Mechanisms of Arsenic Exposure-Induced Hypertension and Atherosclerosis: an Updated Overview

Balarastaghi, Soudabeh; Rezaee, Ramin; Hayes, A. Wallace; Yarmohammadi, Fatemeh; Karimi, Gholamreza

doi:10.1007/s12011-022-03153-2

Cited by 27 publications

(7 citation statements)

References 140 publications

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“…Potential mechanisms of As-induced CVDs may involve oxidative stress, the impairment of nitric oxide and calcium homeostasis in the cardiac cells, metabolic disorder and altered mitochondrial and enzyme activity. , Oxidative stress is a key driver of As-induced toxicity, leading to apoptosis and cardiac injury. , As exposure induces heart damage through a signal pathway involving oxidative stress and inflammation. Arsenic-induced oxidative stress activates nuclear factor-kappa B (NF-κB), resulting in heart tissue inflammation .…”

Section: Resultsmentioning

confidence: 99%

Assessing the Impact of PM_2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability

Qi,

Zhao,

et al. 2024

Environ. Sci. Technol.

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Inhalation of fine particulate matter PM 2.5 -bound arsenic (PM 2.5 -As) may cause significant cardiovascular damage, due to its high concentration, long transmission range, and good absorption efficiency in organisms. However, both the contribution and the effect of the arsenic exposure pathway, with PM 2.5 as the medium, on cardiovascular system damage in nonferrous smelting sites remain to be studied. In this work, a one-year site sample collection and analysis work showed that the annual concentration of PM 2.5 -As reached 0.74 μg/m 3 , which was 120 times the national standard. The predominant species in the PM 2.5 samples were As (V) and As (III). A panel study among workers revealed that PM 2.5 -As exposure dominantly contributed to human absorption of As. After exposure of mice to PM 2.5 -As for 8 weeks, the accumulation of As in the high exposure group reached equilibrium, and its bioavailability was 24.5%. A series of animal experiments revealed that PM 2.5 -As exposure induced cardiac injury and dysfunction at the environmental relevant concentration and speciation. By integrating environmental and animal exposure assessments, more accurate health risk assessment models exposed to PM 2.5 -As were established for metal smelting areas. Therefore, our research provides an important scientific basis for relevant departments to formulate industry supervision, prevention and control policies.

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Section: Resultsmentioning

confidence: 99%

Assessing the Impact of PM_2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability

Qi,

Zhao,

et al. 2024

Environ. Sci. Technol.

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“…As in drinking water can cause vascular endothelial dysfunction, manifesting as a mismatch between vascular relaxation and contraction. These consequences, in turn, raise the risk of vascular disorders like hypertension and atherosclerosis [ 66 , 76 ]. The endothelium is activated by oxidized low-density lipoprotein (oxLDL).…”

Section: Arsenic-associated Cardiotoxicity Via Lipid Metabolismmentioning

confidence: 99%

Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements—A Focused Review

et al. 2022

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Heavy metals and metalloids like cadmium, arsenic, mercury, and lead are frequently found in the soil, water, food, and atmosphere; trace amounts can cause serious health issues to the human organism. These toxic trace elements (TTE) affect almost all the organs, mainly the heart, kidney, liver, lungs, and the nervous system, through increased free radical formation, DNA damage, lipid peroxidation, and protein sulfhydryl depletion. This work aims to advance our understanding of the mechanisms behind lipid accumulation via increased free fatty acid levels in circulation due to TTEs. The increased lipid level in the myocardium worsens the heart function. This dysregulation of the lipid metabolism leads to damage in the structure of the myocardium, inclusive fibrosis in cardiac tissue, myocyte apoptosis, and decreased contractility due to mitochondrial dysfunction. Additionally, it is discussed herein how exposure to cadmium decreases the heart rate, contractile tension, the conductivity of the atrioventricular node, and coronary flow rate. Arsenic may induce atherosclerosis by increasing platelet aggregation and reducing fibrinolysis, as exposure interferes with apolipoprotein (Apo) levels, resulting in the rise of the Apo-B/Apo-A1 ratio and an elevated risk of acute cardiovascular events. Concerning mercury and lead, these toxicants can cause hypertension, myocardial infarction, and carotid atherosclerosis, in association with the generation of free radicals and oxidative stress. This review offers a complete overview of the critical factors and biomarkers of lipid and TTE-induced cardiotoxicity useful for developing future protective interventions.

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“…Numerous prevention therapies, such as high-intensity statins, angiotensin II receptor blockers, and antihyperglycemic agents, have been established for the management of atherosclerosis in diabetic patients because of their anti-inflammatory, antioxidant, and anti-apoptotic properties [ 9 – 13 ]. Several investigations have shown that angiotensin II receptor antagonists are effective anti-atherosclerotic drugs because they inhibit lipid oxidation, restore normal oxidase activity, and boost endothelial function [ 14 – 18 ]. They also reduce hyperglycemia by increasing the body’s sensitivity to insulin [ 14 – 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…Several investigations have shown that angiotensin II receptor antagonists are effective anti-atherosclerotic drugs because they inhibit lipid oxidation, restore normal oxidase activity, and boost endothelial function [ 14 – 18 ]. They also reduce hyperglycemia by increasing the body’s sensitivity to insulin [ 14 – 18 ]. It has been estimated that between 53.1 and 72.0% of people with diabetes and atherosclerosis take angiotensin II receptor blockers [ 9 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

Design, optimization, and in vivo evaluation of invasome-mediated candesartan for the control of diabetes-associated atherosclerosis

Fouad,

Ali,

Naguib

et al. 2023

Drug Deliv. and Transl. Res.

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Atherosclerosis is an inflammatory disease characterized by the accumulation of arterial plaque. Diabetes mellitus stands out as a major risk factor for atherosclerosis. Candesartan is a potent angiotensin II receptor antagonist that enhances arterial blood flow and reduces insulin resistance. However, oral candesartan has limited activity because of its low bioavailability, water solubility, hepatic first-pass degradation, and efficacy. The current study aims to develop nasal candesartan-loaded invasome (CLI) drops to improve candesartan’s permeation, release, and bioavailability as a potential treatment for diabetes-associated atherosclerosis. Design expert software was used to prepare various CLI formulations to determine the impact of the concentrations of ethanol, cineole, and phospholipid. The desirability index was used to estimate the optimized formulation composition to maximize entrapment efficiency and minimize vesicle size. The optimized formulation had a 1% ethanol concentration, a 1.5% cineole concentration, and a 2.32% phospholipid concentration. The selected optimized formulation was then tested in a rat model of diabetes and atherosclerosis to evaluate its activity. The results showed that nasal CLI drops significantly raised serum HDL levels by a ratio of 1.42 and lowered serum glucose, cholesterol, triglycerides, LDL, and VLDL levels by 69.70%, 72.22%, 36.52%, 58.0%, and 65.31%, respectively, compared with diabetic atherosclerotic rats, throwing an insight on the potential for promising anti-diabetic and anti-atherosclerotic activities. Additionally, atherosclerotic lesions were improved in rats treated with CLI, as shown in histopathology. In conclusion, the results of this investigation showed that treatment with nasal CSN-loaded invasome formulation drops prevented the initiation and progression of diabetes-associated atherosclerosis. Graphical Abstract

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Mechanisms of Arsenic Exposure-Induced Hypertension and Atherosclerosis: an Updated Overview

Cited by 27 publications

References 140 publications

Assessing the Impact of PM_2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability

Assessing the Impact of PM_2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability

Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements—A Focused Review

Design, optimization, and in vivo evaluation of invasome-mediated candesartan for the control of diabetes-associated atherosclerosis

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Mechanisms of Arsenic Exposure-Induced Hypertension and Atherosclerosis: an Updated Overview

Cited by 27 publications

References 140 publications

Assessing the Impact of PM2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability

Assessing the Impact of PM2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability

Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements—A Focused Review

Design, optimization, and in vivo evaluation of invasome-mediated candesartan for the control of diabetes-associated atherosclerosis

Contact Info

Product

Resources

About

Assessing the Impact of PM_2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability

Assessing the Impact of PM_2.5-Bound Arsenic on Cardiovascular Risk among Workers in a Non-ferrous Metal Smelting Area: Insights from Chemical Speciation and Bioavailability