Lead Exposure and Oxidative Stress: A Systematic Review

Lopes, Ana Carolina B. Almeida; Peixe, Tiago Severo; Mesas, Arthur Eumann; Paoliello, Mônica Maria Bastos

doi:10.1007/978-3-319-20013-2_3

Cited by 89 publications

(79 citation statements)

References 79 publications

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“…8-OHdG urinary concentration is one of the most relevant effects of free radicalinduced oxidative lesions in DNA structure. This biomarker has been also used to evaluate DNA damage in humans after exposure to mutagenic agents, such as tobacco smoke, hydrocarbons derivatives and heavy metals which are known indeed to generate reactive oxygen species either in humans and inside the ecosystem [36][37][38][39]. In this respect, our study confirmed prior observations about a significant direct correlation between urinary concentration of 8-OHdG and composite heavy metal exposure [26].…”

Section: Discussionsupporting

confidence: 87%

Chelator in Environmentally-exposed Poor Detoxifiers: An Adjuvant Hepatoprotective Treatment for Poly-drug Users?

Marotta¹

2016

Mol Biol (Los Angel)

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Glutathione-S-Transferase (GST) genes, including GSTT1, GSTP1, and GSTM1, play a major role in detoxification and metabolism of xenobiotics. The aim of the present study was to test an orally bioavailable GSH-based compound in poor detoxifier subjects regarding their oxidative stress, ammonia metabolism and heavy metal clearance. Eligibility was established with a telephone questionnaire followed by a clinical examination to obtain height, weight, blood pressure and screening blood chemistry and GSTM-1 gene test. Seventy-five GSTM1-null, non-smoking healthy individuals were introduced in the study who were teetotallers or were using a maximum of 20 g alcohol/day men (n = 47) and women (n = 28) aged 38-69 years (mean: 49.7) with body-mass index ranging from 22 to 29 kg/m 2 ) participated in the study. All enrolled participants were free from acute or chronic diseases and did not eat a diet or take medications that might interfere with outcome markers namely antioxidant supplements, high intake of dietary polyphenols including coffee, grapefruit juice or anti-inflammatory medications. Subjects were divided in 3 groups (25 subjects each): a) Given an oral bioabsorbable glutathione-based compound added with selenium, L-cysteine and vitamin C (GLU-9599, Named Research Co., Lesmo, Italy) at the dosage of 1 tab a day for two months; b) 600 mg of glutathione in 250 saline, given intravenously over 90 min, twice a week for 2 months; and c) Given 3 g a day of a strong cation-exchange oral chelator consisting of a mixture of chabasite-phillipsite for two months. Dietary questionnaire was administered to all subjects. Either at baseline, at one month or at the end of the study the following parameters were tested: erythrocytes (RBC) level of GSH/GSSG and Glutathione Peroxidise (GPx), urinary 8-OHdG, 24 h urinary measurement of main heavy metals, faecal metals, ammonia and oxidative stress. GLU-9599 showed to significantly lower either RBC oxidative stress or urinary 8-OHdG as compared to either IV glutathione or oral chelator (p<0.01). There was a significant correlation between urinary 8-OHdG and overall heavy metal excretion (r: 0.58, p<0.005) but no correlation occurred with RBC oxidative stress. Few subjects with fatty liver and abnormal transaminases improved their value during treatment with GLU-9599. Only oral chelator was effective in significantly lower faecal metals, ammonia and faecal oxidative stress (p<0.005). There was a not significant trend increase of mercury faecal excretion and GLU-9599. Overall, it would appear that in poor-detoxifier (GSTM1-null genotype) subjects, an effective orally-absorbable stabilised-glutathione can efficiently restore antioxidant defences in view of a potential wider application as an integrative adjuvant co-treatment in patients environmentally-exposed and also under pharmacological burden. Effective heavy metal clearance remains a still unresolved issue which may benefit from the rational addition of high cation-exchange oral chelators with a likely association with via...

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Section: Discussionsupporting

confidence: 87%

Chelator in Environmentally-exposed Poor Detoxifiers: An Adjuvant Hepatoprotective Treatment for Poly-drug Users?

Marotta¹

2016

Mol Biol (Los Angel)

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“…Because of this, Pb 2+ can modify biomolecules, resulting in another molecular mechanism that can result in lead toxicity. Finally, biochemical reactions promoted by exposure to heavy metals, in general, are particularly important in generating cellular free radical oxidants (Dietz et al 1999;Lopes et al 2016;Patrick 2006a).…”

Section: Introductionmentioning

confidence: 99%

“…Utilizing the various mechanisms stated above, Pb 2+ can interfere with ion channels, receptors and transporters, altering intracellular Ca 2+ homeostasis, and these actions can explain, in part, the pathogenesis of lead poisoning and its production of symptoms in animals and humans (Atchison 2003;Audesirk 1993;Oortgiesen et al 1993). Thus, lead ions can alter the direct function of ion channels by binding to calcium affinity sites or by redox modification (Atchison 2003;Lopes et al 2016). Neurotoxicity of lead exposure has been extensively studied and many ion channels, receptors, transporters and pumps have been directly or indirectly implicated in lead toxic effects (Baranowska-Bosiacka et al 2012; Kursula and Majava 2007;Neal and Guilarte 2010).…”

Section: Introductionmentioning

confidence: 99%

Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels

et al. 2017

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Lead ions (Pb) possess characteristics similar to Ca. Because of this and its redox capabilities, lead causes different toxic effects. The neurotoxic effects have been well documented; however, the toxic effects on cardiac tissues remain allusive. We utilized isolated guinea pig hearts and measured the effects of Pb on their contractility and excitability. Acute exposure to extracellular Pb had a negative inotropic effect and increased diastolic tension. The speed of contraction and relaxation were affected, though the effects were more dramatic on the speed of contraction. Excitability was also altered. Heart beat frequency increased and later diminished after lead ion exposure. Pro-arrhytmic events, such as early after-depolarization and a reduction of the action potential plateau, were also observed. In isolated cardiomyocytes and tsA 201 cells, extracellular lead blocked currents through Cav1.2 channels, diminished their activation, and enhanced their fast inactivation, negatively affecting their gating currents. Thus, Pb was cardiotoxic and reduced cardiac contractility, making the heart prone to arrhythmias. This was due, in part, to Pb effects on the Cav1.2 channels; however, other channels, transporters or pathways may also be involved. Acute cardiotoxic effects were observed at Pb concentrations achievable during acute lead poisoning. The results suggest how Cav1.2 gating can be affected by divalent cations, such as Pb, and also suggest a more thorough evaluation of heart function in individuals affected by lead poisoning.

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“…Several mechanisms have been explained so far as mode of lead toxicity, including disruption of endogenous oxidant-antioxidant balance. Elicitation of oxidative stress by overproduction of oxidative and nitosative free radicals during the metabolism of lead in the body is considered to be pertinent event in exertion of lead toxicity (Patra et al 2011;Lopes et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Probiotics against alleviation of lead toxicity: recent advances

Bhattacharya

2019

Interdisciplinary Toxicology

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Lead is a toxic heavy metal and there is no specific, safe and efficacious therapeutic management of lead toxicity. Scientific literature reported that some probiotic microorganisms alleviated experimentally induced lead toxicity. The present review attempts to collate the experimental studies on probiotics with ameliorative effects. Literature survey revealed that four (4) types of probiotic microorganisms exhibited significant protection from lead toxicity in experimental pre-clinical studies. No clinical study with significant outcome was found in the literature. From the outcomes of the preclinical studies it appears that probiotics are prospective for alleviation and treatment of lead toxicity.

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Lead Exposure and Oxidative Stress: A Systematic Review

Cited by 89 publications

References 79 publications

Chelator in Environmentally-exposed Poor Detoxifiers: An Adjuvant Hepatoprotective Treatment for Poly-drug Users?

Chelator in Environmentally-exposed Poor Detoxifiers: An Adjuvant Hepatoprotective Treatment for Poly-drug Users?

Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels

Probiotics against alleviation of lead toxicity: recent advances

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