Lactational exposure to inorganic mercury: Evidence of neurotoxic effects

Franco, Jeferson Luís; Braga, Hugo C.; Nunes, Adriana Kleist Clark; Ribas, Camila Mafalda; Stringari, James; Silva, Aline P.; Garcia, Solange Cristina; Moro, Ângela M.; Bohrer, Denise; Santos, Adair R.S.; Dafre, Alcir Luiz; Farina, Marcelo

doi:10.1016/j.ntt.2006.11.009

Cited by 40 publications

(22 citation statements)

References 49 publications

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“…The toxicity of Hg exposure is partly a function of enhanced oxidative stress (OS). Enhancement of OS probably arises from the inhibition of antioxidant enzymes and the consumption of thiol compounds (especially GSH) (Franco et al, 2007) giving rise to cell injury, damage to biomolecules, and lipid peroxidation (Leonard et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Al3+ and Hg2+ on Glucose 6-Phosphate Dehydrogenase From Capoeta Umbla Kidney

Kırıcı¹

2016

Appl Ecol Env Res

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Abstract. Glucose 6-phosphate dehydrogenase (EC 1.1.1.49; G6PD) is an important enzyme found in all mammal tissues, and produces NADPH in the metabolism. NADPH provides a reductive potential to maintain a balanced redox state within the cell. The aim of this study was to purify G6PD from Capoeta umbla kidney and determination of inhibition or activation effects of aluminium and mercury on enzyme activity. In this purpose, glucose 6-phosphate dehydrogenase was purified from Capoeta umbla kidney by using preparation of homogenate, ammonium sulphate precipitation and 2',5'-ADP Sepharose 4B affinity chromatography. Molecular weight of the enzyme was determined on sodium dodecyl sulphatepolyacrylamide gel electrophoresis (SDS-PAGE) and the purified enzyme showed a single band on the gel with a molecular weight of 75 kDa. Moreover, K i constants of Al 3+ and Hg 2+ were found as 0.98 ± 0.084 and 0.57 ± 0.019 mM, respectively. In conclusion, affinity of the Hg 2+ to the enzyme was higher than Al 3+

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Section: Introductionmentioning

confidence: 99%

The Effect of Al3+ and Hg2+ on Glucose 6-Phosphate Dehydrogenase From Capoeta Umbla Kidney

Kırıcı¹

2016

Appl Ecol Env Res

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“…Currently, our understanding of MeHg’s associations with the glutathione system, specifically the relative balance of reduced glutathione (GSH) and oxidized glutathione (glutathione disulfide, GSSG), is limited. One hypothesis is that MeHg lowers GSH levels (Franco et al, 2006, 2007; Grotto et al, 2010) by binding to sulfhydryl groups, reducing the availability of GSH, and GSH relative to GSSG, and increasing the accumulation of reactive oxygen species (Ercal et al, 2001; Wu et al, 2004). Alternatively, MeHg may induce oxidative stress by inhibiting the activity of antioxidant enzymes (e.g., glutathione peroxidase (GPX), glutathione reductase (GR), glutathione -S -transferase (GST), and catalase).…”

Section: Introductionmentioning

confidence: 99%

“…Alternatively, MeHg may induce oxidative stress by inhibiting the activity of antioxidant enzymes (e.g., glutathione peroxidase (GPX), glutathione reductase (GR), glutathione -S -transferase (GST), and catalase). Both human (Franco et al, 2007, 2009) and animal studies (Berntssen et al, 2003; Franco et al, 2009; Hoffman and Heinz, 1998; Larose et al, 2008) have found MeHg exposure associated with decreases in glutathione enzyme activities. Third, in response to MeHg exposure and binding to GSH, an organism may ramp up GSH production, by increasing the activity of GR, catalase, GPX and GST (Franco et al, 2006; Larose et al, 2008; Pinheiro et al, 2008; Woods and Ellis, 1995).…”

Section: Introductionmentioning

confidence: 99%

Mercury exposure and a shift toward oxidative stress in avid seafood consumers

Karimi

Vacchi-Suzzi

Meliker

2016

Environmental Research

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Mechanisms of mercury (Hg) toxicity at low doses from seafood consumption, the most common exposure route, are not well understood. We tested the hypothesis that seafood Hg exposure is related to a shift in redox status, indicated by a decrease in the ratio of reduced to oxidized glutathione (GSH:GSSG) in blood, or increase in redox potential (Eh). We also examined whether key seafood nutrients (selenium (Se), omega-3 fatty acids) confound or modify this shift. We measured blood concentrations of total Hg, Se, GSH, GSSG, and the Omega-3 Index (% omega-3s of total fatty acids in red blood cell membranes) in seafood consumers in Long Island, NY. We examined relationships between Hg, GSH:GSSG ratio and Eh. Elevated blood Hg (> 5.8 μg L−1) was associated with lower GSH:GSSG (β = −116.73, p = 0.01), with no evidence of confounding by Se or Omega-3 Index. However, in models stratified by Omega-3 Index levels, Hg-GSH:GSSG associations were weakened among those with high Omega-3 Index levels (> 6% of fatty acids, β = −63.46, p = 0.28), and heightened among those with low Omega-3 Index (β = −182.53, p < 0.01). We observed comparable patterns for Eh in relation to Hg. These results support the hypothesis that Hg exposure from seafood is linked to a shift in redox status toward oxidative stress, modified by omega-3 fatty acids in this population. Further work should examine the role of different seafood nutrients and Hg-induced shifts in redox status in the diverse health effects associated with elevated Hg exposure.

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“…5 Mercuric chloride is one of the most toxic forms of mercury because it easily forms organo-mercury complexes with proteins. 6 It is well known as hepatotoxic, 7 neurotoxic, 8 nephrotoxic, 9,10 hematotoxic 11 and genotoxic. 12 In addition, it is reported that mercuric chloride possesses adverse effects on the reproductive system in experimental animals.…”

Section: Introductionmentioning

confidence: 99%

Nephroprotective potential of selenium and taurine against mercuric chloride induced nephropathy in rats

et al. 2014

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Department of Hormones, National Research Centre, Cairo, Egypt AbstractThe study was aimed to estimate whether pre-treatment with sodium selenite or taurine would reverse kidney damage induced by intraperitoneal injection of mercuric chloride in rats. Animals were divided into six groups: (1) control group; (2) sodium selenite group; (3) taurine group; (4) HgCl 2 group; (5) sodium selenite pretreated group; (6) taurine pretreated group. The results demonstrated that HgCl 2 causes significant enhancement in serum malondialdehyde (MDA), creatinine, N-acetyl-beta-D-glucosaminidase (NAG), cystatin C, nephrin and interleukin 6 (IL-6) levels accompanied with significant reduction in serum nitric oxide (NO) level. Pretreatment with sodium selenite or taurine produces significant depletion in MDA, NAG, cystatin C, nephrin and IL-6 levels in concomitant with significant elevation in serum NO level as compared to HgCl 2 group. HgCl 2 induced pathological alterations in the kidney. The ultrastructural investigation of renal cortex of HgCl 2 -administered group revealed that the glomerular basement membrane is uniform, the fenestrations of endothelial cells are swollen, and the secondary foot processes appear also swollen even fused at some points. The proximal convoluted tubules showed apical short and few microvilli, while, some tubular cells showed relatively normal microvilli. In contrast, sodium selenite or taurine pretreatment could significantly reduce the pathological alterations in the kidney caused by HgCl 2 intoxication. The current results suggested that selenium and taurine possess nephroprotective efficacy due to their antioxidative capacity and anti-inflammatory activity.

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Lactational exposure to inorganic mercury: Evidence of neurotoxic effects

Cited by 40 publications

References 49 publications

The Effect of Al3+ and Hg2+ on Glucose 6-Phosphate Dehydrogenase From Capoeta Umbla Kidney

The Effect of Al3+ and Hg2+ on Glucose 6-Phosphate Dehydrogenase From Capoeta Umbla Kidney

Mercury exposure and a shift toward oxidative stress in avid seafood consumers

Nephroprotective potential of selenium and taurine against mercuric chloride induced nephropathy in rats

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