 on RNA from peripheral blood. Arsenic exposure was assessed by HPLC-ICPMS. In the Argentinean women, the major AS3MT haplotype, associated with more efficient arsenic metabolism, showed increased methylation of AS3MT (p = 10(-6)) and also differential methylation of several other genes within about 800 kilobasepairs: CNNM2 (p<10(-16)), NT5C2 (p<10(-16)), C10orf26 (p = 10(-8)), USMG5 (p = 10(-5)), TRIM8 (p = 10(-4)), and CALHM2 (p = 0.038) (adjusted for multiple comparisons). Similar, but weaker, associations between AS3MT haplotype and DNA methylation in 10q24 were observed in cord blood (Bangladesh). The haplotype-associated altered CpG methylation was correlated with reduced expression of AS3MT and CNNM2 (r(s) = -0.22 to -0.54), and with increased expression of NT5C2 and USMG5 (r(s) = 0.25 to 0.58). Taking other possibly influential variables into account in multivariable linear models did only to a minor extent alter the strength of the associations. In conclusion, the AS3MT haplotype status strongly predicted DNA methylation and gene expression of AS3MT as well as several genes in 10q24. This raises the possibility that several genes in this region are important for arsenic metabolism.

A practice-oriented desktop reference for medical professionals, toxicologists and pharmaceutical researchers, this handbook provides systematic coverage of the metabolic pathways of all major classes of xenobiotics in the human body. The first part comprehensively reviews the main enzyme systems involved in biotransformation and how they are orchestrated in the body, while parts two to four cover the three main classes of xenobiotics: drugs, natural products, environmental pollutants. The part on drugs includes more than 300 substances from five major therapeutic groups (central nervous system, cardiovascular system, cancer, infection, and pain) as well as most drugs of abuse including nicotine, alcohol and \"designer\" drugs. Selected, well-documented case studies from the most important xenobiotics classes illustrate general principles of metabolism, making this equally useful for teaching courses on pharmacology, drug metabolism or molecular toxicology. Of particular interest, and unique to this volume is the inclusion of a wide range of additional xenobiotic compounds, including food supplements, herbal preparations, and agrochemicals.

The gut microbiota contributes to diverse aspects of host physiology, ranging from immunomodulation to drug metabolism. Changes in the gut microbiota composition are associated with various diseases as well as with the response to medications. It is therefore important to understand how different lifestyle and environmental factors shape gut microbiota composition. Beyond the commonly considered factor of diet, small-molecule drugs have recently been identified as major effectors of the microbiota composition. Other xenobiotics, such as environmental or chemical pollutants, can also impact gut bacterial communities. Here, we review the mechanisms of interactions between gut bacteria and antibiotics, host-targeted drugs, natural food compounds, food additives and environmental pollutants. While xenobiotics can impact bacterial growth and metabolism, bacteria in turn can bioaccumulate or chemically modify these compounds. These reciprocal interactions can manifest in complex xenobiotic–microbiota–host relationships. Our Review highlights the need to study mechanisms underlying interactions with pollutants and food additives towards deciphering the dynamics and evolution of the gut microbiota.We take up a multitude of foreign substances, so called xenobiotics, such as medications, food additives and pollutants, which affect the composition and function of the gut microbiota. In this Review, Lindell, Zimmermann-Kogadeeva and Patil discuss these reciprocal interactions and their mechanisms.

Endocrine-disrupting chemicals (EDCs) are exogenous chemicals that interfere with hormone action, thereby increasing the risk of adverse health outcomes, including cancer, reproductive impairment, cognitive deficits and obesity. A complex literature of mechanistic studies provides evidence on the hazards of EDC exposure, yet there is no widely accepted systematic method to integrate these data to help identify EDC hazards. Inspired by work to improve hazard identification of carcinogens using key characteristics (KCs), we have developed ten KCs of EDCs based on our knowledge of hormone actions and EDC effects. In this Expert Consensus Statement, we describe the logic by which these KCs are identified and the assays that could be used to assess several of these KCs. We reflect on how these ten KCs can be used to identify, organize and utilize mechanistic data when evaluating chemicals as EDCs, and we use diethylstilbestrol, bisphenol A and perchlorate as examples to illustrate this approach.

In the last 3 years alone, over 10,000 publications have appeared on the topic of dye removal, including over 300 reviews. Thus, the topic is very relevant, although there are few articles on the practical applications on an industrial scale of the results obtained in research laboratories. Therefore, in this review, we focus on advanced oxidation methods integrated with biological methods, widely recognized as highly efficient treatments for recalcitrant wastewater, that have the best chance of industrial application. It is extremely important to know all the phenomena and mechanisms that occur during the process of removing dyestuffs and the products of their degradation from wastewater to prevent their penetration into drinking water sources. Therefore, particular attention is paid to understanding the mechanisms of both chemical and biological degradation of dyes, and the kinetics of these processes, which are important from a design point of view, as well as the performance and implementation of these operations on a larger scale.

Plant absorption is important for the entry of many pollutants into food chains. Although terrestrial microplastics (MPs) can be absorbed by the roots 1 , 2 , their upward translocation is slow 1 . Meanwhile, atmospheric MPs are widely present 3 , 4 , but strong evidence on their direct absorption by plants is still lacking. Here, analyses using mass spectrometry detection show the widespread occurrence of polyethylene terephthalate (PET) and polystyrene (PS) polymers and oligomers in plant leaves, and identify that their levels increase with atmospheric concentrations and the leaf growth duration. The concentrations of PET and PS polymers can reach up to 10 4  ng per g dry weight in leaves at the high-pollution areas studied, such as the Dacron factory and a landfill site, and 10 2 –10 3 ng per g dry weight of PET and PS can be detected in the open-air-grown leafy vegetables. Nano-sized PET and PS particles in the leaves were visually detected by hyperspectral imaging and atomic force microscopy–infrared spectroscopy. Absorption of the proactively exposed non-labelled, fluorescently labelled or europium-labelled plastic particles by maize ( Zea mays L.) leaves through stomatal pathways, as well as their translocation to the vascular tissue through the apoplastic pathway, and accumulation in trichomes was identified using hyperspectral imaging, confocal microscopy and laser-ablation inductively coupled plasma mass spectrometry. Our results demonstrate that the absorption and accumulation of atmospheric MPs by plant leaves occur widely in the environment, and this should not be neglected when assessing the exposure of humans and other organisms to environmental MPs. Absorption and accumulation of atmospheric microplastics by plant leaves occurs widely in the environment.

Plastics, including poly(ethylene terephthalate) (PET), possess many desirable characteristics and thus are widely used in daily life. However, non-biodegradability, once thought to be an advantage offered by plastics, is causing major environmental problem. Recently, a PET-degrading bacterium, Ideonella sakaiensis , was identified and suggested for possible use in degradation and/or recycling of PET. However, the molecular mechanism of PET degradation is not known. Here we report the crystal structure of I. sakaiensis PETase ( Is PETase) at 1.5 Å resolution. Is PETase has a Ser–His-Asp catalytic triad at its active site and contains an optimal substrate binding site to accommodate four monohydroxyethyl terephthalate (MHET) moieties of PET. Based on structural and site-directed mutagenesis experiments, the detailed process of PET degradation into MHET, terephthalic acid, and ethylene glycol is suggested. Moreover, other PETase candidates potentially having high PET-degrading activities are suggested based on phylogenetic tree analysis of 69 PETase-like proteins. Poly(ethylene terephthalate) (PET) is a widely used plastic and its accumulation in the environment has become global problem. Here the authors report the crystal structure of a Ideonella sakaiensis PET-degrading enzyme and propose a molecular mechanism for PET degradation.

Experimental liver injury with hepatocelluar necrosis and abnormal liver tests is caused by exposure to heavy metals (HMs) like aluminum, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, mercury, molybdenum, nickel, platinum, thallium, titanium, vanadium, and zinc. As pollutants, HMs disturb the ecosystem, and as these substances are toxic, they may affect the health of humans and animals. HMs are not biodegradable and may be deposited preferentially in the liver. The use of animal models can help identify molecular and mechanistic steps leading to the injury. HMs commonly initiate hepatocellular overproduction of ROS (reactive oxygen species) due to oxidative stress, resulting in covalent binding of radicals to macromolecular proteins or lipids existing in membranes of subcellular organelles. Liver injury is facilitated by iron via the Fenton reaction, providing ROS, and is triggered if protective antioxidant systems are exhausted. Ferroptosis syn pyroptosis was recently introduced as mechanistic concept in explanations of nickel (Ni) liver injury. NiCl2 causes increased iron deposition in the liver, upregulation of cyclooxygenase 2 (COX-2) protein and mRNA expression levels, downregulation of glutathione eroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), nuclear receptor coactivator 4 (NCOA4) protein, and mRNA expression levels. Nickel may cause hepatic injury through mitochondrial damage and ferroptosis, defined as mechanism of iron-dependent cell death, similar to glutamate-induced excitotoxicity but likely distinct from apoptosis, necrosis, and autophagy. Under discussion were additional mechanistic concepts of hepatocellular uptake and biliary excretion of mercury in exposed animals. For instance, the organic anion transporter 3 (Oat3) and the multidrug resistance-associated protein 2 (Mrp2) were involved in the hepatic handling of mercury. Mercury treatment modified the expression of Mrp2 and Oat3 as assessed by immunoblotting, partially explaining its impaired biliary excretion. Concomitantly, a decrease in Oat3 abundance in the hepatocyte plasma membranes was observed that limits the hepatic uptake of mercury ions. Most importantly and shown for the first time in liver injury caused by HMs, titanium changed the diversity of gut microbiota and modified their metabolic functions, leading to increased generation of lipopolysaccharides (LPS). As endotoxins, LPS may trigger and perpetuate the liver injury at the level of gut-liver. In sum, mechanistic and molecular steps of experimental liver injury due to HM administration are complex, with ROS as the key promotional compound. However, additional concepts such as iron used in the Fenton reaction, ferroptosis, modification of transporter systems, and endotoxins derived from diversity of intestinal bacteria at the gut-liver level merit further consideration.

This review proposes a new bioremediation method based on the diverse functionalities of algae. A greenway for cleansing wastewater is more ecologically friendly and environmentally sustainable than prior methods with other bacteria. New bioremediation technology employing algae and cyanobacteria for the removal of a wide range of organic contaminants is reasonable and has great potential. The prevalence of organic contaminants in aquatic habitats may endanger the health and well-being of several marine creatures. Agriculture, industry, and household trash are just a few of the human-caused sources of organic pollutants that contaminate waterways around the world. Before wastewater can be released into waterways, it must be cleaned. Algae-based wastewater treatment systems are becoming increasingly popular because of their environmental sustainability and lack of secondary pollutants. According to the kind of pollutant, the physicochemical properties of wastewater, and the algal species, algae and cyanobacteria can absorb and accumulate a wide spectrum of organic pollutants at different rates. In addition, phytoremediation is a cost-effective alternative to conventional treatments for degrading organic contaminants. Phycoremediationally produced algal biomass may also be an important part of the bioenergy value chain. This article focuses on microalgae and cyanobacteria species, which may remove many organic contaminants from water systems.

Contamination of soil and natural water bodies driven by increased organic pollutants remains a universal concern. Naturally, organic pollutants contain carcinogenic and toxic properties threatening all known life forms. The conventional physical and chemical methods employed to remove these organic pollutants ironically produce toxic and non-ecofriendly end-products. Whereas microbial-based degradation of organic pollutants provides an edge, they are usually cost-effective and take an eco-friendly approach towards remediation. Bacterial species, including Pseudomonas , Comamonas , Burkholderia , and Xanthomonas , have the unique genetic makeup to metabolically degrade toxic pollutants, conferring their survival in toxic environments. Several catabolic genes, such as alkB , xylE , catA , and nahAc , that encode enzymes and allow bacteria to degrade organic pollutants have been identified, characterized, and even engineered for better efficacy. Aerobic and anaerobic processes are followed by bacteria to metabolize aliphatic saturated and unsaturated hydrocarbons such as alkanes, cycloalkanes, aldehydes, and ethers. Bacteria use a variety of degrading pathways, including catechol, protocatechuate, gentisate, benzoate, and biphenyl, to remove aromatic organic contaminants such as polychlorinated biphenyls, polycyclic aromatic hydrocarbons, and pesticides from the environment. A better understanding of the principle, mechanisms, and genetics would be beneficial for improving the metabolic efficacy of bacteria to such ends. With a focus on comprehending the mechanisms involved in various catabolic pathways and the genetics of the biotransformation of these xenobiotic compounds, the present review offers insight into the various sources and types of known organic pollutants and their toxic effects on health and the environment.