Zinc and N-acetylcysteine modify mercury distribution and promote increase in hepatic metallothionein levels

Oliveira, Vinicius de Abreu; Oliveira, Cláudia S.; Mesquita, Mariana; Pedroso, Taíse F.; Costa, Lidiane; Fiuza, Tiago da Luz; Pereira, Maria Estér

doi:10.1016/j.jtemb.2015.06.006

Cited by 13 publications

(7 citation statements)

References 40 publications

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“…It is likely that they are mutually antagonistic in absorption, metabolism and accumulation. Oliveira et al found that zinc is antagonistic to mercury toxicity . We found that co‐feeding of zinc and mercury resulted in reduced mercury accumulation in the placenta and better fetal development.…”

Section: Discussionsupporting

confidence: 50%

“…Oliveira et al found that zinc is antagonistic to mercury toxicity. 23 We found that co-feeding of zinc and mercury resulted in reduced mercury accumulation in the placenta and better fetal development. Furthermore, co-feeding also resulted in reduced S100B expression, suggesting that zinc sulfate may inhibit mercury-induced apoptosis by regulating S100B expression to block Ca 2+ apoptosis signaling.…”

Section: Discussionmentioning

confidence: 74%

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Zinc protection in fetal rats for maternal mercury exposure‐induced growth retardation is probably associated with S100B expression

Weng

Liu

Zhang

et al. 2016

J of Obstet and Gynaecol

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 74%

Zinc protection in fetal rats for maternal mercury exposure‐induced growth retardation is probably associated with S100B expression

Weng

Liu

Zhang

et al. 2016

J of Obstet and Gynaecol

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“…Thus, NAC acts in the detoxification of ROS produced by leukocytes [ 60 ] and is able to chelate transition metals such as Cu 2+ , Fe 3+ and heavy metals such as Cd 2+ , Hg 2+ and Pb 2+ [ 61 ], primarily through its thiol side chain to form complexes, which are easily excreted from the body, being removed from the intra- and extracellular media [ 40 ]. At a physiological pH, NAC may chelate Hg 2+ and thus act as an antidote against HgCl 2 poisoning [ 62 ]. Although NAC has the ability to directly scavenge free radicals, the constant reaction rate with ROS are smaller than in relation to the antioxidant enzymes such as SOD, CAT and GPx [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress and Inflammation in Hepatic Diseases: Therapeutic Possibilities of N-Acetylcysteine

Andrade

Moura

Santos

et al. 2015

IJMS

198

140

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Liver disease is highly prevalent in the world. Oxidative stress (OS) and inflammation are the most important pathogenetic events in liver diseases, regardless the different etiology and natural course. N-acetyl-l-cysteine (the active form) (NAC) is being studied in diseases characterized by increased OS or decreased glutathione (GSH) level. NAC acts mainly on the supply of cysteine for GSH synthesis. The objective of this review is to examine experimental and clinical studies that evaluate the antioxidant and anti-inflammatory roles of NAC in attenuating markers of inflammation and OS in hepatic damage. The results related to the supplementation of NAC in any form of administration and type of study are satisfactory in 85.5% (n = 59) of the cases evaluated (n = 69, 100%). Within this percentage, the dosage of NAC utilized in studies in vivo varied from 0.204 up to 2 g/kg/day. A standard experimental design of protection and treatment as well as the choice of the route of administration, with a broader evaluation of OS and inflammation markers in the serum or other biological matrixes, in animal models, are necessary. Clinical studies are urgently required, to have a clear view, so that, the professionals can be sure about the effectiveness and safety of NAC prescription.

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“…The main mechanism of Hg toxicity is associated with oxidative stress, as reported by numerous studies (Ansar, 2015;Ansar and Iqbal, 2016;Berlin et al, 2007;Li et al, 2009). The oxidative action after Hg exposition may be linked to the fact that this metal increases lipid peroxidation (Ansar 2015), reduces nonenzymatic and enzymatic antioxidants (Agarwal et al, 2010;Pal and Ghosh, 2012;Su et al, 2008) and TSH and NPSH defenses (Farina et al, 2003;Oliveira V.A. 2015).…”

Section: Discussionmentioning

confidence: 95%

“…The oxidative action after Hg exposition may be linked to the fact that this metal increases lipid peroxidation (Ansar ), reduces nonenzymatic and enzymatic antioxidants (Agarwal et al, ; Pal and Ghosh, ; Su et al, ) and TSH and NPSH defenses (Farina et al, ; Oliveira V.A. ). Furthermore, the high affinity of Hg with the SH group contributes to its toxicity, because induces the formation of a stable complex which changes several proteins fundamental for the correct function of the cells and tissues (Berlin et al, ; Farina et al, ; Rooney, ).…”

Section: Discussionmentioning

confidence: 99%

Acute mercury exposition of virgin, pregnant, and lactating rats: Histopathological kidney and liver evaluations

Oliveira

Favero

Stacchiotti

et al. 2016

Environmental Toxicology

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This work investigated the effects of mercury chloride (HgCl ) acute exposure on virgin, pregnant and lactating rats by determination of renal and hepatic morphological and ultrastructural parameters and the expression of oxidative stress and stress tolerance markers, due to kidney and liver are the organs that more accumulate inorganic mercury. Adult Wistar rats virgin (90 days old), pregnant (18 gestation day) and lactating (7 lactation day) were injected once with HgCl (5 mg/kg) or saline (controls). We observed that HgCl exposure of virgin rats caused significant inflammatory infiltration and severe morphological variations, like glomeruli atrophy, dilatation of Bowman's capsule, tubular degeneration and hepatocytes alteration. Moreover, virgin rats presented mitochondrial modification, important oxidative stress and increase in stress tolerance proteins at both kidney and liver level, compared with virgin controls. In detail, virgin rats exposed to HgCl presented significantly elevated level of inducible nitric oxide synthase, heat shock protein 27 and glucose regulated proteins 75 expressions at both renal tubular and hepatocytes level, respect untreated virgin rats. Interestingly, pregnant and lactating rats exposed to HgCl presented weak renal and liver morphological alterations, showing weak inflammatory infiltration and no significant difference in structural mitochondrial transmembrane protein, oxidative stress markers and stress tolerance proteins expressions respect controls (virgin, pregnant and lactating rats). Although, both control and HgCl -exposed pregnant and lactating rats showed renal glomeruli greater in diameter respect virgin rats. In conclusion, we believe that virgin rats are more sensitive to HgCl toxicity respect pregnant and lactating rats. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1500-1512, 2017.

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Zinc and N-acetylcysteine modify mercury distribution and promote increase in hepatic metallothionein levels

Cited by 13 publications

References 40 publications

Zinc protection in fetal rats for maternal mercury exposure‐induced growth retardation is probably associated with S100B expression

Zinc protection in fetal rats for maternal mercury exposure‐induced growth retardation is probably associated with S100B expression

Oxidative Stress and Inflammation in Hepatic Diseases: Therapeutic Possibilities of N-Acetylcysteine

Acute mercury exposition of virgin, pregnant, and lactating rats: Histopathological kidney and liver evaluations

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