Long-term arsenic exposure and ischemic heart disease in arseniasis-hyperendemic villages in Taiwan

Tseng, Chao‐Hsiung; Chong, Choon-Khim; Tseng, Ching Ping; Hsueh, Yu Mei; Chiou, Hung Yi; Tseng, Ching Chung; Chen, Chien Jen

doi:10.1016/s0378-4274(02)00377-6

Cited by 227 publications

(131 citation statements)

References 16 publications

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“…While the roles of environmental contaminants in the etiology of vascular diseases and in the vascular contributions to organ dysfunction remain poorly defined, epidemiological studies have associated arsenic exposures with increased risk of cardiovascular diseases (Navas-Acien et al, 2005;Wu et al, 2006;Tseng et al, 2003;Engel et al, 1994) and vascular contributions to liver disease (Mazumder, 2005). Recent reports indicated that high environmental levels of arsenic (10-100 ppm in drinking water) accelerate atherosclerosis (Bunderson et al, 2004;Simeonova et al, 2003) and promote liver vascular channel formation in rodent models (Mazumder, 2005).…”

Section: Introductionmentioning

confidence: 99%

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Straub

Stolz

Vin

et al. 2007

Toxicology and Applied Pharmacology

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The vascular effects of arsenic in drinking water are global health concerns contributing to human disease worldwide. Arsenic targets the endothelial cells lining blood vessels and endothelial cell activation or dysfunction may underlie the pathogenesis of both arsenic-induced vascular diseases and arsenic-enhanced tumorigenesis. The purpose of the current studies was to demonstrate that exposing mice to drinking water containing environmentally relevant levels of arsenic promoted endothelial cell dysfunction and pathologic vascular remodeling. Increased angiogenesis, neovascularization, and inflammatory cell infiltration was observed in Matrigel plugs implanted in C57BL/6 mice following 5 week exposures to 5-500 ppb arsenic (Soucy et al., 2005). Therefore, functional in vivo effects of arsenic on endothelial cell function and vessel remodeling in an endogenous vascular bed were investigated in the liver. Liver sinusoidal endothelial cells (LSEC) became progressively defenestrated and underwent capillarization to decrease vessel porosity following exposure to 250 ppb arsenic for 2 weeks. Sinusoidal expression of PECAM-1 and laminin-1 proteins, a hallmark of capillarization, was also increased by 2 weeks of exposure. LSEC caveolin-1 protein and caveolae expression were induced after 2 weeks of exposure indicating a compensatory change. Likewise, CD45/CD68 positive inflammatory cells did not accumulate in the livers until after LSEC porosity was decreased; indicating that inflammation is a consequence and not a cause of the arsenic-induced LSEC phenotype. The data demonstrate that the liver vasculature is an early target of pathogenic arsenic effects and that the mouse liver vasculature is a sensitive model for investigating vascular health effects of arsenic.

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Section: Introductionmentioning

confidence: 99%

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Straub

Stolz

Vin

et al. 2007

Toxicology and Applied Pharmacology

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“…Epidemiological studies analyzing the correlation between cardiovascular diseases and arsenic exposure, have linked arsenic to atherosclerosis (Wang et al, 2002), ischemic heart disease (Tseng et al, 2003) and hypertension (Rahman et al, 1999). Drinking water is a significant source of arsenic exposure to humans.…”

Section: Introductionmentioning

confidence: 99%

Activation of protein kinase C and disruption of endothelial monolayer integrity by sodium arsenite—Potential mechanism in the development of atherosclerosis

Pereira

Coffin

Beall

2007

Toxicology and Applied Pharmacology

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Arsenic exposure has been shown to exacerbate atherosclerosis, beginning with activation of the endothelium that lines the vessel wall. Endothelial barrier integrity is maintained by proteins of the adherens junction (AJ) such as vascular endothelial cadherin (VE-cadherin) and β-catenin and their association with the actin cytoskeleton. In the present study, human aortic endothelial cells (HAECs) were exposed to 1, 5 and 10 μM sodium arsenite [As(III)] for 1, 6, 12 and 24 h, and the effects on endothelial barrier integrity were determined. Immunofluorescence studies revealed formation of actin stress fibers and non-uniform VE-cadherin and β-catenin staining at cell-cell junctions that were concentration and time-dependent. Intercellular gaps were observed with a measured increase in endothelial permeability. In addition, concentration-dependent increases in tyrosine phosphorylation (PY) of β-catenin and activation of protein kinase Cα (PKCα) were observed. Inhibition of PKCα restored VE-cadherin and β-catenin staining at cell-cell junctions and abolished the As(III) induced formation of actin stress fibers and intercellular gaps. Endothelial permeability and PY of β-catenin were also reduced to basal levels. These results demonstrate that As(III) induces activation of PKCα, which leads to increased PY of β-catenin downstream of PKCα activation. Phosphorylation of β-catenin plausibly severs the association of VE-cadherin and β-catenin, which along with formation of actin stress fibers, results in intercellular gap formation and increased endothelial permeability. To the best of our knowledge, this is the first report demonstrating that As(III) causes a loss of endothelial monolayer integrity, which potentially could contribute to the development of atherosclerosis.

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“…Deficiency of chromium results in impaired growth and disturbances in glucose, lipid, and protein metabolism [23]. It has also been reported that long term exposure to Cr can cause damage to liver, kidney circulatory and nerve tissues, as well as skin irritation [29,30]. The concentration of Cr in Kiri ranges between 0.08-m 3 .…”

Section: Concentration Of the Selected Heavy Metals In The Fish Samplesmentioning

confidence: 99%

“…Arsenic concentrations as high as 170 mg/kg have been reported in crustaceans and other shellfish [23]. Chronic arsenic poisoning symptoms include pigmented skin lesions, gangrene of the lower extremities (blackfoot disease), along with neuritis and paralysis, anemia and disturbances of the liver and circulatory system [5,19,22,29]. From Figure 2, it is observed that the concentration of these selected heavy metals is higher in Catfish than Tilapia irrespective of the location.…”

Section: Physio-chemical Parameters Of Water Samples Collected From Kmentioning

confidence: 99%

Determination of Selected Heavy Metals and Human Health Risk Assessment in Fishes from Kiri Dam and River Gongola, Northeastern Nigeria

Mm¹,

Tchokossa²,

Ro³

et al. 2017

J Phys Chem Biophys

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Long-term arsenic exposure and ischemic heart disease in arseniasis-hyperendemic villages in Taiwan

Cited by 227 publications

References 16 publications

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice

Activation of protein kinase C and disruption of endothelial monolayer integrity by sodium arsenite—Potential mechanism in the development of atherosclerosis

Determination of Selected Heavy Metals and Human Health Risk Assessment in Fishes from Kiri Dam and River Gongola, Northeastern Nigeria

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