Chronic atrophic gastritis in association with hair mercury level

Xue, Zeyun; Han, Xue; Jiang, Jifa; Li, Bing; Zeng, Si; Huang, Xin; An, Jianfu

doi:10.1007/s13277-014-2475-y

Cited by 8 publications

(2 citation statements)

References 18 publications

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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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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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“…There was a statistically significant association between Pb topsoil levels and incidence of human gastric cancer, while Hg topsoil levels were associated with the incidence of human liver cancer [ 17 ]. Meanwhile, other reports have revealed that changes in hair Hg levels may reflect the transition of normal gastric mucosal to superficial gastritis and atrophic gastritis, or even cancer [ 18 ]. Chronic low-dose exposure to heavy metals may play an important role in the process of tumorigenesis, and high concentrations are not required to induce tumorigenesis [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Advances in Understanding How Heavy Metal Pollution Triggers Gastric Cancer

Wang

Yang

2016

BioMed Research International

129

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With the development of industrialization and urbanization, heavy metals contamination has become a major environmental problem. Numerous investigations have revealed an association between heavy metal exposure and the incidence and mortality of gastric cancer. The mechanisms of heavy metals (lead, cadmium, mercury, chromium, and arsenic) contamination leading to gastric cancer are concluded in this review. There are four main potential mechanisms: (1) Heavy metals disrupt the gastric mucosal barrier by decreasing mucosal thickness, mucus content, and basal acid output, thereby affecting the function of E-cadherin and inducing reactive oxygen species (ROS) damage. (2) Heavy metals directly or indirectly induce ROS generation and cause gastric mucosal and DNA lesions, which subsequently alter gene regulation, signal transduction, and cell growth, ultimately leading to carcinogenesis. Exposure to heavy metals also enhances gastric cancer cell invasion and metastasis. (3) Heavy metals inhibit DNA damage repair or cause inefficient lesion repair. (4) Heavy metals may induce other gene abnormalities. In addition, heavy metals can induce the expression of proinflammatory chemokine interleukin-8 (IL-8) and microRNAs, which promotes tumorigenesis. The present review is an effort to underline the human health problem caused by heavy metal with recent development in order to garner a broader perspective.

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