ArticleToxicological sciences : an official journal of the Society of Toxicology2015
Mercury Reduces the Enzymatic Activity of Neprilysin in Differentiated SH-SY5Y Cells.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Mercury toxicity resulting from enzyme alterations- minireview.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Review
- Dopamine D1-Like Receptor Stimulation Induces CREB, Arc, and BDNF Dynamic Changes in Differentiated SH-SY5Y Cells.Neurochemical research · 2024Article
- Interaction of mercury species with proteins: towards possible mechanism of mercurial toxicology.Toxicology research · 2023Review
- Mercury and Alzheimer's disease: a look at the links and evidence.Metabolic brain disease · 2021Review
- The Function of the Metals in Regulating Epigenetics During Parkinson's Disease.Frontiers in genetics · 2020Review
- Fungicide Residues Exposure andEnvironmental health perspectives · 2020Article
- Insights into the Potential Role of Mercury in Alzheimer's Disease.Journal of molecular neuroscience : MN · 2019Review
- The Phenolic Components ofOxidative medicine and cellular longevity · 2018Article
- Biometal Dyshomeostasis and Toxic Metal Accumulations in the Development of Alzheimer's Disease.Frontiers in molecular neuroscience · 2017Review
- Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases.Frontiers in cellular neuroscience · 2015Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Levels of amyloid beta (Aβ) in the central nervous system are regulated by the balance between its synthesis and degradation. Neprilysin (NEP) is associated with Alzheimer's disease (AD) by its ability to degrade Aβ. Some studies have involved the exposure to mercury (Hg) in AD pathogenesis; therefore, our aim was to investigate the effects on the anabolism and catabolism of Aβ in differentiated SH-SY5Y cells incubated with 1-20 μM of Hg. Exposure to 20 µM of Hg induced an increase in Aβ-42 secretion, but did not increase the expression of the amyloid precursor protein (APP). Hg incubation (10 and 20 µM) increased NEP protein levels; however, it did not change NEP mRNA levels nor the levels of the amyloid intracellular domain peptide, a protein fragment with transcriptional activity. Interestingly, Hg reduced NEP activity at 10 and 20 µM, and circular dichroism analysis using human recombinant NEP showed conformational changes after incubation with molar equivalents of Hg. This suggests that the Hg-induced inhibition of NEP activity may be mediated by a conformational change resulting in reduced Aβ-42 degradation. Finally, the comparative effects of lead (Pb, 50 μM) were evaluated. We found a significant increase in Aβ-42 levels and a dramatic increase in APP protein levels; however, no alteration in NEP levels was observed nor in the enzymatic activity of this metalloprotease, despite the fact that Pb slightly modified the rhNEP conformation. Overall, our data suggest that Hg and Pb increase Aβ levels by different mechanisms.
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