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Environmental Toxicology and... May 2019Lead (Pb) is a highly toxic metal in aquatic environments. Fish are at the top of the food chain in most aquatic environments, and are the most susceptible to the toxic... (Review)
Review
Lead (Pb) is a highly toxic metal in aquatic environments. Fish are at the top of the food chain in most aquatic environments, and are the most susceptible to the toxic effects of Pb exposure. In addition, fish are one of the most abundant vertebrates, and they can directly affect humans through food intake; therefore, fish can be used to assess the extent of environmental pollution in an aquatic environment. Pb-induced toxicity in fish exposed to toxicants is primarily induced by bioaccumulation in specific tissues, and the accumulation mechanisms vary depending on water habitat (freshwater or seawater) and pathway (waterborne or dietary exposure). Pb accumulation in fish tissues causes oxidative stress due to excessive ROS production. Oxidative stress by Pb exposure induces synaptic damage and neurotransmitter malfunction in fish as neurotoxicity. Moreover, Pb exposure influences immune responses in fish as an immune-toxicant. Therefore, the purpose of this review was to examine the various toxic effects of Pb exposure, including bioaccumulation, oxidative stress, neurotoxicity, and immune responses, and to identify indicators to evaluate the extent of Pb toxicity by based on the level of Pb exposure.
Topics: Animals; Fishes; Immune System; Lead; Neurotoxicity Syndromes; Oxidative Stress; Water Pollutants, Chemical
PubMed: 30884452
DOI: 10.1016/j.etap.2019.03.010 -
Neuroscience Letters Jun 20152,5-Hexanedione (HD) and acrylamide (ACR) are considered to be prototypical among chemical toxicants that cause central-peripheral axonopathies characterized by distal... (Review)
Review
2,5-Hexanedione (HD) and acrylamide (ACR) are considered to be prototypical among chemical toxicants that cause central-peripheral axonopathies characterized by distal axon swelling and degeneration. Because the demise of distal regions was assumed to be causally related to the onset of neurotoxicity, substantial effort was devoted to deciphering the respective mechanisms. Continued research, however, revealed that expression of the presumed hallmark morphological features was dependent upon the daily rate of toxicant exposure. Indeed, many studies reported that the corresponding axonopathic changes were late developing effects that occurred independent of behavioral and/or functional neurotoxicity. This suggested that the toxic axonopathy classification might be based on epiphenomena related to dose-rate. Therefore, the goal of this mini-review is to discuss how quantitative morphometric analyses and the establishment of dose-dependent relationships helped distinguish primary, mechanistically relevant toxicant effects from non-specific consequences. Perhaps more importantly, we will discuss how knowledge of neurotoxicant chemical nature can guide molecular-level research toward a better, more rational understanding of mechanism. Our discussion will focus on HD, the neurotoxic γ-diketone metabolite of the industrial solvents n-hexane and methyl-n-butyl ketone. Early investigations suggested that HD caused giant neurofilamentous axonal swellings and eventual degeneration in CNS and PNS. However, as our review will point out, this interpretation underwent several iterations as the understanding of γ-diketone chemistry improved and more quantitative experimental approaches were implemented. The chemical concepts and design strategies discussed in this mini-review are broadly applicable to the mechanistic studies of other chemicals (e.g., n-propyl bromine, methyl methacrylate) that cause toxic neuropathies.
Topics: Axons; Central Nervous System Diseases; Environmental Pollutants; Hexanones; Humans; Peripheral Nervous System Diseases
PubMed: 25218479
DOI: 10.1016/j.neulet.2014.08.054 -
Cellular & Molecular Biology Letters 2019Common environmental pollutants and drugs encountered in everyday life can cause toxic damage to the body through oxidative stress, inflammatory stimulation, induction... (Review)
Review
Common environmental pollutants and drugs encountered in everyday life can cause toxic damage to the body through oxidative stress, inflammatory stimulation, induction of apoptosis, and inhibition of energy metabolism. Silent information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide-dependent deacetylase, is a member of the evolutionarily highly conserved Sir2 (silent information regulator 2) superprotein family, which is located in the nucleus and cytoplasm. It can deacetylate protein substrates in various signal transduction pathways to regulate gene expression, cell apoptosis and senescence, participate in the process of neuroprotection, energy metabolism, inflammation and the oxidative stress response in living organisms, and plays an important role in toxic damage caused by toxicants and in the process of SIRT1 activator/inhibitor antagonized toxic damage. This review summarizes the role that SIRT1 plays in toxic damage caused by toxicants via its interactions with protein substrates in certain signaling pathways.
Topics: Animals; Humans; Models, Biological; Signal Transduction; Sirtuin 1; Toxins, Biological
PubMed: 31164908
DOI: 10.1186/s11658-019-0158-9 -
Toxicology Letters Sep 2019Human populations are chronically exposed to mixtures of toxic chemicals. Predicting the health effects of these mixtures require a large amount of information on the... (Review)
Review
Human populations are chronically exposed to mixtures of toxic chemicals. Predicting the health effects of these mixtures require a large amount of information on the mode of action of their components. Xenobiotic metabolism by bacteria inhabiting the gastrointestinal tract has a major influence on human health. Our review aims to explore the literature for studies looking to characterize the different modes of action and outcomes of major chemical pollutants, and some components of cosmetics and food additives, on gut microbial communities in order to facilitate an estimation of their potential mixture effects. We identified good evidence that exposure to heavy metals, pesticides, nanoparticles, polycyclic aromatic hydrocarbons, dioxins, furans, polychlorinated biphenyls, and non-caloric artificial sweeteners affect the gut microbiome and which is associated with the development of metabolic, malignant, inflammatory, or immune diseases. Answering the question 'Who is there?' is not sufficient to define the mode of action of a toxicant in predictive modeling of mixture effects. Therefore, we recommend that new studies focus to simulate real-life exposure to diverse chemicals (toxicants, cosmetic/food additives), including as mixtures, and which combine metagenomics, metatranscriptomics and metabolomic analytical methods achieving in that way a comprehensive evaluation of effects on human health.
Topics: Environmental Pollutants; Gastrointestinal Microbiome; Hazardous Substances; Humans
PubMed: 31034867
DOI: 10.1016/j.toxlet.2019.04.014 -
Environmental Science & Technology Mar 2020Breathing air is a fundamental human need, yet its safety, when challenged by various harmful or lethal substances, is often not properly guarded. For example, air...
Breathing air is a fundamental human need, yet its safety, when challenged by various harmful or lethal substances, is often not properly guarded. For example, air toxicity is currently monitored only for a single or a limited number of known toxicants, thus failing to warn against possible hazardous air fully. Here, we discovered that, within minutes, living rats emitted distinctive profiles of volatile organic compounds (VOCs) via breath when exposed to various airborne toxicants such as endotoxin, O, ricin, and CO. Compared to background indoor air, when exposed to ricin or endotoxin aerosols, breath-borne VOC levels, especially that of carbon disulfide, were shown to decrease, while their elevated levels were observed for exposure to O and CO. A clear contrast in breath-borne VOC profiles of rats exposed to different toxicants was observed with a statistical significance. Differences in microRNA regulations such as miR-33, miR-146a, and miR-155 from rats' blood samples revealed different mechanisms used by rats in combating different air toxicant challenges. Similar to dogs, rats were found here to be able to sniff off toxic air by releasing a specific breath-borne VOC profile. The discovered science opens a new arena for online monitoring of air toxicity and health effects of pollutants.
Topics: Air Pollutants; Air Pollution, Indoor; Animals; Dogs; Environmental Monitoring; Hazardous Substances; Humans; Rats; Volatile Organic Compounds
PubMed: 31958948
DOI: 10.1021/acs.est.9b07592 -
Environmental Research Mar 2021It is becoming increasingly difficult to avoid exposure to man-made endocrine disrupting chemicals (EDCs) and environmental toxicants. This escalating yet constant... (Review)
Review
It is becoming increasingly difficult to avoid exposure to man-made endocrine disrupting chemicals (EDCs) and environmental toxicants. This escalating yet constant exposure is postulated to partially explain the concurrent decline in human fertility that has occurred over the last 50 years. Controversy however remains as to whether associations exist, with conflicting findings commonly reported for all major EDC classes. The primary aim of this extensive work was to identify and review strong peer-reviewed evidence regarding the effects of environmentally-relevant EDC concentrations on adult male and female fertility during the critical periconception period on reproductive hormone concentrations, gamete and embryo characteristics, as well as the time to pregnancy in the general population. Secondly, to ascertain whether individuals or couples diagnosed as sub-fertile exhibit higher EDC or toxicant concentrations. Lastly, to highlight where little or no data exists that prevents strong associations being identified. From the greater than 1480 known EDCs, substantial evidence supports a negative association between exposure to phthalates, PCBs, PBDEs, pyrethroids, organochloride pesticides and male fertility and fecundity. Only moderate evidence exists for a negative association between BPA, PCBs, organochloride pesticides and female fertility and fecundity. Overall fewer studies were reported in women than men, with knowledge gaps generally evident for both sexes for all the major EDC classes, as well as a paucity of female fertility studies following exposure to parabens, triclosans, dioxins, PFAS, organophosphates and pyrethroids. Generally, sub-fertile individuals or couples exhibit higher EDC concentrations, endorsing a positive association between EDC exposure and sub-fertility. This review also discusses confounding and limiting factors that hamper our understanding of EDC exposures on fertility and fecundity. Finally, it highlights future research areas, as well as government, industry and social awareness strategies required to mitigate the negative effects of EDC and environmental toxicant exposure on human fertility and fecundity.
Topics: Adult; Endocrine Disruptors; Environmental Exposure; Environmental Pollutants; Female; Fertility; Humans; Male; Parabens; Pregnancy
PubMed: 33385395
DOI: 10.1016/j.envres.2020.110694 -
TheScientificWorldJournal 2015In clinical medicine, increasing attention is being directed towards the important areas of nutritional biochemistry and toxicant bioaccumulation as they relate to human... (Review)
Review
In clinical medicine, increasing attention is being directed towards the important areas of nutritional biochemistry and toxicant bioaccumulation as they relate to human health and chronic disease. Optimal nutritional status, including healthy levels of vitamin D and essential minerals, is requisite for proper physiological function; conversely, accrual of toxic elements has the potential to impair normal physiology. It is evident that vitamin D intake can facilitate the absorption and assimilation of essential inorganic elements (such as calcium, magnesium, copper, zinc, iron, and selenium) but also the uptake of toxic elements (such as lead, arsenic, aluminum, cobalt, and strontium). Furthermore, sufficiency of essential minerals appears to resist the uptake of toxic metals. This paper explores the literature to determine a suitable clinical approach with regard to vitamin D and essential mineral intake to achieve optimal biological function and to avoid harm in order to prevent and overcome illness. It appears preferable to secure essential mineral status in conjunction with adequate vitamin D, as intake of vitamin D in the absence of mineral sufficiency may result in facilitation of toxic element absorption with potential adverse clinical outcomes.
Topics: Dietary Supplements; Hazardous Substances; Humans; Minerals; Nutrition Disorders; Nutritional Physiological Phenomena; Vitamin D
PubMed: 26347061
DOI: 10.1155/2015/318595 -
The Journal of Nutrition Nov 2022Concerns have been raised regarding toxic-element (arsenic, cadmium, lead, and mercury) contamination of commercially available infant foods around the world. Young...
Concerns have been raised regarding toxic-element (arsenic, cadmium, lead, and mercury) contamination of commercially available infant foods around the world. Young children are vulnerable to the effects of toxic elements, based on higher absorption levels and potentially poorer detoxification capacities. Toxic-element exposures in early life exact high societal costs, but it is unclear how much dietary exposure to these elements contributes to adverse health outcomes. Well-designed epidemiological studies conducted in different geographical and socioeconomic contexts need to estimate dietary toxicant exposure in young children and to determine whether causal links exist between toxicants in children's diets and health outcomes. This commentary outlines the methodological considerations and data needs to advance such research.
Topics: Infant; Humans; Child; Child, Preschool; Dietary Exposure; Mercury; Arsenic; Cadmium; Diet; Environmental Exposure
PubMed: 36774123
DOI: 10.1093/jn/nxac185 -
Environmental Science and Pollution... May 2019Surface or ground waters can be contaminated with numerous toxic substances. The duckweeds Lemna minor and Lemna gibba are widely used for assaying waterborne toxicity...
Surface or ground waters can be contaminated with numerous toxic substances. The duckweeds Lemna minor and Lemna gibba are widely used for assaying waterborne toxicity to higher plants in terms of growth inhibition and photosynthetic pigment reduction. These tests cannot, however, in themselves determine the nature of the agents responsible for toxicity. Morphological, developmental, physiological, biochemical, and genetic responses of duckweeds to exposure to toxic water contaminants constitute biomarkers of toxic effect. In principle, the very detection of these biomarkers should enable the contaminants having elicited them (and being responsible for the toxicity) to be identified. However, in practice, this is severely compromised by insufficient specificity of biomarkers for their corresponding toxicants and by the lack of documentation of biomarker/toxin relationships. The present contribution illustrates the difficulties of using known water contaminant-related duckweed biomarkers to identify toxins, and discusses possibilities for achieving this goal.
Topics: Araceae; Biomarkers; Water Pollutants, Chemical
PubMed: 30397749
DOI: 10.1007/s11356-018-3427-7 -
Toxics Sep 2021Introduction to a collection. This article is intended to introduce a collection of papers on toxic neuropathies. Toxic neuropathies can be caused by a variety of... (Review)
Review
Introduction to a collection. This article is intended to introduce a collection of papers on toxic neuropathies. Toxic neuropathies can be caused by a variety of substances and by different mechanisms. Toxic agents are numerous and can be distinguished between drugs, recreational agents, heavy metals, industrial agents, pesticides, warfare agents, biologic substances and venoms. Toxic agents reach the nervous system by ingestion, transcutaneously, via the mucous membranes, parenterally and by aerosols. The most frequent types are cumulative toxicities. Other types are acute or delayed toxicities. Pathogenetic mechanisms range from a specific toxic substance profile causing axonal or demyelinating lesions, towards ion channel interferences, immune-mediated mechanisms and a number of different molecular pathways. In addition, demyelination, focal lesions and small fiber damage may occur. Clinically, neurotoxicity presents most frequently as axonal symmetric neuropathies. In this work, we present a panoramic view of toxic neuropathy, in terms of symptoms, causes, mechanisms and classification.
PubMed: 34564369
DOI: 10.3390/toxics9090218