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Chemosphere Apr 2020Minamata disease in Japan and the large-scale poisoning by methylmercury (MeHg) in Iraq caused wide public concerns about the risk emanating from mercury for human... (Review)
Review
Minamata disease in Japan and the large-scale poisoning by methylmercury (MeHg) in Iraq caused wide public concerns about the risk emanating from mercury for human health. Nowadays, it is widely known that all forms of mercury induce toxic effects in mammals, and increasing evidence supports the concern that environmentally relevant levels of MeHg could impact normal biological functions in wildlife. The information of mechanism involved in mercurial toxicity is growing but knowledge gaps still exist between the adverse effects and mechanisms of action, especially at the molecular level. A body of data obtained from experimental studies on mechanisms of mercurial toxicity in vivo and in vitro points to that disruption of the antioxidant system may play an important role in the mercurial toxic effects. Moreover, the accumulating evidence indicates that signaling transduction, protein or/and enzyme activity, and gene regulation are involving in mediating toxic and adaptive response to mercury exposure. We conducted here a comprehensive review of mercurial toxic effects on wildlife and human, in particular synthesized key findings of molecular pathways involved in mercurial toxicity from the cells to human. We discuss the molecular evidence related mercurial toxicity to the adverse effects, with particular emphasis on the gene regulation. The further studies relying on Omic analysis connected to adverse effects and modes of action of mercury will aid in the evaluation and validation of causative relationship between health outcomes and gene expression.
Topics: Animals; Environmental Exposure; Environmental Pollutants; Humans; Japan; Mercury; Mercury Poisoning, Nervous System; Methylmercury Compounds
PubMed: 31881386
DOI: 10.1016/j.chemosphere.2019.125586 -
Frontiers in Pharmacology 2021The industrial activities of the last century have caused massive increases in human exposure to heavy metals. Mercury, lead, chromium, cadmium, and arsenic have been... (Review)
Review
The industrial activities of the last century have caused massive increases in human exposure to heavy metals. Mercury, lead, chromium, cadmium, and arsenic have been the most common heavy metals that induced human poisonings. Here, we reviewed the mechanistic action of these heavy metals according to the available animal and human studies. Acute or chronic poisonings may occur following exposure through water, air, and food. Bioaccumulation of these heavy metals leads to a diversity of toxic effects on a variety of body tissues and organs. Heavy metals disrupt cellular events including growth, proliferation, differentiation, damage-repairing processes, and apoptosis. Comparison of the mechanisms of action reveals similar pathways for these metals to induce toxicity including ROS generation, weakening of the antioxidant defense, enzyme inactivation, and oxidative stress. On the other hand, some of them have selective binding to specific macromolecules. The interaction of lead with aminolevulinic acid dehydratase and ferrochelatase is within this context. Reactions of other heavy metals with certain proteins were discussed as well. Some toxic metals including chromium, cadmium, and arsenic cause genomic instability. Defects in DNA repair following the induction of oxidative stress and DNA damage by the three metals have been considered as the cause of their carcinogenicity. Even with the current knowledge of hazards of heavy metals, the incidence of poisoning remains considerable and requires preventive and effective treatment. The application of chelation therapy for the management of metal poisoning could be another aspect of heavy metals to be reviewed in the future.
PubMed: 33927623
DOI: 10.3389/fphar.2021.643972 -
The New England Journal of Medicine Nov 2022
Topics: Humans; Mercury Poisoning
PubMed: 36383715
DOI: 10.1056/NEJMicm2202896 -
Neurotoxicology Jul 2020
Topics: Age Factors; Animals; Child; Child Development; Child Nutritional Physiological Phenomena; Dietary Exposure; Fishes; Food Contamination; Humans; Mercury Poisoning, Nervous System; Methylmercury Compounds; Nervous System; Nutritional Status; Nutritive Value; Risk Assessment; Risk Factors; Seafood; Seychelles
PubMed: 32387194
DOI: 10.1016/j.neuro.2020.04.001 -
Handbook of Clinical Neurology 2015Metals are frequently used in industry and represent a major source of toxin exposure for workers. For this reason governmental agencies regulate the amount of metal... (Review)
Review
Metals are frequently used in industry and represent a major source of toxin exposure for workers. For this reason governmental agencies regulate the amount of metal exposure permissible for worker safety. While essential metals serve physiologic roles, metals pose significant health risks upon acute and chronic exposure to high levels. The central nervous system is particularly vulnerable to metals. The brain readily accumulates metals, which under physiologic conditions are incorporated into essential metalloproteins required for neuronal health and energy homeostasis. Severe consequences can arise from circumstances of excess essential metals or exposure to toxic nonessential metal. Herein, we discuss sources of occupational metal exposure, metal homeostasis in the human body, susceptibility of the nervous system to metals, detoxification, detection of metals in biologic samples, and chelation therapeutic strategies. The neurologic pathology and physiology following aluminum, arsenic, lead, manganese, mercury, and trimethyltin exposures are highlighted as classic examples of metal-induced neurotoxicity.
Topics: Animals; Heavy Metal Poisoning; Humans; Metals; Neurotoxicity Syndromes; Poisoning
PubMed: 26563789
DOI: 10.1016/B978-0-444-62627-1.00011-1 -
The Journal of the Association of... Jul 2022
Topics: Embolism; Humans; Mercury; Mercury Poisoning; Pulmonary Embolism
PubMed: 35833404
DOI: No ID Found -
Advances in Neurobiology 2017The paraoxonases (PONs) are a three-gene family which includes PON1, PON2, and PON3. PON1 and PON3 are synthesized primarily in the liver and a portion is secreted in... (Review)
Review
The paraoxonases (PONs) are a three-gene family which includes PON1, PON2, and PON3. PON1 and PON3 are synthesized primarily in the liver and a portion is secreted in the plasma, where they are associated with high-density lipoproteins (HDLs), while PON2 is an intracellular enzyme, expressed in most tissues and organs, including the brain. PON1 received its name from its ability to hydrolyze paraoxon, the active metabolite of the organophosphorus (OP) insecticide parathion, and also more efficiently hydrolyzes the active metabolites of several other OPs. PON2 and PON3 do not have OP-esterase activity, but all PONs are lactonases and are capable of hydrolyzing a variety of lactones, including certain drugs, endogenous compounds, and quorum-sensing signals of pathogenic bacteria. In addition, all PONs exert potent antioxidant effects. PONs play important roles in cardiovascular diseases and other oxidative stress-related diseases, modulate susceptibility to infection, and may provide neuroprotection (PON2). Hence, significant attention has been devoted to their modulation by a variety of dietary, pharmacological, lifestyle, or environmental factors. A number of metals have been shown in in vitro, animal, and human studies to mostly negatively modulate expression of PONs, particularly PON1, the most studied in this regard. In addition, different levels of expression of PONs may affect susceptibility to toxicity and neurotoxicity of metals due to their aforementioned antioxidant properties.
Topics: Animals; Antioxidants; Aryldialkylphosphatase; Cadmium; Cadmium Poisoning; Disease Susceptibility; Heavy Metal Poisoning, Nervous System; Humans; Lead; Lead Poisoning, Nervous System; Lipoproteins, HDL; Liver; Manganese; Manganese Poisoning; Mercury; Mercury Poisoning, Nervous System; Metals; Oxidative Stress
PubMed: 28889264
DOI: 10.1007/978-3-319-60189-2_5 -
Journal of Trace Elements in Medicine... Sep 2016The brain pathology in autism spectrum disorders (ASD) indicates marked and ongoing inflammatory reactivity with concomitant neuronal damage. These findings are... (Review)
Review
The brain pathology in autism spectrum disorders (ASD) indicates marked and ongoing inflammatory reactivity with concomitant neuronal damage. These findings are suggestive of neuronal insult as a result of external factors, rather than some type of developmental mishap. Various xenobiotics have been suggested as possible causes of this pathology. In a recent review, the top ten environmental compounds suspected of causing autism and learning disabilities were listed and they included: lead, methyl-mercury, polychorinated biphenyls, organophosphate pesticides, organochlorine pesticides, endocrine disruptors, automotive exhaust, polycyclic aromatic hydrocarbons, polybrominated diphenyl ethers, and perfluorinated compounds. This current review, however, will focus specifically on mercury exposure and ASD by conducting a comprehensive literature search of original studies in humans that examine the potential relationship between mercury and ASD, categorizing, summarizing, and discussing the published research that addresses this topic. This review found 91 studies that examine the potential relationship between mercury and ASD from 1999 to February 2016. Of these studies, the vast majority (74%) suggest that mercury is a risk factor for ASD, revealing both direct and indirect effects. The preponderance of the evidence indicates that mercury exposure is causal and/or contributory in ASD.
Topics: Autistic Disorder; Environmental Exposure; Humans; Mercury; Mercury Poisoning; Risk Factors
PubMed: 27473827
DOI: 10.1016/j.jtemb.2016.06.002