Biomarkers of oxidative stress and damage in human populations exposed to arsenic

Vizcaya-Ruiz, Andrea De; Barbier, Olivier; Ruíz-Ramos, Rubén; Cebrián, Mariano E.

doi:10.1016/j.mrgentox.2008.09.020

Cited by 162 publications

(107 citation statements)

References 71 publications

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“…Chronic exposure to arsenic has been recognized to cause various types of human diseases, including metabolic syndrome, T2D, CVD and various cancers, [40][41][42][43][44] which may contribute to the prevalence of metabolic syndrome in arsenic-polluted areas. The mechanism underlying arsenic toxicity is believed to be due to methyl depletion-induced aberrant DNA methylation, and excessive ROS generation and subsequent oxidative cell injury.…”

Section: Arsenicmentioning

confidence: 99%

“…The mechanism underlying arsenic toxicity is believed to be due to methyl depletion-induced aberrant DNA methylation, and excessive ROS generation and subsequent oxidative cell injury. [40][41][42]45 Niacin Niacin (nicotinic acid and nicotinamide) is a water-soluble vitamin and a common methyl consumer. 46 Dietary nicotinic acid is derived from plant foods, while nicotinamide is derived from animal foods and typically used for food fortification.…”

Section: Arsenicmentioning

confidence: 99%

“…35 The increased appetite may lead to an increase in energy intake and subsequent obesity. As a result, the long-term persistent b-cell compensation together with the oxidative b-cell damage may eventually induce b-cell failure and T2D, which may account for the associations between arsenic [42][43][44] or niacin 34,35 exposure and the prevalence of metabolic syndrome and its related diseases.…”

Section: Proposed Mechanism For the Effects Of Methyl Consumersmentioning

confidence: 99%

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Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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The metabolic syndrome, a major risk factor for type 2 diabetes and cardiovascular disease, is a cluster of metabolic abnormalities including obesity, insulin resistance, hypertension and dyslipidemia. Although systemic oxidative stress and aberrant methylation status are known to have important roles in the development of metabolic syndrome, how they occur remains unclear. The metabolism of methyl-consuming compounds generates reactive oxygen species and consumes labile methyl groups; therefore, a chronic increase in the levels of methyl-consuming compounds in the body can induce not only oxidative stress and subsequent tissue injury, but also methyl-group pool depletion and subsequent aberrant methylation status. In the past few decades, the intake amount of methyl-consuming compounds has substantially increased primarily due to pollution, food additives, niacin fortification and high meat consumption. Thus, increased methyl consumers might have a causal role in the development and prevalence of metabolic syndrome and its related diseases. Moreover, factors that decrease the elimination/ metabolism of methyl-consuming compounds and other xenobiotics (for example, sweat gland inactivity and decreased liver function) or increase the generation of endogenous methyl-consuming compounds (for example, mental stress-induced increase in catecholamine release) may accelerate the progression of metabolic syndrome. Based on current nutrition knowledge and the available evidence from epidemiological, ecological, clinical and laboratory studies on metabolic syndrome and its related diseases, this review outlines the relationship between methyl supply-consumption imbalance and metabolic syndrome, and proposes a novel mechanism for the pathogenesis and prevalence of metabolic syndrome and its related diseases.

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Section: Arsenicmentioning

confidence: 99%

Section: Arsenicmentioning

confidence: 99%

Section: Proposed Mechanism For the Effects Of Methyl Consumersmentioning

confidence: 99%

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Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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“…Inorganic arsenic exposure increases ROS generation and cellular oxidative insults (4,12). Imbalance between oxygen-derived radicals generation and cellular antioxidant capacity mediated by arsenic, plays a principal role in disease manifestation (1,4).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, oxidative stress causes damage to cellular components (e.g. DNA, proteins, and lipids) and their functions (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

The Evaluation of the Ameliorative Effect of Montelukast Against Arsenic Trioxide-Induced Cardiotoxicity in Rats

Hemmati

Olapour

Varzi

et al. 2017

Jundishapur J Nat Pharm Prod

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Background: Arsenic trioxide (As2O3) is used for treating patients with acute promyelocytic leukemia (APL). The extensive application of this drug has been limited due to its severe cardiotoxicity. Montelukast is a selective leukotriene receptor antagonist with antioxidant and anti-inflammatory properties. Objectives: This study evaluated whether montelukast could protect against As2O3-induced cardiotoxicity in vivo. Methods: Thirty-two male Wistar rats (150 to 200 g) were divided to 4 treatment groups: control (0.2 mL of saline, ip), As2O3 (5 mg/kg, ip), As2O3 plus MONT, and MONT (20 mg/kg, po). All drugs were administered daily for 10 days and pretreatment with MONT was performed 1 hour prior to As2O3 administration. Cardiotoxicity was estimated by electrocardiological, biochemical, and histopathological evaluations. Results:The results indicated that the combination treatment of montelukast and As2O3 markedly (P < 0.05) inhibited As2O3-induced lipid peroxidation and attenuated QT interval (QT) prolongation and histopathological alterations. Pretreatment with montelukast also suppressed increased troponin I and creatinine kinase-muscle brain (CK-MB) isoenzyme levels in response to As2O3 (P < 0.01). Conclusions:In conclusion, the current results demonstrated that montelukast possesses beneficial cardio-protective properties against As2O3 toxicity. It was also proposed that these protective effects were mediated by antioxidant modifications of montelukast.

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Hepatotoxicity

Arteel¹

2015

Arsenic

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Biomarkers of oxidative stress and damage in human populations exposed to arsenic

Cited by 162 publications

References 71 publications

Dietary methyl-consuming compounds and metabolic syndrome

Dietary methyl-consuming compounds and metabolic syndrome

The Evaluation of the Ameliorative Effect of Montelukast Against Arsenic Trioxide-Induced Cardiotoxicity in Rats

Hepatotoxicity

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