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Journal of Biochemical and Molecular... Dec 2023Gut microbiota plays a functionally important part in retaining the homeostasis of host physiology, however, under exposure of various heavy metals, the composition of... (Review)
Review
Gut microbiota plays a functionally important part in retaining the homeostasis of host physiology, however, under exposure of various heavy metals, the composition of gut biota is disturbed in relation to species diversity and richness. Ever since the increase of microbiome-related studies during the last decade, many research studies have delivered an understanding of the reasons and concerns of gut microbiota-related modifications. During the past decade, it's been confirmed from various studies that heavy metals poisoning alters the microbial composition, which results in changes in gene expression, alteration in metabolism, immunity, neurological dysfunction, and causes various other disorders. The present comprehensive review is summarizing an attempt to enumerate the key findings from recent clinical or preclinical studies related to the influence of heavy metals on gut microbiota published recently. Google, PubMed, Science Direct, Scopus, and Google Scholar were employed as primary search engines using the keywords such as "heavy metals, gut microbiota, dysbiosis, and intestinal microbiota" for finding relevant research articles from the past 10 years and some old important articles. Here, we tried to provide insight into some of the key timelines and scientific findings from reported literature, like the effects of heavy metals such as arsenic, cadmium, lead, and mercury on the general body and specifically on the gut microbiota of different model organisms. So, it is important to increase awareness against heavy metal-induced toxicity and formulate guidelines for the benefit of the environment.
Topics: Gastrointestinal Microbiome; Metals, Heavy; Cadmium; Arsenic
PubMed: 37593904
DOI: 10.1002/jbt.23485 -
Iranian Journal of Public Health Feb 2023
PubMed: 37089162
DOI: 10.18502/ijph.v52i2.11900 -
Pediatric Emergency Care Oct 2019Elemental mercury is a toxic liquid element that is used widely in the home, medicine, agriculture, and industry. It is readily vaporized and inhaled at room...
OBJECTIVE
Elemental mercury is a toxic liquid element that is used widely in the home, medicine, agriculture, and industry. It is readily vaporized and inhaled at room temperature. Thereby, inhalation can cause acute or chronic poisoning. Mercury can be found in environmental naturally find but some dangers sources give rise to contaminations. It can be very dangerous to all living organisms, especially children.
METHODS
This study presents the features of mercury poisoning in a group of pediatric cases. Data were obtained for 29 pediatric cases exposed to elemental mercury in a high school chemistry laboratory in Turkey. Patients with a blood mercury level exceeding 10 μg/L or a urine mercury level exceeding 15 μg/L were considered to have mercury poisoning. The patients were treated with 2,3-dimercaptopropane sulfonic acid or D-penicillamine.
RESULTS
Twenty-nine children with mercury poisoning were admitted to the hospital. The median duration of exposure was 58 (range, 15-120) minutes. Ten (29%) children were asymptomatic. Physical and neurological examinations were normal in 19 (65.5%) children. The most common presenting complaint was headache. The most common neurological abnormality, partly dilated/dilated pupils, was present in 9 (31%) children. Mercury levels were measured in blood samples every 5 days, and the median blood mercury level was 51.98 (range, 24.9-86.4) μg/L. There was a positive correlation between the duration of exposure and maximum blood/urine mercury levels (P = 0.001).
CONCLUSIONS
Elemental mercury exposure is potentially toxic; its symptomatology varies, especially in children. Secure storage of mercury and other toxic substances and provision of information about this subject to individuals who might be exposed to mercury and their families might help to prevent mercury poisoning.
Topics: Acute Disease; Adolescent; Chelating Agents; Child; Environmental Exposure; Female; Humans; Male; Mercury; Mercury Poisoning; Pediatric Emergency Medicine; Penicillamine; Schools; Turkey; Unithiol
PubMed: 27977534
DOI: 10.1097/PEC.0000000000001011 -
Foods (Basel, Switzerland) Mar 2024Polysaccharides are functional foods or drugs that can be used to alleviate heavy metal poisoning by cadmium, lead, mercury, and arsenic. Industries generate substantial... (Review)
Review
Polysaccharides are functional foods or drugs that can be used to alleviate heavy metal poisoning by cadmium, lead, mercury, and arsenic. Industries generate substantial quantities of toxic heavy metal wastes, such as wastewater discharges, paints, electronic waste, batteries, pigments, and plastics, into the environment that pose a risk to human health. Therefore, it is imperative to eliminate accumulated heavy metal ions from the body and the environment. Heavy metal toxicity can lead to decreased energy levels and impair the functioning of vital organs, such as the brain, lungs, kidneys, liver, and blood. Prolonged exposure can result in progressive physical, muscular, and neurological degeneration that resembles conditions such as multiple sclerosis, Parkinson's disease, Alzheimer's disease, and muscular dystrophy. Polysaccharides operate through mechanisms such as chelation, antioxidant defense, immunomodulation, and tissue repair. Polysaccharides involved in heavy metal removal include methionine and cysteine, together with N-acetylcysteine, an acetylated form of cysteine, S-adenosylmethionine, a metabolite of methionine, α-lipoic acid, and the tripeptide glutathione (GSH). These compounds effectively bind with harmful heavy metals to create a stable complex and defend biological targets from metal ions, thus decreasing their harmful effects and causing them to be excreted from the body. This review also highlights the importance of polysaccharides' ability to mitigate oxidative stress, enhance immune responses, and support tissue repair processes. Polysaccharides are ubiquitous in nature and take part in diverse processes, making them potential natural therapies for heavy metal-related diseases. This review discusses the effectiveness of natural polysaccharides and the mechanisms that allow them to bind with heavy metals to alleviate their effects from the body and the environment. Polysaccharides have inherent features that enable them to function as pharmacological agents and regulate the immune response.
PubMed: 38540843
DOI: 10.3390/foods13060853 -
Journal of Hazardous Materials Jan 2020The role of natural gas in mitigating greenhouse gas emissions and advancing renewable energy resource integration is undoubtedly critical. With the progress of... (Review)
Review
The role of natural gas in mitigating greenhouse gas emissions and advancing renewable energy resource integration is undoubtedly critical. With the progress of hydrocarbons exploration and production, the target zones become deeper and the possibility of mercury contamination increases. This impacts on the industry from health and safety risks, due to corrosion and contamination of equipment, to catalyst poisoning and toxicity through emissions to the environment. Especially mercury embrittlement, being a significant problem in LNG plants using aluminum cryogenic heat exchangers, has led to catastrophic plant incidents worldwide. The aim of this review is to critically discuss the conventional and alternative materials as well as the processes employed for mercury removal during gas processing. Moreover, comments on studies examining the geological occurrence of mercury species are included, the latest developments regarding the detection, sampling and measurement are presented and updated information with respect to mercury speciation and solubility is displayed. Clean up and passivation techniques as well as disposal methods for mercury-containing waste are also explained. Most importantly, the environmental as well as the health and safety implications are addressed, and areas that require further research are pinpointed.
PubMed: 31473516
DOI: 10.1016/j.jhazmat.2019.121036 -
MMWR. Morbidity and Mortality Weekly... Sep 2023Two siblings aged 5 and 15 years from Connecticut were hospitalized with petechial rash, oral mucositis, and severe thrombocytopenia approximately 10 days after they...
Two siblings aged 5 and 15 years from Connecticut were hospitalized with petechial rash, oral mucositis, and severe thrombocytopenia approximately 10 days after they played with a jar of elemental mercury they found in their home. Before the mercury exposure was disclosed, the siblings were treated with platelet transfusions, intravenous immune globulin (IVIG) for possible immune thrombocytopenic purpura, and antibiotics for possible infectious causes. When their conditions did not improve after 6 days, poison control facilitated further questioning about toxic exposures including mercury, testing for mercury, and chelation with dimercaptosuccinic acid. The older sibling soon recovered, but the younger child required a prolonged hospitalization for severe thrombocytopenia, ultimately receiving repeated doses of IVIG, steroids, and romiplostim, a thrombopoietin receptor agonist. Close collaboration among multiple agencies was required to identify the extent of mercury contamination, evaluate and treat the other family members, and decontaminate the home. These cases demonstrate the importance of ongoing public health outreach to promote early detection of elemental mercury toxicity, and the need to evaluate for environmental exposures when multiple close contacts experience similar signs and symptoms.
Topics: Child; Humans; Siblings; Connecticut; Immunoglobulins, Intravenous; Mercury Poisoning; Thrombocytopenia; Mercury
PubMed: 37733629
DOI: 10.15585/mmwr.mm7238a2 -
The Journal of Toxicological Sciences 2021Methylmercury (MeHg), the causal substrate in Minamata disease, can lead to severe and chronic neurological disorders. The main symptom of Minamata disease is sensory...
Methylmercury (MeHg), the causal substrate in Minamata disease, can lead to severe and chronic neurological disorders. The main symptom of Minamata disease is sensory impairment in the four extremities; however, the sensitivity of individual sensory modalities to MeHg has not been investigated extensively. In the present study, we performed stimulus-response behavioral experiments in MeHg-exposed rats to compare the sensitivities to pain, heat, cold, and mechanical sensations. MeHg (6.7 mg/kg/day) was orally administered to 9-week-old Wistar rats for 5 days and discontinued for 2 days, then administered daily for another 5 days. The four behavioral experiments were performed daily on each rat from the beginning of MeHg treatment for 68 days. The pain sensation decreased significantly from day 11 onwards, but recovered to control levels on day 48. Other sensory modalities were not affected by MeHg exposure. These findings suggest that the pain sensation is the sensory modality most susceptive to MeHg toxicity and that this sensitivity is reversible following discontinuation of the exposure.
Topics: Animals; Hypesthesia; Male; Mercury Poisoning, Nervous System; Methylmercury Compounds; Pain; Rats, Wistar; Rats
PubMed: 34078837
DOI: 10.2131/jts.46.303 -
International Journal of Environmental... Dec 2019Mercury is one of the most toxic elements and causes a multitude of health problems. It is ten times more toxic to neurons than lead. This study was created to determine...
Mercury is one of the most toxic elements and causes a multitude of health problems. It is ten times more toxic to neurons than lead. This study was created to determine if mercury could be causing Alzheimer's disease (AD) by cross referencing the effects of mercury with 70 factors associated with AD. The results found that all these factors could be attributed to mercury. The hallmark changes in AD include plaques, beta amyloid protein, neurofibrillary tangles, phosphorylated tau protein, and memory loss-all changes that can be caused by mercury. Neurotransmitters such as acetylcholine, serotonin, dopamine, glutamate, and norepinephrine are inhibited in patients with Alzheimer's disease, with the same inhibition occurring in mercury toxicity. Enzyme dysfunction in patients with Alzheimer's disease include BACE 1, gamma secretase, cyclooxygenase-2, cytochrome-c-oxidase, protein kinases, monoamine oxidase, nitric oxide synthetase, acetyl choline transferase, and caspases, all which can be explained by mercury toxicity. Immune and inflammatory responses seen in patients with Alzheimer's disease also occur when cells are exposed to mercury, including complement activation, cytokine expression, production of glial fibrillary acid protein antibodies and interleukin-1, transforming growth factor, beta 2 microglobulins, and phosphodiesterase 4 stimulation. Genetic factors in patients with Alzheimer's disease are also associated with mercury. Apolipoprotein E 4 allele increases the toxicity of mercury. Mercury can inhibit DNA synthesis in the hippocampus, and has been associated with genetic mutations of presenilin 1 and 2, found in AD. The abnormalities of minerals and vitamins, specifically aluminum, calcium, copper, iron, magnesium, selenium, zinc, and vitamins B1, B12, E, and C, that occur in patients with Alzheimer's disease, also occur in mercury toxicity. Aluminum has been found to increase mercury's toxicity. Likewise, similar biochemical factors in AD are affected by mercury, including changes in blood levels of homocysteine, arachidonic acid, DHEA sulfate, glutathione, hydrogen peroxide, glycosamine glycans, acetyl-L carnitine, melatonin, and HDL. Other factors seen in Alzheimer's disease, such as increased platelet activation, poor odor identification, hypertension, depression, increased incidences of herpes virus and chlamydia infections, also occur in mercury exposure. In addition, patients diagnosed with Alzheimer's disease exhibit higher levels of brain mercury, blood mercury, and tissue mercury in some studies. The greatest exogenous sources of brain mercury come from dental amalgams. Conclusion: This review of the literature strongly suggests that mercury can be a cause of Alzheimer's Disease.
Topics: Alzheimer Disease; Brain; Dental Amalgam; Humans; Mercury; Mercury Poisoning; Neurons
PubMed: 31861093
DOI: 10.3390/ijerph16245152 -
Environmental Science and Pollution... Dec 2020Toxicity due to heavy metals (HM), specifically mercury (Hg), arsenic (As), lead (Pb), and cadmium (Cd) remains a challenge to scientists till date. This review gives... (Review)
Review
Toxicity due to heavy metals (HM), specifically mercury (Hg), arsenic (As), lead (Pb), and cadmium (Cd) remains a challenge to scientists till date. This review gives insights into natural antidotes for the management and prevention of HM toxicity. Various databases such as PubMed, Embase, and Science Direct were searched for available facts on natural antidotes and their commercial products against HM toxicity till date. Toxicity owing to such metals needs prevention rather than therapy. Natural antidotes, fruits and vegetables, rich in antioxidant are the answers to such toxicities. Synthetic chelators impart a major drawback of removing essential metals required for normal body function, along with the toxic one. Natural antioxidants are bestowed with scavenging and chelation properties and can be alternative for synthetic chelating agents. Natural compounds are abundantly available, economic, and have minimal side effects when compared with classical chelators. Prevention is better than cure and thus adding plentiful vegetables and fruits to our diet can combat HM toxicity-related illness. Graphical abstract.
Topics: Antidotes; Arsenic; Cadmium; Chelating Agents; Heavy Metal Poisoning; Humans; Metals, Heavy
PubMed: 32951168
DOI: 10.1007/s11356-020-10783-3 -
Neurotoxicology Dec 2020Methyl mercury (MeHg) poisoning or Minamata disease (MD) from fish consumption is a public health concern throughout the world because all fish contain small amounts....
Methyl mercury (MeHg) poisoning or Minamata disease (MD) from fish consumption is a public health concern throughout the world because all fish contain small amounts. The lowest exposure level needed to impair children's development is controversial. Actual poisoning with MeHg from fish consumption has been reliably reported only two times. It occurred in Minamata, Japan in the 1950s and then in Niigata, Japan in the 1960s. On each occasion, massive industrial pollution led to local fish having mercury levels as high as 40ppm. In Niigata the pollution was on the Agano River and there were over 2000 commercial fishermen active at that time. We studied adult subjects who had been exposed perinatally to MeHg from fish consumption during the Niigata poisoning to determine the long-term impact of exposure. We identified mothers with elevated levels of exposure during the epidemic and those diagnosed with MeHg poisoning. The subjects of the study were their adult children, born during the epidemic. The evaluation consisted of a questionnaire (administered by interview) focusing on development, symptoms, and current function and a standard medical and neurological examination. The subjects were divided into four groups based upon prenatal levels of mercury in maternal hair or the presence of MD. For Group A the hair mercury levels were 50ppm or more, for Group B the mercury levels were 25-49ppm, and for Group C 10-24ppm. The subjects in Group D were born to mothers diagnosed with MD, but their mercury levels were not measured. Exposure was predominantly prenatal, but some mothers also breast fed their infants. Group A included 13 subjects among whom two were diagnosed with congenital MeHg poisoning and in two others it was suspected. Group B included 10 subjects, of whom three had symptoms compatible with MeHg poisoning. Group C had nine subjects including one with intellectual deficit and another with hearing loss. Group D had eight subjects of whom four had symptoms compatible with MeHg exposure, but only one had abnormal neurological findings. Among the subjects thought to have congenital or childhood MeHg poisoning, intelligence did not appear to have declined over time. More children were affected by prenatal and postnatal MeHg exposure at Niigata than was previously reported.
Topics: Animals; Female; Humans; Pregnancy; Fishes; Food Contamination; Hair; Japan; Mercury; Mercury Poisoning, Nervous System; Methylmercury Compounds; Prenatal Exposure Delayed Effects
PubMed: 35587140
DOI: 10.1016/j.neuro.2020.09.031