Mercury Exposure and Endothelial Dysfunction

Omanwar, Swati; Fahim, Mohammad

doi:10.1177/1091581815589766

Cited by 28 publications

(12 citation statements)

References 83 publications

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“…A large number of studies have well identified and characterised the negative effects of mercury on organism health. It was discovered that mercury can increase oxidative stress, reduced oxidative defence, thrombosis, mitochondrial dysfunction, hyperlipidaemia, inflammation and vascular/endothelial dysfunction [36,37], all of which can contribute to cardiovascular disease development and progression by initiating the development of atherosclerosis. It was demonstrated that endothelial function can be improved by the treatment with atorvastatin, in the case of patients with hyperlipidaemia, while the measurement of intima media thickness (IMT) together with the determination of high sensitive C reactive protein (hsCRP) can have a predicting value for future CAD events [38,39].…”

Section: Resultsmentioning

confidence: 99%

The Effects of Hg2+ on Endothelial Function in Electronic Cigarette Smokers with Coronary Artery Disease

Balint¹,

Borugă²,

Iovănescu³

et al. 2017

Rev. Chim.

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The present available data on the harmful effects of electronic cigarettes (EC) is inconsistent and contradicting. Even though EC is considered a healthier alternative to the traditional cigarettes, several studies reported a large range of toxic compounds. The objective of this study is to determine whether the mercury found in the solutions used for electronic cigarettes is involved in the initiation and aggravation of endothelial dysfunction found in smoking persons with coronary artery disease (CAD). Endothelial function was evaluated by performing organ bath studies of vascular rings from patients with CAD, and was determined as a response to cumulative doses of endothelial-dependent/independent vasodilators, in the presence of Hg2+. Hg2+ extraction was realised using ion exchanging resin PUROLITE S920 from the liquid solution used in EC. The results of this study suggests that Hg2+ may be responsible for the aggravation of the endothelial dysfunction found in smoker of EC patients with CAD.

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Section: Resultsmentioning

confidence: 99%

The Effects of Hg2+ on Endothelial Function in Electronic Cigarette Smokers with Coronary Artery Disease

Balint¹,

Borugă²,

Iovănescu³

et al. 2017

Rev. Chim.

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“…Ros has been shown to have multiple effects besides inhibition of HMG-CoA reductase, such as increasing nitric oxide synthase expression (Huang et al, 2012;Omanwar and Fahim, 2015), decreasing ROS-mediated stress (Mahalwar and Khanna, 2013), and exerting anti-inflammatory actions (Srivastava et al, 2009). However, its effect on ER stress has not previously been reported.…”

Section: Discussionmentioning

confidence: 99%

Effect of rosuvastatin on high glucose-induced endoplasmic reticulum stress in human umbilical vein endothelial cells

Chai

Zhang

2016

Genet. Mol. Res.

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ABSTRACT. It is well established that endothelial injury plays an essential role in atherosclerotic plaque formation. Accumulating evidence has shown that high glucose levels may detrimentally affect cultured endothelial cells through endoplasmic reticulum (ER) stress. In this study, we investigated the effect of rosuvastatin on high glucoseinduced ER stress in human umbilical vein endothelial cells (HUVECs). HUVECs treated with 30 mM glucose were used to simulate high-glucose conditions, and rosuvastatin concentrations ranging from 0.1 to 10 nM were used. Cell viability was analyzed by thiazolyl blue tetrazolium bromide assay, and apoptosis rate was measured using flow cytometry. Expression of GRP78, IRE1α, XBP1s, and CHOP was quantified using western blot and real-time polymerase chain reaction. Compared to cells treated with high glucose alone, cell viability increased and apoptosis rate decreased significantly in the rosuvastatin + high-glucose groups. Furthermore, GRP78, IRE1α, XBP1s, and CHOP expression was downregulated as a result of rosuvastatin administration. These results suggest that rosuvastatin may protect HUVECs from injury induced by high glucose levels, through alleviation of ER stress.

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“…Endothelial cells are vulnerable to oxidative stress, which when increased by MeHg causes endothelial dysfunction, leading to the development of atherosclerosis, thrombosis, vasospasm, and inflammation [37,38]. Consequently, it is associated with risk of atherothrombotic diseases, such as hypertension, cerebrovascular diseases, renal dysfunction, and acute myocardial infarction [39,40,41,42,43].…”

Section: Systemic Vascular Effects Of Mehg Intoxicationmentioning

confidence: 99%

Vascular Dysfunction Induced by Mercury Exposure

Shimohata

2019

IJMS

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Methylmercury (MeHg) causes severe damage to the central nervous system, and there is increasing evidence of the association between MeHg exposure and vascular dysfunction, hemorrhage, and edema in the brain, but not in other organs of patients with acute MeHg intoxication. These observations suggest that MeHg possibly causes blood–brain barrier (BBB) damage. MeHg penetrates the BBB into the brain parenchyma via active transport systems, mainly the l-type amino acid transporter 1, on endothelial cell membranes. Recently, exposure to mercury has significantly increased. Numerous reports suggest that long-term low-level MeHg exposure can impair endothelial function and increase the risks of cardiovascular disease. The most widely reported mechanism of MeHg toxicity is oxidative stress and related pathways, such as neuroinflammation. BBB dysfunction has been suggested by both in vitro and in vivo models of MeHg intoxication. Therapy targeted at both maintaining the BBB and suppressing oxidative stress may represent a promising therapeutic strategy for MeHg intoxication. This paper reviews studies on the relationship between MeHg exposure and vascular dysfunction, with a special emphasis on the BBB.

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Mercury Exposure and Endothelial Dysfunction

Cited by 28 publications

References 83 publications

The Effects of Hg2+ on Endothelial Function in Electronic Cigarette Smokers with Coronary Artery Disease

The Effects of Hg2+ on Endothelial Function in Electronic Cigarette Smokers with Coronary Artery Disease

Effect of rosuvastatin on high glucose-induced endoplasmic reticulum stress in human umbilical vein endothelial cells

Vascular Dysfunction Induced by Mercury Exposure

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