Superoxide anion generation and oxidative stress in methylmercury-induced endothelial toxicity in vitro

Ghizoni, Heloisa; Souza, Viviane de Oliveira Nogueira; Straliotto, Marcos Raniel; de, Andreza Fabro; Farina, Marcelo; Hort, Mariana Appel

doi:10.1016/j.tiv.2016.10.010

Cited by 17 publications

(8 citation statements)

References 47 publications

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“…Oxidative stress has been suggested as a fundamental component of Hg‐induced testicular dysfunction (Venkatesan & Sadiq, 2017). Hg disturbs mitochondrial function and enhances the production of free radicals, including superoxide anions and peroxide radicals, which further trigger membrane LPO (Ghizoni et al, 2017). NO is a biological molecule that regulates blood pressure, neurotransmission, and immune response (Pierini & Bryan, 2015).…”

Section: Discussionmentioning

confidence: 99%

Berberine mitigates oxidative damage associated with testicular impairment following mercury chloride intoxication

2020

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In this study, we assessed the protective effect of berberine (BBR) against mercuric chloride (HgCl2)‐induced reproductive impairment. Twenty‐eight adult male Wistar albino rats were placed into four equal groups: control, BBR, HgCl2, and BBR + HgCl2. All the treatments were orally administered for seven consecutive days. The rats exposed to HgCl2 showed a marked decrease in testosterone accompanied by an increase in lipid peroxidation (LPO) and nitric oxide (NO). Additionally, HgCl2 decreased glutathione (GSH) content, deactivated catalase (CAT) and glutathione reductase (GR), and suppressed the activities and mRNA expression of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the testicular tissue. In addition, histological deformations and testicular cell loss were recorded, as evidenced by the upregulation of caspase‐3 following HgCl2 intoxication. Notably, BBR administration reversed the testicular impairments associated with HgCl2 exposure. These findings suggest that BBR protected the testicular tissue following HgCl2 exposure through inhibiting the disturbance in the testosterone level and enhanced the antioxidant capacity. Practical applications Heavy metals are naturally existing metallic elements in the earth’s crust. These trace metals have the potential to cause multiple adverse reactions to the living systems, even at low exposure doses. Human exposure may also result from industrial, agricultural, and domestic activities. Berberine (BBR, a naturally occurring quaternary benzylisoquinoline alkaloid) is a protoberberine and is the representative main active ingredient in all parts of Berberis species. BBR has been used widely in folk medicine worldwide for its multiple pharmacological and therapeutic activities; for example, in the treatment of digestive and reproductive system disorders, microorganism infections, hemorrhage and wound healing, and cardiovascular and ophthalmic diseases. We found that BBR administration was able to abrogate significantly the reproductive toxicity associated with Hg intoxication. This protective effect comes from its strong antioxidant, anti‐inflammatory, and antiapoptotic activities; suggesting that BBR may be applied to alleviate reproductive toxicity associated with Hg intoxication.

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Section: Discussionmentioning

confidence: 99%

Berberine mitigates oxidative damage associated with testicular impairment following mercury chloride intoxication

2020

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“…Calpain belongs to families of cysteine proteases and plays essential roles in the regulation and execution of necrotic cell death 45 . In addition to Bcl-2, Fas, and calpain, reactive oxygen species (ROS) such as hydrogen peroxide and superoxide have been shown to induce both apoptotic and necrotic forms of cell death 46 . A study by Ghizoni et al 46 aimed to determine the effects of MeHg exposure on superoxide generation and cellular glutathione (GSH) and toxicity in cultured bovine aortic endothelial cells (BAECs).…”

Section: Mercury-induced Apoptotic and Necrotic Cell Death Apoptosismentioning

confidence: 99%

“…In addition to Bcl-2, Fas, and calpain, reactive oxygen species (ROS) such as hydrogen peroxide and superoxide have been shown to induce both apoptotic and necrotic forms of cell death 46 . A study by Ghizoni et al 46 aimed to determine the effects of MeHg exposure on superoxide generation and cellular glutathione (GSH) and toxicity in cultured bovine aortic endothelial cells (BAECs). Results showed that exposure of 1 µM MeHg for 6 h significantly increased superoxide production and decreased levels of intracellular GSH 46 .…”

Section: Mercury-induced Apoptotic and Necrotic Cell Death Apoptosismentioning

confidence: 99%

“…A study by Ghizoni et al 46 aimed to determine the effects of MeHg exposure on superoxide generation and cellular glutathione (GSH) and toxicity in cultured bovine aortic endothelial cells (BAECs). Results showed that exposure of 1 µM MeHg for 6 h significantly increased superoxide production and decreased levels of intracellular GSH 46 . The BAECs exposed to exposure to 1 μM MeHg also showed a decrease in mitochondrial potential (ΔΨm).…”

Section: Mercury-induced Apoptotic and Necrotic Cell Death Apoptosismentioning

confidence: 99%

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Uptake, efflux, and toxicity of inorganic and methyl mercury in the endothelial cells (EA.hy926)

Liu

Tsui

Lee

et al. 2020

Sci Rep

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Cardiovascular disease (CVD) is the major cause of morbidity, mortality, and health care costs in the United States, and possibly around the world. Among the various risk factors of CVD, environmental and dietary exposures to mercury (Hg), a highly toxic metal traditionally regarded as a neurotoxin, has been recently suggested as a potential contributor towards human atherosclerotic development. In this study, we investigated the toxicity, type of cell death, dose-dependent uptake, and efflux of inorganic HgII (as HgCl2) and methylmercury or MeHg (as CH3HgCl) in EA.hy926 endothelial cells, as these two forms of Hg are often reported to be present in human blood among the general populations (~20–30% as HgII and ~70–80% as MeHg). Our results showed that HgII is more toxic than MeHg to the endothelial cells, owing to the higher uptake into the cytoplasm and perhaps importantly lower efflux of HgII by the cells, thus the “net” accumulation by the endothelial cells is higher for HgII than MeHg when exposed to the same Hg levels in the media. Furthermore, both HgII and MeHg were found to induce apoptotic and necrotic cell death. This study has important implications for the contributions of these two common Hg species to the development of atherosclerosis, an important process leading to CVD.

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“…The increased formation of reactive oxygen species (ROS) is generally agreed to be one of the key mechanisms responsible for Hg-induced toxicity [ 26 – 28 ]. Mercury is endowed with high affinity for sulfhydryl groups, and it is therefore able to react with low-molecular-weight thiols, including glutathione (GSH) [ 29 , 30 ].…”

Section: Introductionmentioning

confidence: 99%

Comparative Analysis of the Effects of Olive Oil Hydroxytyrosol and Its 5‐S‐Lipoyl Conjugate in Protecting Human Erythrocytes from Mercury Toxicity

Officioso

Panzella

Tortora

et al. 2018

Oxidative Medicine and Cellular Longevity

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Oxidative stress is one of the underlying mechanisms of the toxic effects exerted by mercury (Hg) on human health. Several antioxidant compounds, including the olive oil phenol hydroxytyrosol (HT), were investigated for their protective action. Recently, we have reported that 5-S-lipoylhydroxytyrosol (Lipo-HT) has shown increased antioxidant activities compared to HT and exerted potent protective effects against reactive oxygen species (ROS) generation and oxidative damage in human hepatocellular carcinoma HepG2 cell lines. In this study, the effects of Lipo-HT and HT on oxidative alterations of human erythrocytes induced by exposure to 40 μM HgCl2 were comparatively evaluated. When administered to the cells, Lipo-HT (5–20 μM) proved nontoxic and it decreased the Hg-induced generation of ROS, the hemolysis, and the depletion of intracellular GSH levels. At all tested concentrations, Lipo-HT exhibited higher ability to counteract Hg-induced cytotoxicity compared to HT. Model studies indicated the formation of a mercury complex at the SH group of Lipo-HT followed by a redox reaction that would spare intracellular GSH. Thus, the enhanced erythrocyte protective action of Lipo-HT from Hg-induced damage with respect to HT is likely due to an effective chelating and reducing ability toward mercury ions. These findings encourage the use of Lipo-HT in nutraceutical strategies to contrast heavy metal toxicity in humans.

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Superoxide anion generation and oxidative stress in methylmercury-induced endothelial toxicity in vitro

Cited by 17 publications

References 47 publications

Berberine mitigates oxidative damage associated with testicular impairment following mercury chloride intoxication

Berberine mitigates oxidative damage associated with testicular impairment following mercury chloride intoxication

Uptake, efflux, and toxicity of inorganic and methyl mercury in the endothelial cells (EA.hy926)

Comparative Analysis of the Effects of Olive Oil Hydroxytyrosol and Its 5‐S‐Lipoyl Conjugate in Protecting Human Erythrocytes from Mercury Toxicity

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