In vitro evaluation of inorganic mercury and methylmercury effects on the intestinal epithelium permeability

Vázquez, Marta; Vélez, Dinoraz; Devesa, Vicenta

doi:10.1016/j.fct.2014.10.022

Cited by 29 publications

(11 citation statements)

References 49 publications

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“…Although direct data on the impact of Hg on airway epithelium permeability are insufficient, it has been demonstrated that Hg exposure affects expression of tight junction proteins in colonic epithelial cells ( Vazquez et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases

Skalny

Lima

Tao

et al. 2020

Food and Chemical Toxicology

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Multiple medical, lifestyle, and environmental conditions, including smoking and particulate pollution, have been considered as risk factors for CO rona VI rus D isease 2019 (COVID-19) susceptibility and severity. Taking into account the high level of toxic metals in both particulate matter (PM2.5) and tobacco smoke, the objective of this review is to discuss recent data on the role of heavy metal exposure in development of respiratory dysfunction, immunotoxicity, and severity of viral diseases in epidemiological and experimental studies, as to demonstrate the potential crossroads between heavy metal exposure and COVID-19 severity risk. The existing data demonstrate that As, Cd, Hg, and Pb exposure is associated with respiratory dysfunction and respiratory diseases (COPD, bronchitis). These observations corroborate laboratory findings on the role of heavy metal exposure in impaired mucociliary clearance, reduced barrier function, airway inflammation, oxidative stress, and apoptosis. The association between heavy metal exposure and severity of viral diseases, including influenza and respiratory syncytial virus has been also demonstrated. The latter may be considered a consequence of adverse effects of metal exposure on adaptive immunity. Therefore, reduction of toxic metal exposure may be considered as a potential tool for reducing susceptibility and severity of viral diseases affecting the respiratory system, including COVID-19.

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Section: Introductionmentioning

confidence: 99%

Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases

Skalny

Lima

Tao

et al. 2020

Food and Chemical Toxicology

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“…Mercury induces mitochondrial-dependent apoptosis in human ( 140 ) and murine ( 141 ) cells, induces mitochondrial dysfunction in rodent liver and brain tissue ( 142 ), impairs the carnitine transporter ( 143 ), and reduces mitochondrial enzyme function in cells from murine ( 141 , 144 , 145 ) and zebrafish ( 146 ). Mercury causes dysfunction of human intestinal epithelium cells ( 147 ) and has been linked to chronic atrophic gastritis ( 148 ) while it also appears to significantly change the bacterial community structures in the gut microbiome in animal models ( 149 ).…”

Section: Environmental and Iatrogenic Exposures Can Disrupt Both Gi Amentioning

confidence: 99%

Gastrointestinal dysfunction in autism spectrum disorder: the role of the mitochondria and the enteric microbiome

Frye

Rose

Slattery

et al. 2015

Microbial Ecology in Health & Disease

113

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Autism spectrum disorder (ASD) affects a significant number of individuals worldwide with the prevalence continuing to grow. It is becoming clear that a large subgroup of individuals with ASD demonstrate abnormalities in mitochondrial function as well as gastrointestinal (GI) symptoms. Interestingly, GI disturbances are common in individuals with mitochondrial disorders and have been reported to be highly prevalent in individuals with co-occurring ASD and mitochondrial disease. The majority of individuals with ASD and mitochondrial disorders do not manifest a primary genetic mutation, raising the possibility that their mitochondrial disorder is acquired or, at least, results from a combination of genetic susceptibility interacting with a wide range of environmental triggers. Mitochondria are very sensitive to both endogenous and exogenous environmental stressors such as toxicants, iatrogenic medications, immune activation, and metabolic disturbances. Many of these same environmental stressors have been associated with ASD, suggesting that the mitochondria could be the biological link between environmental stressors and neurometabolic abnormalities associated with ASD. This paper reviews the possible links between GI abnormalities, mitochondria, and ASD. First, we review the link between GI symptoms and abnormalities in mitochondrial function. Second, we review the evidence supporting the notion that environmental stressors linked to ASD can also adversely affect both mitochondria and GI function. Third, we review the evidence that enteric bacteria that are overrepresented in children with ASD, particularly Clostridia spp., produce short-chain fatty acid metabolites that are potentially toxic to the mitochondria. We provide an example of this gut–brain connection by highlighting the propionic acid rodent model of ASD and the clinical evidence that supports this animal model. Lastly, we discuss the potential therapeutic approaches that could be helpful for GI symptoms in ASD and mitochondrial disorders. To this end, this review aims to help better understand the underlying pathophysiology associated with ASD that may be related to concurrent mitochondrial and GI dysfunction.

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“…Riverside populations regularly consume predatory fishes (being fish and seafood basic dietary products). Therefore, following ingestion of contaminated food, MeHg is rapidly absorbed by the gastrointestinal tract and rapidly biodistributed in the body, a process further magnified by toxicity-induced vulnerability of the intestinal barrier (Vázquez et al, 2014). Moreover, as we discuss in a recent manuscript, MeHg has been shown to affect microbiota, potentially leading to dysbiosis.…”

Section: The Environmental Impact Of Mercurymentioning

confidence: 91%

Methylmercury Impact on Adult Neurogenesis: Is the Worst Yet to Come From Recent Brazilian Environmental Disasters?

Raposo

Pinto

Moreira

et al. 2020

Front. Aging Neurosci.

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Worldwide environmental tragedies of anthropogenic origin causing massive release of metals and other pollutants have been increasing considerably. These pollution outbreaks affect the ecosystems and impact human health. Among those tragedies, recent large-scale environmental disasters in Brazil strongly affected riverside populations, leading to high-risk exposure to methylmercury (MeHg). MeHg is highly neurotoxic to the developing brain. This toxicant causes neural stem cell dysfunction and neurodevelopmental abnormalities. However, less is known about the effects of MeHg in the postnatal neurogenic niche, which harbors neural stem cells and their progeny, in the adult brain. Therefore, taking in consideration the impact of MeHg in human health it is urgent to clarify possible associations between exposure to mercury, accelerated cognitive decline, and neurodegenerative diseases. In this perspectives paper, we discuss the neurotoxic mechanisms of MeHg on postnatal neurogenesis and the putative implications associated with accelerated brain aging and early-onset cognitive decline in populations highly exposed to this environmental neurotoxicant.

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In vitro evaluation of inorganic mercury and methylmercury effects on the intestinal epithelium permeability

Cited by 29 publications

References 49 publications

Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases

Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases

Gastrointestinal dysfunction in autism spectrum disorder: the role of the mitochondria and the enteric microbiome

Methylmercury Impact on Adult Neurogenesis: Is the Worst Yet to Come From Recent Brazilian Environmental Disasters?

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