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International Journal of Molecular... Mar 2021Methylmercury (MeHg) toxicity is a major environmental concern. In the aquatic reservoir, MeHg bioaccumulates along the food chain until it is consumed by riverine... (Review)
Review
Methylmercury (MeHg) toxicity is a major environmental concern. In the aquatic reservoir, MeHg bioaccumulates along the food chain until it is consumed by riverine populations. There has been much interest in the neurotoxicity of MeHg due to recent environmental disasters. Studies have also addressed the implications of long-term MeHg exposure for humans. The central nervous system is particularly susceptible to the deleterious effects of MeHg, as evidenced by clinical symptoms and histopathological changes in poisoned humans. In vitro and in vivo studies have been crucial in deciphering the molecular mechanisms underlying MeHg-induced neurotoxicity. A collection of cellular and molecular alterations including cytokine release, oxidative stress, mitochondrial dysfunction, Ca and glutamate dyshomeostasis, and cell death mechanisms are important consequences of brain cells exposure to MeHg. The purpose of this review is to organize an overview of the mercury cycle and MeHg poisoning events and to summarize data from cellular, animal, and human studies focusing on MeHg effects in neurons and glial cells. This review proposes an up-to-date compendium that will serve as a starting point for further studies and a consultation reference of published studies.
Topics: Animals; Bioaccumulation; Brain; Humans; Inflammation; Methylmercury Compounds; Microbiota; Neurotoxicity Syndromes
PubMed: 33803585
DOI: 10.3390/ijms22063101 -
Pharmacology 2021The presence of mercury in the environment is a worldwide concern. Inorganic mercury is present in industrial materials, is employed in medical devices, is widely used...
INTRODUCTION
The presence of mercury in the environment is a worldwide concern. Inorganic mercury is present in industrial materials, is employed in medical devices, is widely used in batteries, is a component of fluorescent light bulbs, and it has been associated with human poisoning in gold mining areas. The nephrotoxicity induced by inorganic mercury is a relevant health problem mainly in developing countries. The primary mechanism of mercury toxicity is oxidative stress. Trimetazidine (TMZ) is an anti-ischemic drug, which inhibits cellular oxidative stress, eliminates oxygen-free radicals, and improves lipid metabolism. The aim of this study was to evaluate whether the administration of TMZ protects against mercuric chloride (HgCl2) kidney damage.
METHODS
Adult male Wistar rats received only HgCl2 (4 mg/kg bw, sc) (Hg group, n = 5) or TMZ (3 mg/kg bw, ip) 30 min before HgCl2 administration (4 mg/kg bw, sc) (TMZHg group, n = 7). Simultaneously, a control group of rats (n = 4) was studied. After 4 days of HgCl2 injection, urinary flow, urea and creatinine (Cr) plasma levels, Cr clearance, urinary glucose, and sodium-dicarboxylate cotransporter 1 (NaDC1) in urine were determined. Lipid peroxidation (MDA) and glutathione (GSH) levels were measured in kidney homogenates.
RESULTS
Rats only treated with HgCl2 showed an increase in urea and Cr plasma levels, urinary flow, fractional excretion of water, glucosuria, and NaDC1 urinary excretion as compared with the control group and a decrease in Cr clearance. TMZHg group showed a decrease in urea and Cr plasma levels, urinary flow, fractional excretion of water, glucosuria, NaDC1 urinary excretion, and an increase in Cr clearance when compared to the Hg group. Moreover, MDA and GSH levels observed in Hg groups were decreased and increased, respectively, by TMZ pretreatment.
CONCLUSION
TMZ exerted a renoprotective action against HgCl2-induced renal injury, which might be mediated by the reduction of oxidative stress. Considering the absence of toxicity of TMZ, its clinical application against oxidative damage due to HgCl2-induced renal injury should be considered. The fact that TMZ is commercially available should simplify and accelerate the translation of the present data "from bench to bedside." In this context, TMZ become an interesting new example of drug repurposing.
Topics: Animals; Creatinine; Dicarboxylic Acid Transporters; Glutathione; Glycosuria; Kidney Diseases; Lipid Peroxidation; Male; Malondialdehyde; Mercuric Chloride; Mercury Poisoning; Organic Anion Transporters, Sodium-Dependent; Oxidative Stress; Protective Agents; Rats, Wistar; Sodium Chloride; Symporters; Trimetazidine; Urea; Urination; Rats
PubMed: 33849026
DOI: 10.1159/000514843 -
Environmental Research Oct 2022Early exposure to mercury has been related to endocrine disruption. Steroid hormones play a crucial role in neural cell migration, differentiation, etc., as well as...
Early exposure to mercury has been related to endocrine disruption. Steroid hormones play a crucial role in neural cell migration, differentiation, etc., as well as protecting against several neurotoxic compounds. We investigate the relation between mercury exposure and children's sexual development, and we evaluate the possible influence of different brain-derived neurotrophic factor (BDNF) polymorphisms on this association. Our study sample comprised 412 9-year-old children participating in the INMA cohort (2004-2015). Mercury concentrations were measured at birth (cord blood) and at 4 and 9 years of age (hair). Sexual development was assessed by levels of sex steroid hormones (estradiol and testosterone) in saliva and the Tanner stages of sex development at 9 years (categorized as 1: prepuberty and >1: pubertal onset). Covariates and confounders were collected through questionnaires during pregnancy and childhood. Polymorphisms in the BDNF gene were genotyped in cord blood DNA. Multivariate linear regression analyses were performed between mercury levels and children's sexual development by sex. Effect modification by genetic polymorphisms and fish intake was assessed. We found marginally significant inverse associations between postnatal exposure to mercury (at 9 years) and testosterone levels (β[95%CI] = -0.16[-0.33,0.001], and -0.20[-0.42,0.03], for boys and girls, respectively). Additionally, we found that prenatal mercury was negatively associated with Tanner stage >1 in boys. Finally, we found significant genetic interactions for some single nucleotide polymorphisms in the BDNF gene. In conclusion, pre and postnatal exposure to mercury seems to affect children's sexual development and BDNF may play a role in this association, but further research would be needed.
Topics: Animals; Brain-Derived Neurotrophic Factor; Child; Diet; Female; Fishes; Humans; Mercury; Mercury Poisoning; Pregnancy; Prenatal Exposure Delayed Effects; Sexual Development; Spain; Testosterone
PubMed: 35697081
DOI: 10.1016/j.envres.2022.113620 -
Reviews on Environmental Health Mar 2020Sri Lanka is an island country located in the Indian Ocean, characterized by tropical weather, with an estimated population of 21.4 million in 2017, one third of them... (Review)
Review
Sri Lanka is an island country located in the Indian Ocean, characterized by tropical weather, with an estimated population of 21.4 million in 2017, one third of them being children. Advancing and rapidly changing technology, novel industries, consumer goods and equipment have introduced new health hazards of a chemical, biological and physical nature to future generations. The infant mortality rate has declined to around 8-9 per 100,000 since 2015. Congenital malformations were the most significant cause of neonatal death. Thus, there might be unproven environmental factors which affect infant mortality rates despite robust field and hospital services. Air pollution is a major environmental health hazard to children, largely due to hazardous industries, vehicular emissions and traditional cooking stoves. The health of children living in urban households and attending schools in cities is adversely affected by air pollution. Usage of polythene and plastic for toys, utensils, bags, lunch sheets and other daily essentials leads to overusage and improper waste management and open burning. This emits dioxins, which are carcinogens, hormone disruptors, and which can be transferred to the fetus via the placenta. In rural areas, the burning of agricultural waste and certain agro-forestry activities have also led to air pollution. Indoor air pollution (IAP) remains a large threat as 66% of the population use biomass for cooking. Use of inefficient stoves and biomass, poor ventilation and absence of chimneys, contribute to IAP. Other indoor air pollutants such as tobacco smoke, volatile organic compounds, asbestos, pesticides, kerosene, mercury, mosquito coils and biological pollutants also prevail. Biological pollutants, such as dust mites, droppings and urine from pets, insects and rodents, pollen from indoor plants and outdoor air, and fungi, including moulds in poorly maintained buildings, can trigger asthma or cause allergic reactions and infections among children inhabiting these environments. In rural areas, chemicals were accountable for 30.2% of acute poisonings, with kerosene oil being the most common cause, followed by paracetamol. More than 80% of agricultural workers in the country work in the informal sector with limited personal protective equipment use, while pesticide usage is increasing. Children who engage in agriculture-related work and hazardous industries are at risk of developing health consequences at early stages. Dengue remains a major environmental health problem as the reduction of mosquito breeding sites has been a challenging task for many years. It is essential to gain more evidence of existing environmental risk factors and their associations with the health of children. Information dissemination among local and international experts on Children's Environmental Health (CEH) issues needs to be enhanced and properly established. Training programs should be conducted for healthcare workers to update their knowledge. Pediatricians are needed for remote hospitals and primary healthcare centers. Environmental parameters and biological parameters are not routinely monitored in most of the hazardous environments.
Topics: Adolescent; Adolescent Health; Child; Child Health; Child, Preschool; Environmental Health; Female; Humans; Infant; Infant, Newborn; Male
PubMed: 32134739
DOI: 10.1515/reveh-2019-0091 -
Food Research International (Ottawa,... Feb 2022Potentially toxic elements (PTEs) as non-degradable elements (especially carcinogenic types for humans such as lead (Pb), cadmium (Cd), mercury (Hg), and arsenic (As))... (Review)
Review
Potentially toxic elements (PTEs) as non-degradable elements (especially carcinogenic types for humans such as lead (Pb), cadmium (Cd), mercury (Hg), and arsenic (As)) are widely distributed in the environment. They are one of the most concerned pollutants that can be absorbed and accumulated in the human body, primarily via contaminated water and foods. Acute or chronic poisoning of humans to PTEs can pose some serious risks for human health even at low concentrations. In this context, some methods are introduced to eliminate or reduce their concentration. While the biological treatment by bacterial strains, particularly probiotic bacteria, is considered as an effective method for reducing or eliminating of them. The consumption of probiotics as nonpathogenic microorganisms at regular and adequate dose offer some beneficial health impacts, it can also be applied to remove PTEs in both alive and non-alive states. This review aimed to provide an overview regarding the efficacy of different types of probiotic bacteria for PTEs removal from various environments such as food, water, in vitro, and in vivo conditions.
Topics: Arsenic; Bacteria; Cadmium; Humans; Mercury; Probiotics
PubMed: 35181105
DOI: 10.1016/j.foodres.2021.110324 -
Journal of Medical Toxicology :... Oct 2020This is a case series of 3 children from a single family who developed symptomatic elemental mercury poisoning requiring hospitalization and chelation. The mercury...
This is a case series of 3 children from a single family who developed symptomatic elemental mercury poisoning requiring hospitalization and chelation. The mercury exposure primarily occurred in the home but the mercury was also tracked to one of their schools requiring environmental cleanup at both the home and school. The clinical assessment and management, as well as public health investigation and response, are discussed. There are many lessons learned in this difficult, often delayed, diagnosis. Early recognition of this environmental toxic exposure is essential. Communication between the clinicians and public health officials played a critical role. Public education prevented panic. Proper environmental sampling, and assessment and management of those exposed, were a few of the many challenges faced in this complicated case series.
Topics: Adolescent; Chelating Agents; Child; Diagnosis, Differential; Exanthema; Female; Fever; Hospitalization; Humans; Male; Mercury Poisoning; Predictive Value of Tests; Treatment Outcome
PubMed: 32572678
DOI: 10.1007/s13181-020-00792-6 -
Journal of the Neurological Sciences Dec 2023We had an opportunity to perform a general autopsy of a case with chronic organic mercury toxicosis in 2017. He had been engaged in synthesizing a variety of organic...
We had an opportunity to perform a general autopsy of a case with chronic organic mercury toxicosis in 2017. He had been engaged in synthesizing a variety of organic mercury compounds throughout the four years from 1966 and developed chronic organic mercury poisoning in 1969. Almost forty years on, he still remained to complain of persistent paresthesia at finger tips and tongue, and of narrowed visual field. Neurological examinations clarified a rise of two-point discrimination thresholds, a systemic increase of touch thresholds, constriction of the visual field caused by general visual depression, and sensorineural hearing loss while primary modalities of his somatic, visual, and auditory sensations were preserved. These symptoms and signs are characteristic of human organic mercury poisoning. Furthermore, he had difficulty in processing a lot of visual and auditory information at a time. His two-point discrimination thresholds and systemic elevation of touch thresholds were comparable to those of mild organic mercury poisoning cases. He had slight sensory ataxia, but not cerebellar ataxia. Brain [F]-2-fluorodeoxyglucose positron emission tomography analysis exhibited marked hypometabolism at bilateral postcentral gyrus, striate cortex, and superior temporal gyrus, but not the cerebellum. Histopathological studies revealed considerable decrease of granular neurons and neuronal networks in bilateral primary somatosensory, visual, and auditory cortices. Those characteristic brain lesions fairly explain increase of thresholds of somatic, visual, and auditory sensations, and degradation of integrating sensory information. It is noted that damages to the peripheral nervous system and the cerebellum were not detected and that his intellectual faculties were preserved.
Topics: Male; Humans; Mercury Poisoning, Nervous System; Brain; Mercury Poisoning; Nervous System Diseases; Autopsy
PubMed: 38000298
DOI: 10.1016/j.jns.2023.122802 -
The Science of the Total Environment Jan 2024Colorectal cancer is a major public health concern, with increasing incidence and mortality rates worldwide. Environmental factors, including exposure to toxic metals,... (Review)
Review
Colorectal cancer is a major public health concern, with increasing incidence and mortality rates worldwide. Environmental factors, including exposure to toxic metals, such as lead, chromium, cadmium, aluminium, copper, arsenic and mercury, have been suggested to play a significant role in the development and progression of this neoplasia. In particular, the bioaccumulation of toxic metals can play a significant role in colorectal cancer by regulating biological phenomenon associated to both cancer occurrence and progression, such as cell death and proliferation. Also, frequently these metals can induce DNA mutations in well-known oncogenes. This review provides a critical analysis of the current evidence, highlighting the need for further research to fully grasp the complex interplay between toxic metal bioaccumulation and colorectal cancer. Understanding the contribution of toxic metals to colorectal cancer occurrence and progression is essential for the development of targeted preventive strategies and social interventions, with the ultimate goal of reducing the burden of this disease.
Topics: Humans; Bioaccumulation; Metals; Arsenic; Cadmium; Mercury; Heavy Metal Poisoning; Colorectal Neoplasms; Metals, Heavy
PubMed: 37813250
DOI: 10.1016/j.scitotenv.2023.167667 -
Health Science Reports Jun 2021Elemental mercury toxicity is a rare condition which can be difficult to diagnose due to its nonspecific signs and symptoms. The purpose of this investigation is to...
BACKGROUND AND AIMS
Elemental mercury toxicity is a rare condition which can be difficult to diagnose due to its nonspecific signs and symptoms. The purpose of this investigation is to describe the presenting characteristics and treatment of adult and pediatric patients with elemental mercury poisoning.
METHODS
A retrospective review was performed in six patients with elemental mercury exposure or intoxication who were treated in an outpatient medical toxicology clinic. Clinical signs and symptoms, laboratory assessments, and public health responses were reviewed.
RESULTS
Headache, anorexia, rash, and personality changes were commonly reported symptoms in pediatric patients; the adult patients were asymptomatic or reported signs and symptoms included myalgias, tremors, and hypertension. Delays in diagnosis were common. Symptomatic patients had 24-hour urine mercury concentrations greater than 20 mcg/L. Treatment, including removal from the exposure source as well as chelation with dimercaptosuccinic acid, resulted in resolution of signs and symptoms within 6 months of diagnosis.
CONCLUSION
The evaluation and treatment of patients with suspected elemental mercury poisoning frequently require a multidisciplinary approach including medical toxicologists and public health officials. A heightened awareness of the clinical presentations of this condition, as well as early identification and removal of patients from the source of exposure and consideration of chelation therapy, can result in accelerated patient recovery.
PubMed: 34136656
DOI: 10.1002/hsr2.293 -
The Science of the Total Environment Sep 2024Mercury is a well-known neurotoxicant for humans and wildlife. The epidemic of mercury poisoning in Japan has clearly demonstrated that chronic exposure to methylmercury... (Review)
Review
Mercury is a well-known neurotoxicant for humans and wildlife. The epidemic of mercury poisoning in Japan has clearly demonstrated that chronic exposure to methylmercury (MeHg) results in serious neurological damage to the cerebral and cerebellar cortex, leading to the dysfunction of the central nervous system (CNS), especially in infants exposed to MeHg in utero. The occurrences of poisoning have caused a wide public concern regarding the health risk emanating from MeHg exposure; particularly those eating large amounts of fish may experience the low-level and long-term exposure. There is growing evidence that MeHg at environmentally relevant concentrations can affect the health of biota in the ecosystem. Although extensive in vivo and in vitro studies have demonstrated that the disruption of redox homeostasis and microtube assembly is mainly responsible for mercurial toxicity leading to adverse health outcomes, it is still unclear whether we could quantitively determine the occurrence of interaction between mercurial and thiols and/or selenols groups of proteins linked directly to outcomes, especially at very low levels of exposure. Furthermore, intracellular calcium homeostasis, cytoskeleton, mitochondrial function, oxidative stress, neurotransmitter release, and DNA methylation may be the targets of mercury compounds; however, the primary targets associated with the adverse outcomes remain to be elucidated. Considering these knowledge gaps, in this article, we conducted a comprehensive review of mercurial toxicity, focusing mainly on the mechanism, and genes/proteins expression. We speculated that comprehensive analyses of transcriptomics, proteomics, and metabolomics could enhance interpretation of "omics" profiles, which may reveal specific biomarkers obviously correlated with specific pathways that mediate selective neurotoxicity.
Topics: Humans; Methylmercury Compounds; Gene Expression Regulation; Mercury; Animals; Oxidative Stress
PubMed: 38852866
DOI: 10.1016/j.scitotenv.2024.173577