Lung and blood superoxide dismutase activity in mercury vapor exposed rats: effect of N-acetylcysteine treatment

Livardjani, F.; Ledig, M.; Kopp, P.; Dahlet, Marc; Leroy, M. J. F.; Jaeger, Albert

doi:10.1016/0300-483x(91)90200-k

Cited by 22 publications

(3 citation statements)

References 11 publications

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“…It is in clinical use for acetaminophen overdose to prevent or decrease hepatic injury, and as an adjuvant mucolytic therapy in patients with abnormal, viscuous mucous secretions in bronchopulmonary diseases and diagnostic bronchial studies [41]. Animal experiments showed that NAC is capable of chelating certain metals, such as inorganic and organic mercury [96][97][98], cadmium [292], chromium and boron [77], arsenic [67], and to a lesser extent gold [292]. Marked urinary excretion of methylmercury is observed in mice orally treated with NAC [98].…”

Section: N-acetylcysteine (Nac)mentioning

confidence: 99%

Chelators as Antidotes of Metal Toxicity: Therapeutic and Experimental Aspects

Blanuša¹,

Varnai²,

Piasek³

et al. 2005

CMC

236

150

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The effects of chelating drugs used clinically as antidotes to metal toxicity are reviewed. Human exposure to a number of metals such as lead, cadmium, mercury, manganese, aluminum, iron, copper, thallium, arsenic, chromium, nickel and platinum may lead to toxic effects, which are different for each metal. Similarly the pharmacokinetic data, clinical use and adverse effects of most of the chelating drugs used in human metal poisoning are also different for each chelating drug. The chelating drugs with worldwide application are dimercaprol (BAL), succimer (meso-DMSA), unithiol (DMPS), D-penicillamine (DPA), N-acetyl-D-penicillamine (NAPA), calcium disodium ethylenediaminetetraacetate (CaNa(2)EDTA), calcium trisodium or zinc trisodium diethylenetriaminepentaacetate (CaNa(3)DTPA, ZnNa(3)DTPA), deferoxamine (DFO), deferiprone (L1), triethylenetetraamine (trientine), N-acetylcysteine (NAC), and Prussian blue (PB). Several new synthetic homologues and experimental chelating agents have been designed and tested in vivo for their metal binding effects. These include three groups of synthetic chelators, namely the polyaminopolycarboxylic acids (EDTA and DTPA), the derivatives of BAL (DMPS, DMSA and mono- and dialkylesters of DMSA) and the carbodithioates. Many factors have been shown to affect the efficacy of the chelation treatment in metal poisoning. Within this context it has been shown in experiments using young and adult animals that metal toxicity and chelation effects could be influenced by age. These findings may have a bearing in the design of new therapeutic chelation protocols for metal toxicity.

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Section: N-acetylcysteine (Nac)mentioning

confidence: 99%

Chelators as Antidotes of Metal Toxicity: Therapeutic and Experimental Aspects

Blanuša¹,

Varnai²,

Piasek³

et al. 2005

CMC

236

150

View full text Add to dashboard Cite

show abstract

“…Changes in the activity of several enzymes involved in antioxidant action, such as glutathione reductase (GR) [22], superoxide dismutase (SOD) [23], and catalase (CAT) [24] are indicative of mercury induced oxidative stress. Glutathione depletion [25, 26], resulting from complexation with mercurials is also a good but unspecific indicator of mercury effects.…”

Section: Introductionmentioning

confidence: 99%

Biomarkers of Adverse Response to Mercury: Histopathology versus Thioredoxin Reductase Activity

Branco

Ramos

Canário

et al. 2012

Journal of Biomedicine and Biotechnology

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Exposure to mercury is normally assessed by measuring its accumulation in hair, blood or urine. Currently, the biomarkers of effect that have been proposed for mercurials, such as coproporphyrines or oxidative stress markers, are not sensitive enough and lack specificity. Selenium and selenoproteins are important targets for mercury and thioredoxin reductase (TrxR) in particular was shown to be very sensitive to mercury compounds bothin vitroandin vivo. In this study we looked into the relation between the inhibition of thioredoxin reductase (TrxR) activity and histopathological changes caused by exposure to mercurials. Juvenile zeabra-seabreams were exposed to Hg2+or MeHg for 28 days and histopathological changes were analyzed in the liver and kidney as well as TrxR activity. Both mercurials caused histopathological changes in liver and kidney, albeit Hg2+caused more extensive and severe lesions. Likewise, both mercurials decreased TrxR activity, being Hg2+a stronger inhibitor. Co-exposure to Hg2+and Se fully prevented TrxR inhibition in the liver and reduced the severity of lesions in the organ. These results show that upon exposure to mercurials, histopathological alterations correlate with the level of TrxR activity and point to the potential use of this enzyme as a biomarker of mercury toxicity.

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“…Mercuric ions may be inactivating superoxide dismutase (SOD) enzymes or binding to glutathione, thus increasing the intracellular concentration of superoxide. Mercury is known to affect the expression and activity of SODs in animal models [13]. It is also possible that Hg 2+ forms a semi‐active complex with SoxR, containing mercury instead of iron ions.…”

Section: Discussionmentioning

confidence: 99%